Showing papers on "Pulsatile flow published in 1993"

Arterial alterations with aging and high blood pressure. A noninvasive study of carotid and femoral arteries.

Abstract: Noninvasive in situ evaluations of pulsatile changes of blood pressure and arterial diameter were performed at the sites of the common carotid and femoral arteries in a population of 78 untreated normotensive and hypertensive subjects. Arterial segments were studied by using an original echo-tracking technique for internal diameter and validated applanation tonometry for local pulse pressure measurements. Whereas mean arterial pressure is known to be identical in all parts of the arterial tree, pulse pressure was significantly lower in the carotid (52.7 +/- 2.2 mm Hg) than in the brachial (62.0 +/- 2.0 mm Hg) or femoral (62.5 +/- 2.5 mm Hg) arteries. Despite a higher pulse pressure and diastolic diameter, the femoral artery had a lower pulsatile change in diameter (3.47 +/- 0.18% versus 6.07 +/- 0.28%; p < 0.0001) and distensibility coefficient (9.36 +/- 0.58 versus 21.60 +/- 1.75 x 10(-3) kPa-1) than the carotid artery. Local cross-sectional compliance of the carotid artery was higher than that of the femoral artery (7.42 +/- 0.46 versus 6.20 +/- 0.28 m2.kPa-1.10(-7); p < 0.05). Whereas age was strongly correlated with arterial parameters at the site of the carotid artery (pulse pressure: r = 0.54, p < 0.0001; pulsatile change in arterial diameter: r = -0.62, p < 0.0001; distensibility coefficient: r = -0.70, p < 0.0001), no significant correlation was observed at the femoral artery. Mean blood pressure was the second factor of carotid artery alterations: the higher the mean blood pressure, the lower the distensibility of this artery (r = -0.36, p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Role of nitric oxide in the control of luteinizing hormone-releasing hormone release in vivo and in vitro

Abstract: Nitric oxide (NO) synthase, the enzyme which converts arginine into citrulline plus NO, a highly active free radical, has been found in many neurons in the brain, including neurons in the hypothalamus. Our previous experiments showed that norepinephrine-induced prostaglandin E2 release from hypothalamic explants incubated in vitro is mediated by NO. Since the release of luteinizing hormone-releasing hormone (LHRH) is also driven by norepinephrine and prostaglandin E2, we hypothesized that NO might also control pulsatile release of LHRH in vivo, resulting in turn in pulsatile release of luteinizing hormone (LH). To ascertain the role of NO in control of pulsatile LH release in vivo, an inhibitor of NO synthase, NG-monomethyl-L-arginine (NMMA), was microinjected into the third cerebral ventricle (1 mg/5 microliters) of conscious castrate male rats at time 0 and 60 min later; blood samples were taken every 10 min during this period. NMMA blocked pulsatile LH release within 20 min, and plasma LH concentration declined further without pulses after the injection at 60 min. Pulsatile release of LH was not altered in diluent-injected controls. NMMA did not alter pulsatile release of follicle-stimulating hormone, which suggests that its release does not require NO. Incubation of medial basal hypothalami with norepinephrine (10 microM) induced an increase in LHRH release that was inhibited by NMMA (300 microM). NMMA alone did not alter basal LHRH release, whereas it was augmented by sodium nitroprusside (100 microM), which releases NO spontaneously. This augmentation was prevented by hemoglobin (2 micrograms/ml), which binds the NO released by nitroprusside. Our previous experiments showed that norepinephrine-induced release of prostaglandin E2 is mediated by NO. Nitric oxidergic neurons were visualized in the median eminence adjacent to the LHRH terminals. The combined in vivo and in vitro results indicate that the pulsatile release of LHRH induced by norepinephrine is brought about by alpha 1-adrenergic activation of NO synthase. NO then induces prostaglandin E2 release that activates exocytosis of LHRH secretory granules into the portal vessels to induce pulsatile LH release.

Cerebrospinal fluid circulation and associated intracranial dynamics. A radiologic investigation using MR imaging and radionuclide cisternography.

