Showing papers on "Pulsatile flow published in 2000"
TL;DR: In older hypertensive patients, pulse pressure not mean pressure is the major determinant of cardiovascular risk, according to a meta-analysis based on individual patient data.
Abstract: Background: Current guidelines for the management of hypertension rest almost completely on the measurement of systolic and diastolic blood pressure. However, the arterial blood pressure wave is more correctly described as consisting of a pulsatile (pulse pressure) and a steady (mean pressure) component. Objective: To explore the independent roles of pulse pressure and mean pressure as determinants of cardiovascular prognosis in older hypertensive patients. Methods: This meta-analysis, based on individual patient data, pooled the results of the European Working Party on High Blood Pressure in the Elderly trial (n = 840), the Systolic Hypertension in Europe Trial (n = 4695), and the Systolic Hypertension in China Trial (n = 2394). The relative hazard rates associated with pulse pressure and mean pressure were calculated using Cox regression analysis, with stratification for the 3 trials and with adjustments for sex, age, previous cardiovascular complications, smoking, and treatment group. Results: A 10-mm Hg wider pulse pressure increased the risk of major cardiovascular complications; after controlling for mean pressure and the other covariates, the increase in risk ranged from approximately 13% for all coronary end points (P = .02) to nearly 20% for cardiovascular mortality (P = .001). In a similar analysis, mean pressure predicted the incidence of cardiovascular complications but only after removal of pulse pressure as an explanatory variable from the model. Furthermore, the probability of a major cardiovascular end point increased with higher systolic blood pressure; at any given level of systolic blood pressure, it also increased with lower diastolic blood pressure, suggesting that the wider pulse pressure was driving the risk of major complications. Conclusions: In older hypertensive patients, pulse pressure not mean pressure is the major determinant of cardiovascular risk. The implications of these findings for the management of hypertensive patients should be further investigated in randomized controlled outcome trials in which the pulsatile component of blood pressure is differently affected by antihypertensive drug treatment. Arch Intern Med. 2000;160:1085-1089
579 citations
TL;DR: The pulsatile flow in an anatomically realistic compliant human carotid bifurcation was simulated numerically and showed good agreement in both computed and measured wall movement, demonstrating the quantitative influence of the vessel wall motion.
312 citations
TL;DR: Pulsatile linear stretch in vitro causes marked upregulation of proteins that form electrical and mechanical junctions, as well as a concomitant increase in propagation velocity that may contribute to arrhythmogenesis in myocardium exposed to acute stretch.
Abstract: Mechanical stretch is thought to play an important role in remodeling atrial and ventricular myocardium and may produce substrates that promote arrhythmogenesis. In the present work, neonatal rat ventricular myocytes were cultured for 4 days as confluent monolayers on thin silicone membranes and then subjected to linear pulsatile stretch for up to 6 hours. Action potential upstrokes and propagation velocity (theta) were measured with multisite optical recording of transmembrane voltage of the cells stained with the voltage-sensitive dye RH237. Expression of the gap junction protein connexin43 (Cx43) and the fascia adherens junction protein N-cadherin was measured immunohistochemically in the same preparations. Pulsatile stretch caused dramatic upregulation of intercellular junction proteins after only 1 hour and a further increase after 6 hours (Cx43 signal increased from 0.73 to 1.86 and 2.02% cell area, and N-cadherin signal increased from 1.21 to 2.11 and 2.74% cell area after 1 and 6 hours, respectively). This was paralleled by an increase in theta from 27 to 35 cm/s after 1 hour and 37 cm/s after 6 hours. No significant change in the upstroke velocity of the action potential or cell size was observed. Increased theta and protein expression were not reversible after 24 hours of relaxation. Nonpulsatile (static) stretch produced qualitatively similar but significantly smaller changes than pulsatile stretch. Thus, pulsatile linear stretch in vitro causes marked upregulation of proteins that form electrical and mechanical junctions, as well as a concomitant increase in propagation velocity. These changes may contribute to arrhythmogenesis in myocardium exposed to acute stretch.
214 citations
TL;DR: PVC MRI is an accurate technique to quantify pulsatile blood flow at a specific location and can be used to noninvasively calculate Qp and Qs under normal flow conditions.