Abstract: UNLABELLED AIMS OF THE PRESENT INVESTIGATION: Observations made in a preliminary study of pulsatile cerebrospinal fluid (CSF) and brain motions using MR imaging called for a reconsideration of the CSF flow model currently accepted. The following questions were addressed: 1) The nature of the CSF-circulation, e.g., the magnitude and pattern of pulsatile and bulk flow; 2) The driving forces of the CSF circulation and assessment of the role of associated hemodynamics and brain motions; 3) The major routes for the absorption of CSF. MATERIAL AND METHODS CSF flow and associated hemodynamics were studied using gated MR imaging, in 26 healthy volunteers, 5 patients with communicating hydrocephalus and 10 with benign intracranial hypertension. Radionuclide cisternography was performed in 10 individuals with venous vasculitis. RESULTS AND CONCLUSIONS 1) The CSF-circulation is propelled by a pulsating flow, which causes an effective mixing. This flow is produced by the alternating pressure gradient, which is a consequence of the systolic expansion of the intracranial arteries causing expulsion of CSF into the compliant and contractable spinal subarachnoid space. 2) No bulk flow is necessary to explain the transport of tracers in the subarachnoid space. 3) The main absorption of the CSF is not through the Pacchionian granulations, but a major part of the CSF transportation to the blood-stream is likely to occur via the paravascular and extracellular spaces of the central nervous system. 4) The intracranial dynamics may be regarded as the result of an interplay between the demands for space by the four components of the intracranial content, i.e. the arterial blood, brain volume, venous blood and the CSF. This interaction is shown to have a time offset within the cerebral hemispheres in a fronto-occipital direction during the cardiac cycle (the fronto-occipital "volume wave"). 5) The outflow from the cranial cavity to the cervical subarachnoid space (SAS) is dependent in size and timing on the intracranial arterial expansion during systole. Similarly, the outflow from the aqueduct mirrors the brain expansion. The brain expansion is typically very small as evident from the minute aqueductal flow observed in healthy individuals. This expansion occurs simultaneously with an inflow of CSF and will be directed inwards towards the ventricular system. The brain expansion is of decisive importance for the formation of the normal transcerebral pressure gradient. 6) The instantaneous increase of flow in the superior sagittal sinus at the beginning of the systole reflects a direct pressure transmission via the SAS from the expanding arteries to the cerebral veins. It is contended that this early increase in venous pressure together with the volume wave is most likely an important prerequisite for sustaining normal intracranial pressure (ICP) and normal cerebral blood flow. This counter pressure should be reduced in hydrocephalus due to the decreased arterial expansion and could explain the reduced blood flow as well as an increased transmantle pressure gradient causing the ventricular dilatation. An increased pressure in the venous system is likely to be the cause of increases in ICP, including the increased pressure observed in benign intracranial hypertension (BIH).

Pulsatile and steady flow induces c-fos expression in human endothelial cells.

Abstract: The effects of pulsatile and steady fluid flow on the mRNA levels of proto-oncogenes c-fos, c-jun, and c-myc in cultured human umbilical vein endothelial cells (HUVEC) were investigated. c-fos mRNA levels in stationary cultures were very low. A 1 Hz pulsatile flow with an average shear stress of 16 dynes/cm2 induced a dramatic increase of c-fos mRNA levels in HUVEC 0.5 h after the onset of flow, which declined rapidly to basal levels within 1 h. Steady flow with a similar shear stress also induced a transient increase of c-fos mRNA levels, but to a lesser extent. In addition, increased c-fos mRNA levels were observed when low shear (2-6 dynes/cm2) was replaced by high shear (16-33 dynes/cm2). Pulsatile and steady flow caused a slight increase of c-jun and c-myc mRNA levels. The role of pulsatility was also investigated in platelet-derived growth factor (PDGF) expression. Pulsatile flow induced a transient increase of PDGF A- and B-chain mRNA levels with peaks at 1.5-2 h. Pulsatile flow, which was more stimulatory in mediating c-fos expression, however, was less stimulatory than steady flow in mediating PDGF expression. By using various inhibitors, protein kinase C was found to be an important mediator in flow-induced c-fos expression, with the involvement of G proteins, phospholipase C, and intracellular calcium. Protein kinase C was previously shown as a possible major mediator in flow-induced PDGF expression which, at least partly, appeared to follow the induction mechanism of c-fos, suggesting a possible connection between c-fos and PDGF induction. However, the c-fos antisense treatment, which significantly inhibited c-fos transcription, failed to block the flow-induced PDGF expression, suggesting that flow-induced c-fos expression may not play an important role in the mechanism of flow-induced PDGF expression. The difference in the induction of c-fos and PDGF expression under pulsatile as compared to steady flow indicates that a complex, flow-mediated regulatory mechanism of gene expression exists in HUVEC. The increased expression of these proto-oncogenes mediated by flow may be important in regulating long-term cellular responses.

On the Pulsatile Nature of Intracranial and Spinal CSF-Circulation Demonstrated by MR Imaging

Abstract: Cerebrospinal fluid (CSF) flow was studied in 24 healthy volunteers using gated MR phase imaging. The subarachnoid space (SAS) was divided into 5 compartments depending on the magnitude of the pulsatile CSF flows: a high velocity compartment in the area of the brain stem and spinal cord, 2 slow ones at the upper and lower extremes of the SAS, and finally 2 intermediate velocity compartments in between. The main pulsatile spinal flow channel had a meandering pattern. The extraventricular CSF-circulation can be explained by pulsatile CSF flow without the necessity of assuming existence of a net flow. A successive time offset during the cardiac cycle has been found in the fronto-occipital direction of the interplay between the arterial expansion, brain expansion, volume changes of the CSF spaces and of the veins. It is proposed to name this time offset the intracranial “volume wave” (VoW).

Hemodynamic Patterns in Two Models of End-to-Side Vascular Graft Anastomoses: Effects of Pulsatility, Flow Division, Reynolds Number, and Hood Length

Abstract: Flow behavior in models of end-to-side vascular graft anastomoses was studied under steady and pulsatile flow conditions. Models were constructed to simulate geometries employed in experimental studies on intimal thickening in a canine model. Reynolds numbers, division of flow in the outflow tracts and the pulsatile waveform employed were taken from measurements obtained in the canine model. Flows in the scaled-up, transparent models were visualized with white, neutrally buoyant particles which were photographed under laser illumination and also recorded on video tape under bright incandescent light. Strong, three-dimensional helical patterns which formed in the anastomotic junction were prominent features of the flow fields. Regions of low wall shear, oscillatory wall shear and long particle residence time were identified from the flow visualization experiments. Comparisons with the limited qualitative data available on intimal thickening in vascular graft anastomoses suggest a relation between localization of vascular intimal thickening and those surfaces experiencing low shear and long particle residence time.

Calcium antagonists differently inhibit proliferation of human coronary smooth muscle cells in response to pulsatile stretch and platelet-derived growth factor.

Abstract: BACKGROUND Vascular smooth muscle cell proliferation is the key event of coronary artery disease. Mechanical forces, in particular, pulsatile stretch and platelet-derived growth factor, may play an important role. METHODS AND RESULTS Vascular smooth muscle cells were cultured from the media of human left descending coronary arteries obtained from organ donors using the explant method. To study effects of pulsatile stretch on vascular smooth muscle cell proliferation, a computer-controlled in vitro pulsatile stretch device was used. Cells were seeded onto Flex I culture plates with deformable membranes and exposed to pulsatile stretch (60 cycles per minute) and/or growth factors. Proliferation of smooth muscle cells was determined by 3H-thymidine incorporation. Pulsatile stretch markedly stimulated 3H-thymidine incorporation of coronary smooth muscle cells (180 +/- 15 to 432 +/- 27 cpm/10(5) cells; P CONCLUSIONS Pulsatile stretch and platelet-derived growth factor are potent stimuli for proliferation of coronary smooth muscle cells. The selective inhibitory effect of a Ca2+ antagonist on smooth muscle cell proliferation stimulated by platelet-derived growth factor but not by pulsatile stretch may explain why the drugs have only modest antiatherogenic effects in patients with coronary artery disease.

Comparison of exogenous gonadotropins and pulsatile gonadotropin-releasing hormone for induction of ovulation in hypogonadotropic amenorrhea.