Abstract: Quantification of blood flow in vessels provides valuable information that aids management decisions in a variety of cardiac conditions. Current flow measurement techniques are often limited by accuracy, time resolution, convenience, or anatomic localization. This study examined the accuracy of a commercially available phase-velocity cine magnetic resonance imaging (PVC MRI) technique to quantify flow rate in a pulsatile flow phantom. In addition, the equivalence of PVC MRI measurements of pulmonary and systemic flow was evaluated in children and adults without any pathologic shunt. Using a pulsatile flow phantom, volume flow rates measured by PVC MRI were compared to those by a transit-time ultrasound flowmeter over a range of flow rates (1.25–3.5 L/min, 13 trials). Close agreement was found between these techniques (y= 1.02x− 0.02, r= 0.99, Bland–Altman bias =−0.045 L/min, 95% limits of agreement =−0.19–0.10 L/min). Twenty subjects (median age 12.8 years, range 0.7–49 years) with no pathologic shunt underwent PVC MRI measurement of blood flow in the main pulmonary artery (Qp) and the ascending aorta (Qs). Data processing time for each location was 20 minutes. The Qp/Qs ratio closely approximated unity (mean = 0.99, SD = 0.10, range 0.85–1.19). Interobserver agreement was excellent (Bland–Altman bias = 0.09 L/min, 95% limits of agreement = 0.15–0.33 L/min). PVC MRI is an accurate technique to quantify pulsatile blood flow at a specific location. It can be used to noninvasively calculate Qp and Qs under normal flow conditions.
190 citations
TL;DR: Direct portal vein sampling in humans revealed that the interpulse interval of insulin pulses in humans is about 5 min, and this frequency is also observed when sampling from the systemic circulation using a highly specific insulin assay and 1-min sampling, but is about 4-fold greater than the frequency observed at this site using single site RIAs.
Abstract: Insulin is secreted in a high frequency pulsatile manner. These pulses are delivered directly into the portal vein and then undergo extraction and dilution before delivery into the systemic circulation. The reported frequency of these insulin pulses estimated in peripheral blood varies from an interpulse interval of 4-20 min. We postulated that this discrepancy is due to the attenuation of the pulse signal in the systemic circulation vs. the portal circulation. In the present study we measured pulsatile insulin release directly in the portal circulation of human subjects who had indwelling transjugular intrahepatic portasystemic stent shunts (TIPSS) to decompress portal hypertension. We quantitated pulsatile insulin secretion in both the overnight fasted state (fasting) and during a hyperglycemic clamp (8 mmol/L). Direct portal vein sampling established that pulsatile insulin secretion in humans has an interval (periodicity) of approximately 5 min. The amplitude (and mass) of the insulin concentration oscillations observed in the portal vein was approximately 5-fold greater than that observed in the arterialized vein and was similar to that observed in the dog. Increased insulin release during hyperglycemia was achieved through amplification of the insulin pulse mass. In conclusion, direct portal vein sampling in humans revealed that the interpulse interval of insulin pulses in humans is about 5 min, and this frequency is also observed when sampling from the systemic circulation using a highly specific insulin assay and 1-min sampling, but is about 4-fold greater than the frequency observed at this site using single site RIAs. We confirm that enhanced insulin release in response to hyperglycemia is achieved by amplification of these high frequency pulses.
179 citations
TL;DR: This new device accurately monitors BP, heart rate, and locomotor activity in conscious, untethered, freely moving mice living in their home cages for periods of at least 150 days.
Abstract: A simple and reliable means for accurate, chronic measurement of pulsatile blood pressure (BP) from conscious, freely moving laboratory mice was developed and validated. The newly developed device ...
176 citations
TL;DR: It was found that the geometry of the carotid bifurcation was highly complex, involving helical curvature and out‐of‐plane branching, which resulted in patterns of flow and wall shear stress significantly different from those found in simplified planar carotids bIfurcation models.
Abstract: The carotid bifurcation is a common site for clinically significant atherosclerosis, and the development of this disease may be influenced by the local hemodynamic environment. It has been shown that vessel geometry and pulsatile flow conditions are the predominant factors that determine the detailed blood flow patterns at the carotid bifurcation. This study was initiated to quantify the velocity profiles and wall shear stress (WSS) distributions in an anatomically true model of the human carotid bifurcation using data acquired from magnetic resonance (MR) imaging scans of an individual subject. A numerical simulation approach combining the image processing and computational fluid dynamics (CFD) techniques was developed. Individual vascular anatomy and pulsatile flow conditions were all incorporated into the computer model. It was found that the geometry of the carotid bifurcation was highly complex, involving helical curvature and out-of-plane branching. These geometrical features resulted in patterns of flow and wall shear stress significantly different from those found in simplified planar carotid bifurcation models. Comparisons between the predicted flow patterns and MR measurement demonstrated good quantitative agreement.
174 citations
TL;DR: In this paper, the influence of three rheology models (i.e., Newtonian, power law and Quemada) on axisymmetric flow through a tube with a smooth local area reduction of 75% is considered.
171 citations
TL;DR: The relative pressure map calculated for pulsatile flow in a compliant phantom was shown to be consistent with independent pressure transducer measurements and the feasibility of performing 4D pressure mapping in vivo is demonstrated.
Abstract: We describe here a method for generating relative pressure maps from magnetic resonance velocity data in three spatial and one temporal dimension (4D). The relative pressure map calculated for pulsatile flow in a compliant phantom was shown to be consistent with independent pressure transducer measurements. The feasibility of performing 4D pressure mapping in vivo is also demonstrated. J. Magn. Reson. Imaging 2000;12: 321‐329. © 2000 Wiley-Liss, Inc.
165 citations
TL;DR: The stress phase angle (SPA), which characterizes the dynamics of the mechanical force pattern applied to the endothelial cell layer, shows that CS and WSS are more out of phase in the coronaries than in any other region of the circulation, suggesting that in addition to WSS, SPA may play a role in localization of coronary atherosclerosis.
Abstract: The endothelial cells (ECs) lining a blood vessel wall are exposed to both the wall shear stress (WSS) of blood flow and the circumferential strain (CS) of pulsing artery wall motion. These two forces and their interaction are believed to play a role in determining remodeling of the vessel wall and development of arterial disease (atherosclerosis). This study focused on the WSS and CS dynamic behavior in a compliant model of a coronary artery taking into account the curvature of the bending artery and physiological radial wall motion. A three-dimensional finite element model with transient flow and moving boundaries was set up to simulate pulsatile flow with physiological pressure and flow wave forms characteristic of the coronary arteries. The characteristic coronary artery curvature and flow conditions applied to the simulation were: aspect ratio (lambda) = 10, diameter variation (DV) = 6 percent, mean Reynolds number (Re) = 150, and unsteadiness parameter (alpha) = 3. The results show that mean WSS is about 50 percent lower on the inside wall than the outside wall while WSS oscillation is stronger on the inside wall. The stress phase angle (SPA) between CS and WSS, which characterizes the dynamics of the mechanical force pattern applied to the endothelial cell layer, shows that CS and WSS are more out of phase in the coronaries than in any other region of the circulation (-220 deg on the outside wall, -250 deg on the inside wall). This suggests that in addition to WSS, SPA may play a role in localization of coronary atherosclerosis.
142 citations
TL;DR: The DeBakey VAD unloads the LV, which leads to a decrease in LV end-diastolic LV diameter and to the restoration of RV function, which provides a nearly physiological pulsatile flow despite the continuous flow of the VAD.
Abstract: Background —Ventricular assist devices (VADs) are an accepted therapy for patients with end-stage heart failure. The implantable devices that are available produce a pulsatile flow and are very large. In 6 patients, beginning in November 1998, we started to use the continuous-flow implantable DeBakey VAD device, which weighs 93 g. To detect the flow in peripheral vessels, we measured transcranial Doppler signals in patients after implantation.
Methods and Results —Transcranial Doppler studies were performed with the MULTI-DOP X4 device with two 2-MHz probes (for the middle cranial arteries) in 4 patients for up to 12 weeks twice weekly after implantation. The blood velocity was measured, and the pulsation index (PI) calculated. The measured pump flow and rotations per minute were registered. The preoperative echocardiographic assessment values were compared with those acquired 6 weeks after implantation. The PI increased continually in all patients after VAD implantation, left ventricular (LV) ejection fraction did not improve, but right ventricular (RV) ejection fraction after implantation improved compared with preoperative values. The LV end-diastolic diameter after implantation decreased between 11% and 46% intraindividually. There was no correlation between PI and blood pressure or, except in 1 patient, between PI and blood flow through the VAD.