Abstract: To compare the efficacy and safety of ovulation induction with exogenous gonadotropins vs. pulsatile GnRH in patients with hypogonadotropic amenorrhea, results from 30 patients in 111 cycles of gonadotropins and 41 patients in 118 cycles of pulsatile GnRH were analyzed retrospectively. Exogenous gonadotropins were administered using an individually adjusted protocol, using a starting dose of 150 IU. Pulsatile GnRH was delivered iv at a physiological frequency based upon our normative data. The doses administered ranged from 75-250 ng/kg. Preovulatory serum estradiol (E2) and luteal phase progesterone (P) levels were compared to those in normal cycling women (n = 87). The mean body mass index, age, and baseline gonadotropin levels were similar in the two groups. Overall ovulatory rates and conception rates per cycle and per patient were not significantly different between the two groups. However, the cumulative chance of conception after six cycles of treatment by life table analysis appeared to be higher with pulsatile GnRH treatment (96%) than with exogenous gonadotropins (72%). The risk of multiple gestation was also higher with exogenous gonadotropins (14.8% vs. 8.3%), although this was not statistically significant. All higher order multiple gestations (triplets or more) occurred in the gonadotropin-treated group. More than two dominant follicles were seen on ultrasound in 47.6% of gonadotropin-treated cycles compared to 18.9% of cycles with pulsatile GnRH treatment (P < 0.01). Three or more follicles were seen in 16.6% of the gonadotropin cycles compared to 5.4% with pulsatile GnRH (P < 0.05). No case of severe ovarian hyperstimulation was observed in either group, although the mean luteal phase ovarian size was significantly higher in the gonadotropin group (P < 0.05). Mean peak preovulatory E2 levels were significantly higher in the gonadotropin group (1684.5 +/- 124.4 vs. 1315.3 +/- 74.9 pmol/L; P < 0.05). The mean luteal phase P level 1 week after ovulation was significantly higher than normal in the gonadotropin group (84.9 +/- 10.8 vs. 61.1 +/- 3.2 nmol/L; P < 0.05), but was not significantly different from that in the pulsatile GnRH group (70.3 +/- 6.0 nmol/L). We conclude that pulsatile GnRH, when compared to exogenous gonadotropins, results in high rates of ovulation and conception, but a decreased risk of multiple folliculogenesis, higher order multiple gestations, and ovarian enlargement.(ABSTRACT TRUNCATED AT 400 WORDS)

Non‐invasive measurement of pulsatile vessel diameter change and elastic properties in human arteries: a methodological study,

Abstract: A recently developed ultrasound phase-locked echo-tracking system makes it possible to measure non-invasive pulsatile vessel diameter changes, and, in combination with blood-pressure measurement, to calculate pressure strain elastic modulus (Ep) and stiffness (beta). The reproducibility in measurements of pulsatile diameter changes with this system was evaluated. Also the precision of indirect blood-pressure measurements, as compared to the simultaneously measured intra-arterial blood pressure was tested. The resulting reproducibility in pressure strain elastic modulus (Ep) and stiffness (beta) was evaluated. Intra-observer variabilities in measuring pulsatile diameter changes were 16% for the abdominal aorta, 10% for the common carotid artery, and 15% for the common femoral artery, respectively. Intra-observer variabilities for Ep and beta were 21% for both in the abdominal aorta, 17% for both in the common carotid artery, and 18% for both in the common femoral artery, respectively. There were only small differences in indirect and direct measurement of systolic blood pressure, whereas indirect blood pressure measurement systematically overestimated the diastolic blood pressure, on average by 20%. The variabilities in indirect blood pressure measurements were 2% for the systolic and 3% for the diastolic blood pressure, respectively. Inter-observer variability in the investigation of the common carotid artery was 10% for the pulsatile diameter changes, and 21% and 23% for Ep and beta, respectively. Thus, the echo-tracking system represents a reliable system for estimation of pressure strain elastic modulus and stiffness. However, Ep and beta are systematically underestimated by 25-30%, when used in combination with indirect blood pressure measurements.

Hepatic blood flow during cardiopulmonary bypass.