Conclusions —The DeBakey VAD unloads the LV, which leads to a decrease in LV end-diastolic LV diameter and to the restoration of RV function. The unloaded LV and partially recovered RV provide a nearly physiological pulsatile flow despite the continuous flow of the VAD. Pulsatility is independent of peripheral vascular resistance. The first clinical experience with the DeBakey VAD was positive and has resulted in its continued use.
TL;DR: In this article, a mathematical model of non-linear two-dimensional blood flow in tapered arteries in the presence of stenosis is developed, where the vascular wall deformability is taken to be elastic while the flowing blood contained in it is treated to be Newtonian.
Abstract: A mathematical model of non-linear two-dimensional blood flow in tapered arteries in the presence of stenosis is developed. An improved shape of the time-variant overlapping stenosis present in the tapered arterial lumen is given mathematically in order to update resemblance to the in vivo situation. The vascular wall deformability is taken to be elastic while the flowing blood contained in it is treated to be Newtonian. The non-linear terms appearing in the Navier–Stokes equations governing blood flow and the instantaneous taper angle are accounted for. The present analytical treatment bears the potential to calculate both the axial and the radial velocity profiles with low computational complexity by exploiting the appropriate boundary conditions and the input pressure gradient arising from the normal functioning of the heart. The computed results are found to converge at a high rate with the tolerance of ∼10−14 and agree well with the corresponding existing data. An extensive quantitative analysis is performed through numerical computations of the desired quantities presented graphically at the end of the paper which help estimating the effects of tapering, the wall motion, the stenosis and the pulsatile pressure gradient on the flow characteristics of blood and thereby the applicability of the present model is established.
TL;DR: These data are the first to demonstrate an increase in nocturnal leptin and GH-induced IGF-I secretion prior to the onset of puberty in the agonadal male monkey and that these developmental changes occur independent of the gonadal influences.
Abstract: The factor(s) responsible for initiating the developmental increase in nocturnal gonadotropin-releasing hormone secretion, defining the onset of puberty, are not known. Although signals regulating prepubertal growth seem to be obvious candidates to control such a process, it is unclear whether prepubertal alterations occur in these growth-related factors such that they might provide the brain information on changing body size. Using samples analyzed previously describing the initiation of nocturnal pulsatile LH secretion in agonadal male monkeys , developmental changes in plasma concentrations of leptin, GH, and insulin-like growth factor I (IGF-I) were determined to test the hypothesis that an increase in circulating levels of one or all of these growth-derived signals precedes the onset of puberty. Hormone concentrations were determined in five juvenile males at 10-day intervals from approximately 60 days before and 50 days after the initiation of pulsatile nocturnal LH secretion. Leptin concentrations ...
TL;DR: The smallest turbulence length scale, which offers a more reliable estimate of the effects of turbulence on blood cell damage, was three times the size of red blood cells and five times thesize of platelets, which suggests that there is more direct interaction with the blood cells, thus causing more damage.
Abstract: This study was focused on a series of in vitro tests on the turbulent flow characteristics of three bileaflet aortic valves: St. Jude Medical (SJM), CarboMedics (CM), and Edwards Tekna (modified Duromedics, DM). The flow fields of the valves were measured in a pulsatile flow model with a laser-Doppler anemometer (LDA) at the aortic sinus area downstream of the valves. The heart rate was set at 70 beats per minute, the cardiac output was maintained at 5 liters per minute, and the aortic pressure wave forms were kept within the physiological range. Cycle-resolved analysis was applied to obtain turbulence data, including mean velocity, Reynolds stresses, autocorrelation coefficients, energy spectral density functions, and turbulence scales. The Reynolds shear stresses of all three valves induced only minor damage to red blood cells, but directly damaged the platelets, increasing the possibility of thrombosis. The smallest turbulence length scale, which offers a more reliable estimate of the effects of turbulence on blood cell damage, was three times the size of red blood cells and five times the size of platelets. This suggests that there is more direct interaction with the blood cells, thus causing more damage.
TL;DR: In addition to systolic and diastolic blood pressures, other hemodynamic indices that have particular relevance for cardiac complications and that originate from pulsatile pressure should be taken into account, with important consequences in cardiovascular epidemiology and in the pathophysiology of hypertensive end-organ damage.
Abstract: Systolic and diastolic blood pressures are the exclusive mechanical factors usually considered as predictors of cardiovascular risk in populations of normotensive and hypertensive subjects at large. However, if hypertension is considered as a mechanical factor acting on the arterial wall with substantial deleterious consequences, the totality of the blood pressure curve should be considered in order to investigate the cardiovascular risk. The purpose of this review is to show that in addition to systolic and diastolic blood pressures, other hemodynamic indices that have particular relevance for cardiac complications and that originate from pulsatile pressure should be taken into account, with important consequences in cardiovascular epidemiology and in the pathophysiology of hypertensive end-organ damage.
TL;DR: This study shows that elevated ureteral pressure, likely acting via interstitial pressure, diminishes the conductance of the renal vascular bed, and the cyclic patterns of flow are altered, resulting in elevated resistive index values.
Abstract: The aim of this study was to evaluate the influence of elevated ureteral pressure on renal arterial distention, and thereby on the Doppler resistive index. Seven isolated rabbit kidneys were subjected to a pulsatile perfusion while the renal pelvis was pressurized via the ureter. Renal vascular pressure, flow, resistance (pressure/flow) and conductance (flow/pressure) were compared to simultaneous resistive index measurements using linear regression analysis. Changes in the Conductance Index (systolic conductance - diastolic conductance/systolic conductance) were likewise compared to the resistive index. Elevations in ureteral pressure were significantly correlated with (1) increased resistive index values, (2) increased mean renal vascular resistance, (3) decreased mean conductance, and (4) increased conductance index values (for all correlations P < 0.05). The increases in the resistive index correlated significantly with increases in the conductance index. This study shows that elevated ureteral pressure, likely acting via interstitial pressure, diminishes the conductance of the renal vascular bed. Because this effect is more dramatic at diastole, the cyclic patterns of flow are altered, resulting in elevated resistive index values. The results indicate the importance of the interaction between vascular distensibility and pulsatile flow, rather than overall mean renal vascular resistance, in determining resistive index values.
TL;DR: PVR was significantly elevated by erbstatin A but not by calmidazolium, suggesting that flow-induced vasodilation was largely caused by tyrosine kinase inhibitor-sensitive activation of NO synthase, indicating that pulsatility significantly enhances the basal and flow-stimulated EDNO release in the peripheral vasculature under in vivo conditions.
Abstract: The effects of pulsatility in blood flow on endothelium-derived nitric oxide (EDNO) release in the peripheral vasculature were investigated. The basal and flow-stimulated EDNO release were compared...
TL;DR: A novel real-time servo-controlled perfusion system that exposes endothelial cells grown in nondistensible or distensible tubes to realistic pulse pressures and phasic shears at physiological mean pressures provides the first in vitro application of realistic mechanical pulsatile forces on vascular cells.
Abstract: We developed a novel real-time servo-controlled perfusion system that exposes endothelial cells grown in nondistensible or distensible tubes to realistic pulse pressures and phasic shears at physio...
TL;DR: The analysis of high-resolution flow profiles allows detection of early hemodynamic changes even at degrees of stenoses not associated with a reduction of mean flow, and Rmax(1/2) allows differentiation of the grade of hemodynamic compromise for a given morphologic stenosis independent ofmean flow in a single comprehensive MR examination.
Abstract: . In a noninvasive comprehensive magnetic resonance (MR) examination, the morphologic degree of renal artery stenosis was correlated to corresponding changes in renal artery flow dynamics. Different degrees of stenosis were created with the use of a chronically implanted inflatable arterial cuff in seven dogs. For each degree of stenosis, an ultrafast three-dimensional gadolinium MR angiography with high spatial resolution was performed, followed by cardiac-gated MR flow measurements with high temporal resolution for determination of pulsatile flow profiles and mean flow. Flow was also measured by a chronically implanted flow probe. In three of the dogs, trans-stenotic pressure gradients (ΔP) also were measured via implanted catheters. Five different degrees of stenosis could be differentiated in the MR angiograms (0%, 30%, 50%, 80%, >90%). The MR flow data agreed with the flow probe within ±20%. Stenoses between 30 and 80% gradually reduced the early systolic peak (Max 1 ) of the flow profile but only minimally affected the midsystolic peak (Max 2 ) or mean flow. Stenoses of more than 90% significantly depressed mean flow by more than 50%. The ratio between Max 1 and Max 2 (Rmax 1/2 ) gradually fell with the degree of stenosis. The onset of significant mean flow reduction and ΔP was indicated by a drop of Rmax 1/2 below 1 to 1.2. Thus, the analysis of high-resolution flow profiles allows detection of early hemodynamic changes even at degrees of stenoses not associated with a reduction of mean flow. Rmax 1/2 allows differentiation of the grade of hemodynamic compromise for a given morphologic stenosis independent of mean flow in a single comprehensive MR examination.