Abstract: OBJECTIVES To establish the effects of different modes of cardiopulmonary bypass on hepatic blood flow, with the aim of increasing understanding of the hemodynamic factors that may lead to hepatic dysfunction in patients after cardiopulmonary bypass. The anatomical and physiologic characteristics that are unique to the hepatic circulation are also reviewed, together with an account of the known specific effects on the liver of several hemodynamic stimuli that are commonly present during cardiopulmonary bypass. DATA SOURCES The entire world literature on the subjects of clinical and experimental cardiopulmonary bypass, extracorporeal circulation, blood gas tensions, hypothermia, hypotension, and hepatic blood flow was searched via Index Medicus, up to and including 1991. DATA EXTRACTION Data are presented only from those studies that employed sound cardiopulmonary bypass or blood flow measurement technique. For investigations on hypothermia, data for temperatures < 28 degrees C are not included. Details of one recent experimental study in the dog by the author are highlighted, in which the relative effects of pump flow rate, temperature, and type of perfusion (pulsatile or nonpulsatile) are presented; the data are critically compared and contrasted with those data obtained by earlier workers. DATA SYNTHESIS Hepatic hemodynamics are characterized by a dual supply of blood from the hepatic artery, actively controlled within the liver, and the portal vein, principally regulated by prehepatic resistance vessels. Portal flow may modulate the hepatic arterial circulation through the "hepatic arterial buffer response." Hypotension caused by hemorrhage causes a decrease in portal blood flow but hepatic arterial flow is maintained by autoregulation and by the "buffer" response. Hypothermia (28 degrees C) has little effect on hepatic arterial flow, but portal flow may increase. During cardiopulmonary bypass, total liver blood flow is better maintained at a pump flow rate of 2.4 than at 1.2 L/min/m2. Perfusion at 28 degrees C causes an increase in portal flow and a slight decrease in hepatic arterial flow. Total hepatic blood flow is better preserved during cardiopulmonary bypass at 1.2 L/min/m2 by pulsatile than by nonpulsatile flow; however, no significant difference was noted between pulsatile and nonpulsatile perfusion at a bypass flow rate of 2.4 L/min/m2, particularly at 28 degrees C. CONCLUSIONS During cardiopulmonary bypass, hepatic blood flow is better maintained by high pump flow than by low pump flow rates. Hypothermic cardiopulmonary bypass may benefit the hepatic circulation, although the additional advantages usually gained by the use of pulsatile perfusion may be partly lost when hypothermia is combined with a high pump flow rate.

Flow characteristics of hepatic tumors at color Doppler sonography: correlation with arteriographic findings.

Abstract: We studied benign and malignant hepatic tumors with color Doppler sonography and arteriography in order to correlate color Doppler flow characteristics with tumor hemodynamics (vascularity, arteriovenous shunting, and portal vein involvement) shown by arteriography. We also evaluated the usefulness of color Doppler flow characteristics in discriminating between tumor types.We performed color Doppler sonography and hepatic arteriography in 58 patients with 72 hepatic lesions larger than 2.0 cm in diameter. Differences in pulsatile flow (peritumoral or intratumoral) and the highest systolic peak flow velocities reached were evaluated on color Doppler sonograms and compared with arteriographic findings.Color flow sonograms were obtained in 43 of 45 hepatocellular carcinomas, 15 of 16 cholangiocellular carcinomas or hepatic metastases, and six of 11 hemangiomas. Mixed peritumoral and intratumoral pulsatile flow was shown by arteriography in highly vascular tumors. The mean peak systolic flow velocity seen in ...

Influence of infusion pump operation and flow rate on hemodynamic stability during epinephrine infusion.