TL;DR: It is demonstrated that failure to respond adequately with regular oscillatory insulin secretion to recurrent high-frequency and (near)-physiological glucose excursion is a manifest feature of beta-cell malfunction in type 2 diabetes.
Abstract: Insulin is released in high-frequency pulsatile bursts at intervals of 6-13 min. Intrapancreatic mechanisms are assumed to coordinate pulsatile insulin release, but small oscillations in plasma glucose concentrations may contribute further. To gain additional insight into beta-cell (patho)physiology, we explored the ability of repetitive small glucose infusions (6 mg/kg over 1 min every 10 min) to modify rapid pulsatile insulin secretion in 10 type 2 diabetic individuals (plasma glucose 9.3 +/- 1.0 mmol/l, HbA1c 7.9 +/- 0.5%, mean +/- SE) and 10 healthy subjects. All subjects were investigated twice in randomly assigned order: during saline and during glucose exposure. Blood was collected every minute for 90 min to create a plasma insulin concentration time-series for analysis using 3 complementary algorithms: namely, spectral analysis, autocorrelation analysis, and approximate entropy (ApEn). During saline infusion, none of the algorithms were able to discriminate between diabetic and control subjects (P > 0.20). During glucose entrainment, spectral density peaks (SP) and autocorrelation coefficients (AC) increased significantly (P < 0.001), and ApEn decreased (P < 0.01), indicating more regular insulin time-series in the healthy volunteers. However, no differences were observed in the diabetic individuals between the glucose and saline conditions. Furthermore, in spite of identical absolute glucose excursions (approximately 0.3 mmol/l) glucose pulse entrainment led to a complete (SP: 4.76 +/- 0.62 [range 2.08-7.60] vs. 17.24 +/- 0.93 [11.70-20.58], P < 0.001; AC: 0.01 +/- 0.05 [0.33-0.24] vs. 0.64 +/- 0.05 [0.35-0.83], P < 0.001) or almost complete (ApEn: 1.59 +/- 0.02 [1.48-1.67] vs. 1.42 +/- 0.05 [1.26-1.74], P < 0.005) separation of the insulin time-series in diabetic and control subjects. Even elevating the glucose infusion rate in the diabetic subjects to achieve comparable relative (and hence higher absolute) glucose excursions (approximately 4.9%) failed to entrain pulsatile insulin secretion in this group. In conclusion, the present study demonstrates that failure to respond adequately with regular oscillatory insulin secretion to recurrent high-frequency and (near)-physiological glucose excursion is a manifest feature of beta-cell malfunction in type 2 diabetes. Whether the model will be useful in unmasking subtle (possible prediabetic) defects in beta-cell sensitivity to glucose drive remains to be determined.
Journal Article•
TL;DR: Results indicate that NO is continuously released in human choroidal and ONH vessels.
Abstract: PURPOSE There is evidence from animal studies that nitric oxide (NO) is a major determinant of ocular blood flow. In humans NO synthase inhibition reduces pulsatile choroidal blood flow, but no data on optic nerve head (ONH) vasculature are available yet. The goal of this study was to investigate the effects of NO synthase inhibition on human choroidal and ONH blood flow using laser Doppler flowmetry. METHODS The study design was a randomized, placebo-controlled, double-masked, balanced three-way crossover. On separate study days 12 healthy male subjects received infusions of N:(G)-nitro-L-arginine (L-NMMA; either 3 mg/kg over 5 minutes followed by 30 microg/kg per minute over 55 minutes or 6 mg/kg over 5 minutes followed by 60 microg/kg per minute over 55 minutes) or placebo. The effects of L-NMMA or placebo on choroidal and ONH blood flow were measured with laser Doppler flowmetry. In addition, laser interferometric measurement of fundus pulsation was performed in the macula to assess pulsatile choroidal blood flow. RESULTS L-NMMA reduced all outcome parameters in the choroid and the ONH. The higher dose of L-NMMA caused a significant decrease in blood flow in the choroid (-26% +/- 9%; P: < 0.001) and the ONH (-20% +/- 16%; P: < 0.001) as evidenced from laser Doppler flowmetry and a significant decrease in fundus pulsation amplitude (-26% +/- 5%; P: < 0.001). CONCLUSIONS These results indicate that NO is continuously released in human choroidal and ONH vessels.
01 Jan 2000
TL;DR: Variations in the patterns of pulsatile activity are important determinants of both basal secretion and acute responses of the HPA axis, with consequent impact upon the response to acute stimuli.
Abstract: A stress-free automated blood sampling system has been employed to demonstrate pulsatile hypothalamo-pituitary-adrenal (HPA) activity in the rat. In females, pulses of corticosterone secretion occur approximately once/hour throughout the 24 h cycle, with variation in pulse amplitude underlying a diurnal rhythm. Males show smaller pulses of secretion which become widely spaced during the early light phase nadir. Ageing does not affect the occurrence of pulses but the diurnal variation is lost. Analysis of the relationship between the HPA response to an acute noise stress and its coincidence with the various phases of the pulse, suggests that pulsatile activity arises from alternating periods of activation and suppression. Responses to i.v. corticotropin-releasing factor are not affected by pulse phase, indicating that this relationship is not generated at the pituitary-adrenal level. This phase relationship holds for all strains of rat except the hyperresponsive Fischer-344 in which an exaggerated stress response arises from a lack of phase-dependent suppression. Patterns of pulsatile activity are also modulated by neonatal programming or chronic HPA activation arising from adjuvant-induced arthritis, with consequent impact upon the response to acute stimuli. Thus, variations in the patterns of pulsatile activity are important determinants of both basal secretion and acute responses of the HPA axis.
TL;DR: A 33‐year‐old patient presented with an incapacitating pulsatile tinnitus of 6 months' duration in the left ear and the radiological workup evidenced an aneurysm of the left sigmoid sinus.
Abstract: We report a newly evidenced cause of venous pulsatile tinnitus--the aneurysm of a dural sigmoid sinus. A 33-year-old patient presented with an incapacitating pulsatile tinnitus of 6 months' duration in the left ear. The radiological workup evidenced an aneurysm of the left sigmoid sinus. Selective endovascular coil occlusion of the aneurysm was followed by complete resolution of the tinnitus.
TL;DR: In this article, it was shown that under the steady flow conditions, a recirculating vortex occupied the entire circular bulge with its core located closer to the distal end of the bulge and the strength of the vortex would increase as the Reynolds number increased but would not exceed more than 10% of the bulk flow in the parent tube.
TL;DR: It is concluded that the FPA is a valid index of pulsatile choroidal perfusion in humans on the basis of the strong correlation between laser interferometry measurements of FPA and pneumotonometric measurements of PA and POBF.
Abstract: Purpose Several methods have been proposed for the investigation of the human choroidal circulation. The aim of the present study was to compare laser interferometric measurements of cardiac synchronous fundus pulsations with pneumotonometric measurements of intraocular pressure pulse and pulsatile ocular blood flow in humans. Methods The association between fundus pulsation amplitude as assessed with laser interferometry and pulse amplitude (PA) and pulsatile ocular blood flow (POBF) as assessed with pneumotonometry was investigated in 28 healthy subjects. Additionally, we investigated the distribution of fundus pulsation amplitude (FPA) in a region of -15° to + 15° around the macula (n = 18) and the influence of accommodation paralysis with cyclopentolate on FPA (n = 10). Results There was a high association between FPA and PA (r = 0.86, p < 0.001) and FPA and POBF (r = 0.70, p < 0.001). Fundus pulsations in the macula were significantly smaller than in the optic disc, but significantly larger than those in peripheral regions of the retina. Administration of cyclopentolate did not influence FPA. Conclusions On the basis of the strong correlation between laser interferometric measurements of FPA and pneumotonometric measurements of PA and POBF, we conclude that the FPA is a valid index of pulsatile choroidal perfusion in humans.
TL;DR: Pulsatile stretch activates ERK1/2 in the arterial wall via pathways different from those induced by steady overstretch, and levels in freshly isolated vessels were equivalent to the levels found in pulsatile vessels.