Abstract: OBJECTIVE To determine whether variations in the flow rate of epinephrine solutions administered via commonly available infusion pumps lead to significant variations in blood pressure (BP) in vivo. DESIGN Prospective, randomized, crossover study with factorial design, using infusion pumps with four different operating mechanisms (pulsatile diaphragm, linear piston/syringe, cyclic piston-valve, and linear peristaltic) and three drug delivery rates (1, 5, and 10 mL/hr). SUBJECTS Two healthy, mixed-breed dogs (12 to 16 kg). INTERVENTIONS Dogs were made hypotensive with methohexital bolus and continuous infusion. BP was restored to normal with constant-dose epinephrine infusion via two pumps at each rate. MEASUREMENTS Femoral mean arterial pressure (MAP) was recorded every 10 secs. Pump-flow continuity was quantitated in vitro using a digital gravimetric technique. Variations in MAP and flow continuity were expressed by the coefficient of variation; analysis of variance was used for comparisons. RESULTS The mean coefficients of variations for MAP varied from 3.8 +/- 3.1% (linear piston/syringe) to 6.1 +/- 6.6% (linear peristaltic), and from 3.4 +/- 2.2% (10 mL/hr) to 7.9 +/- 6.6% (1 mL/hr). The coefficients of variation for in vitro flow continuity ranged from 9 +/- 8% (linear piston-syringe) to 250 +/- 162% (pulsatile diaphragm), and from 35 +/- 44% (10 mL/hr) to 138 +/- 196% (1 mL/hr). Both the type of pump and infusion rate significantly (p < .001) influenced variation in drug delivery rate. The 1 mL/hr infusion rate significantly (p < .01) influenced MAP variation. Cyclic fluctuations in MAP of < or = 30 mm Hg were observed using the pulsatile diaphragm pump at 1 mL/hr. CONCLUSION Factors inherent in the operating mechanisms of infusion pumps may result in clinically important hemodynamic fluctuations when administering a concentrated short-acting vasoactive medication at slow infusion rates.

Simple calculation of the velocity profiles for pulsatile flow in a blood vessel using mathematica

Abstract: The numerical solution of Womersley flow can provide important physical insights to the student of Biofluid dynamics. This computer program is less than 70 lines and can be entered rapidly without extensive knowledge of Mathematica. Through manipulations, the effect of changes in the unsteadiness parameter, Reynolds number, and waveform shape on the pulsatile hemodynamics in straight tubes, can be explored. The exercise reinforces the importance of unsteady forces on the complex processes of physiologic flow and illustrates the usefulness of computers in fluid mechanics analyses.

Measurement of mean velocity during pulsatile flow using time-averaged maximum frequency of doppler ultrasound waveforms

Abstract: It has been suggested that mean velocity of flow could be estimated by the time-averaged maximum frequency over an integral number of cardiac cycles (Gill 1985). The present study verified this theory experimentally with a computer-controlled flow phantom. The effects of some parameters on the relationship between mean velocity and time-averaged maximum frequency were also studied. Parameters investigated included beam-vessel angle, diameter of tubing, pulsatility, flow rate and stenosis. The velocities measured by the Doppler system were compared with the actual velocities. A simple theoretical model was also developed to compare with the experimental results. The results showed that, in a long straight tube, the mean velocity can be estimated to within about 5% from the time-averaged maximum Doppler shift at various flow rates and pulsatilities. The error due to geometrical spectral broadening, especially for large beam-vessel angles, can be estimated to within 3% and therefore corrected.

Right ventricular-vascular interaction in congestive heart failure. Importance of low-frequency impedance.

Abstract: BACKGROUND Vasodilator agents are widely used in congestive heart failure. These agents may have important effects on the pulsatile aspects of right ventricular hydraulic load. METHODS AND RESULTS Fifteen patients with severe congestive heart failure were studied during cardiac catheterization by use of high-fidelity pressure transducers and a catheter-mounted flow velocity probe. Three graded doses of nitroprusside were infused as pulmonary artery (PA) pressure and flow were continuously recorded. From Fourier transforms of signal-averaged waves, PA impedance, hydraulic power, and wave reflection indices were derived. At the highest dose of nitroprusside (66 +/- 41 micrograms/min), cardiac output was significantly improved, whereas PA mean and wedge pressure, resistance, impedance at the first harmonic, characteristic impedance, and wave reflection amplitude were all reduced. At the dose (32 +/- 20 micrograms/min) at which cardiac output first showed improvement, only PA mean pressure and first-harmonic impedance were significantly reduced. Hydraulic power cost per unit of forward flow was also lowered at this dose, despite lack of significant change in pulmonary vascular resistance. At the lowest dose of nitroprusside (11 +/- 4 micrograms/min), six patients experienced a decrease in stroke volume, whereas the other nine were either unchanged (n = 1) or showed an increase (n = 8). Multiple regression revealed that only the change in first-harmonic impedance correlated with this effect, increasing when stroke volume decreased and decreasing when stroke volume increased (P = .02). The change in first-harmonic impedance at this dose appeared to be caused by alterations in the amplitude of PA wave reflections. At higher doses, changes in mean PA pressure (but not in pulmonary vascular resistance) correlated with changes in stroke volume. CONCLUSIONS Nitroprusside vasodilation at low doses alters PA hemodynamics in congestive heart failure primarily through changes in low-frequency impedance. In some patients, this effect is associated with decreased stroke output. At higher doses, favorable alterations in resistance, low- and high-frequency impedance, and wave reflections all contribute to increased forward flow and decreased power requirement per unit forward flow. These findings show that ventricular-vascular interaction is importantly affected by pulmonary vasodilation and that appreciation of pulsatile properties is required to understand the effects of pulmonary vasodilation on cardiac output.