Abstract: Increased steady intraluminal pressure in blood vessels activates the extracellular signal-regulated kinase (ERK)1/2 pathway. However, signal transduction of pulsatile stretch has not been elucidated. Using an organ culture model of rabbit aorta, we studied ERK1/2 activation by pulsatility in vessels maintained at 80 mm Hg for 24 hours. ERK1/2 activity was evaluated by in-gel kinase assays and by Western blot. Compared with control aortas without pulsatility, aortas submitted to a pulsatile 10% variation in vessel diameter displayed a significant increase in ERK1/2 activity (207+/-12%, P<0.001), which remained high after removal of the endothelium. Unlike steady overstretch, pulsatile stretch-induced activation of ERK1/2 was not modified by herbimycin A, a Src family tyrosine kinase inhibitor, but was reduced by other tyrosine kinase inhibitors, tyrphostin A48 and genistein (162+/-27% and 144+/-14%, respectively). Conversely, ERK1/2 activity was markedly decreased in pulsatile vessels treated with staurosporine (114+/-18%) although neither of the more specific protein kinase C inhibitors, Ro-31-8220 or Go-6976, blocked ERK1/2 activation (209+/-24% and 238+/-34%, respectively), whereas staurosporine had no effect on steady overstretch-induced ERK1/2 activation. Pulsatility induced superoxide anion generation, which was prevented by the NADPH oxidase inhibitor diphenyleneiodonium. Furthermore, polyethylene glycol-superoxide dismutase completely abolished ERK1/2 activation by pulsatility (114+/-12%). Finally, ERK1/2 and O(2)(-) levels in freshly isolated vessels were equivalent to the levels found in pulsatile vessels. In conclusion, pulsatile stretch activates ERK1/2 in the arterial wall via pathways different from those induced by steady overstretch. Pulsatility might be considered a physiological stimulus that maintains a certain degree of ERK1/2 activation via oxygen-derived free radical production.
TL;DR: The liver does not appear to play an important role in detecting glucoprivic action of 2DG to suppress pulsatile LH secretion, suggesting that an important glucose-sensing mechanism is located circumventricularly in the fourth ventricle.
Abstract: Changes in glucose availability are proposed to modulate pulsatile GnRH secretion, and at least two anatomical sites, the liver and hindbrain, may serve as glucose sensors. The present study determined the relative importance of these putative glucose-sensing areas in regulating pulsatile LH secretion in the sheep. Our approach was to administer the antimetabolic glucose analog, 2-deoxy-D-glucose (2DG) into either the hepatic portal vein or the fourth ventricle in gonadectomized females in which LH pulse frequency was high. In the first study, a catheter was placed in the ileocolic vein to determine the effects of local injection of 2DG into the hepatic portal system on the release of LH. After monitoring the pattern of LH secretion for 4 h, 2DG (250 mg/kg) was infused (500 microl/min) into the liver for 2 h. For comparison, animals were also given the same dose of 2DG into a jugular vein for 2 h. Administration of 2DG into either the hepatic portal or jugular vein reduced LH pulse frequency to the same extent. Infusion of the lower dose (50 mg/kg) locally into the hepatic portal vein did not affect plasma LH profiles. Collectively, these results are interpreted to indicate that the liver does not contain special glucose-sensing mechanisms for the glucoprivic suppression of LH pulses. In the second study, 2DG (5 mg/kg) was infused (50 l/min) for 30 min into the fourth ventricle or lateral ventricle. During the subsequent 4-h sampling period, pulsatile LH secretion was significantly suppressed, but there was no significant difference in LH pulse frequency between sites of infusion. Peripheral 2DG concentrations were not detectable after either fourth or lateral ventricle infusions, indicating that the 2DG had acted centrally to suppress LH pulses. Plasma cortisol concentrations increased more in animals infused with 2DG into the fourth ventricle than in those infused into the lateral ventricle, suggesting that 2DG infused into lateral ventricle is transported caudally into the fourth ventricle and acts within the area surrounding the fourth ventricle. Overall, these findings suggest that an important glucose-sensing mechanism is located circumventricularly in the fourth ventricle. Moreover, the liver does not appear to play an important role in detecting glucoprivic action of 2DG to suppress pulsatile LH secretion.
TL;DR: A group of three-dimensional computational models of the shunt have been investigated under steady-state and pulsatile conditions by means of a finite element analysis to quantify the effects of shunt diameter, curvature, angle, and pulsatility on the pressure-flow relationship of theShunt.