Development of a miniature intraventricular axial flow blood pump.

Abstract: A new intraventricular axial flow blood pump has been designed and developed as a totally implantable left ventricular assist device (LVAD). This pump consists of an impeller combined with a guide-vane, a tube housing, and a DC motor. The pump is introduced into the LV cavity through the LV apex, and the outlet cannula is passed antegrade across the aortic valve. Blood is withdrawn from the LV through the inlet ports at the pump base, and discharged to the ascending aorta. Our newly developed axial flow pump system has the following advantages: 1) it is a simple and compact system, 2) minimal blood stasis both in the device and the LV cavity, 3) minimal blood contacting surface of the pump, 4) easy accessibility with a less invasive surgical procedure, and 5) low cost. A pump flow > 5 L/min was obtained against 100 mmHg differential pressure in the mock circulatory system. The pump could produce a passive pulsatile flow effect with a beating heart more efficiently than other non-pulsatile pumps because of minimal pressure drop and inertia along the bypass tract. Anatomic fit studies using dissected hearts of dilated cardiomyopathy (DCM) cadavers showed that this pump could smoothly pass through the aortic valve without any interference with mitral valve function. Recently, a dynamic pressure groove bearing and a miniature lip seal have been developed. The dynamic pressure groove bearing has a simple structure and acts as a pressure resistant sealing mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Non-responsiveness of serum gonadotropins and testosterone to pulsatile GnRH in hemochromatosis suggesting a pituitary defect.

Abstract: We investigated the potential pituitary origin of gonadal insufficiency in hemochromatosis. Gonadotropin secretion was studied in seven patients with hemochromatosis and hypogonadism, before and after chronic pulsatile GnRH therapy. Pulsatile LH secretion was studied before (sampling every 10 min for 6 h) and after 15-30 days of chronic pulsatile GnRH therapy (10-12 micrograms per pulse). Prior to GnRH therapy, all the patients had low serum testosterone, FSH and LH levels. LH secretion was non-pulsatile in four patients, while a single pulse was detected in the remaining three. Chronic pulsatile GnRH administration did not increase serum testosterone levels; similarly, serum LH levels remained low: neither pulse frequency nor pulse amplitude was modified. We conclude that hypogonadism in hemochromatosis is due to pituitary lesions.

Cyclic variation of the power of ultrasonic Doppler signals backscattered by polystyrene microspheres and porcine erythrocyte suspensions

Abstract: Factors affecting the power of the ultrasonic Doppler signal within the flow cycle have been evaluated experimentally using a pulsatile flow loop model. Polystyrene microspheres and porcine red cells suspended in saline solution for hematocrits between 2 and 40% were used as scattering fluid in the flow model. Experiments were performed at mean flow velocities of 11, 64, and 76 cm/s. In laminar flow experiments performed at a mean velocity of 11 cm/s, no variation of the Doppler power was found for both polystyrene microspheres and red cell suspensions (40% hematocrit). When turbulence was induced in the flow model, the power increasing during systole, a maximum was observed early after peak systole, and a decrease was obtained in diastole during deceleration of flow. >