Showing papers in "American Journal of Physiology-heart and Circulatory Physiology in 1979"
674 citations
TL;DR: An empirical equation is found that can be used to predict VO2 from PVA, which is equivalent to the area (PVA) bounded by the end-systolic and end-diastolic P-V curves and the systolic limb of the P- V loop trajectory in theP-V plane.
Abstract: Mechanical energy (ENG) required by a time-varying elastance model of the ventricle was compared with oxygen consumption per beat (VO2) of the canine left ventricle contracting under a variety of loading conditions. ENG needed for this model to increase its elastance during systole is shown to be equal to the sum of the potential energy built in the elastance during systole plus the external mechanical stroke work. This ENG is equivalent to the area (PVA) bounded by the end-systolic and end-diastolic P-V curves and the systolic limb of the P-V loop trajectory in the P-V plane. There was a high correlation (r = 0.89) between VO2s documented in the literature and PVAs assessed by the author from the accompanying P-V data from both isovolumic and ejecting contractions in 11 hearts. A linear regression analysis yielded an empirical equation: VO2 (ml O2/beat) = a . PVA (mmHg . ml/beat) + b, where a = 1.37 X 10(-5) and b = 0.027, which can be used to predict VO2 from PVA. A preliminary experimental study in my laboratory confirmed the validity of this empirical equation.
401 citations
TL;DR: The quantitative relations between capillary red cell flux, arterial hematocrit, and total blood flow could be explained by a two-element model of microvascular blood flow that incorporated a relatively slow-moving plasma layer (1.2 micrometer).
Abstract: Microvascular hematocrit and its possible relation to oxygen supply were systematically examined. We studied the red cell volume fraction (hematocrit) in arterial blood and in capillaries under a v...
350 citations
TL;DR: As peak pumping ability markedly declined from 52 to 90 wk of age in the spontaneously hypertensive rats, the free wall of the left ventricle greatly thickened whereas the septum remained unchanged, which may contribute to the decrease in pumping ability observed in long-standing hypertension.
Abstract: To determine the effects of a chronic pressure load on cardiac function and morphology, spontaneously hypertensive rats (SHR) and two normotensive strains of Wistar rats (WKY and NWR) were studied under ether anesthesia at 13, 25, 52, and 90 wk of age. Although resting cardiac index of the SHR was comparable to that of WKY and NWR at all ages, the peak cardiac output and peak stroke volume per gram of left ventricle determined during a rapid intravenous infusion of Tyrode solution was markedly reduced in the SHR only at 90 wk of age. Autonomic inhibition did not alter the peak stroke volume attained, but reduced peak cardiac output at all ages in each of the strains. Absolute left ventricular dimensions in the SHR increased out of proportion to body growth, consistent with concentric hypertrophy. As peak pumping ability markedly declined from 52 to 90 wk of age in the SHR, the free wall of the left ventricle greatly thickened whereas the septum remained unchanged. At this time the right ventricle also hypertrophied. This disproportionate thickening of the walls of the left ventricle and the hypertrophy of the right ventricle were reflected in measurements of their fiber diameters. These alterations in ventricular architecture may contribute to the decrease in pumping ability observed in long-standing hypertension.
237 citations
TL;DR: Despite streamline blood flow within the fetal thoracic inferior vena cava, organ blood flows can be accurately measured with either an umbilical venous or an abdominal inferior v Rena caval injection of microspheres when either is combined with the appropriate reference arterial blood samples.
Abstract: In 16 chronically prepared fetal lambs we compared the systemic distribution of ductus venosus blood flow with that of abdominal inferior vena caval blood by simultaneously injecting microspheres labeled with different radionuclides into an umbilical vein and into the abdominal inferior vena cava. A significantly greater proportion of ductus venosus blood flow than of abdominal inferior vena caval blood flow supplied the brain, heart, and upper body; this resulted from streaming of ductus venosus blood flow within the thoracic inferior vena cava with preferential direction of that blood flow through the foramen ovale. Blood flows to upper and lower body structures and placenta calculated from umbilical venous microsphere injections and reference arterial blood samples did not differ from those computed fromabdominal inferior vena caval injections and reference samples. Thus, despite streamline blood flow within the fetal thoracic inferior vena cava, organ blood flows can be accurately measured with either an umbilical venous or an abdominal inferior vena caval injection of microspheres when either is combined with the appropriate reference arterial blood samples.
191 citations
TL;DR: During Ca2+ depletion, the mechanisms responsible for regulating calcium influx are either lost or inactivated, so that reperfusion-induced changes are governed solely by the driving force favoring calcium influx.
Abstract: Myocardial cation contents were measured in isolated rat hearts perfused under various conditions. Reperfusion of Ca2+-deprived hearts produced marked increases in myocardial Ca2+ and Na+ and decreases in Mg2+ and K+ contents. These changes were dependent on the Ca2+ concentration and duration of perfusion during the periods of Ca2+ deprivation and reperfusion. The loss of Ca2+ and K+ contents normally seen after Ca2+-free exposure as well as the reperfusion-induced changes were prevented if the Ca2+-free medium contained low (35 mM) Na+ or was cooled to 21 degrees C. Reperfusion with normal Ca2+, low Na+ medium augmented the increase in myocardial Ca2+ content, while reducing K+ or Mg2+ or increasing Mg2+ in the reperfusion medium had no effect. Addition of verapamil, D600, or propranolol to the reperfusion solution did not alter the reperfusion-induced cation changes observed using control medium. These data suggest that during Ca2+ depletion, the mechanisms responsible for regulating calcium influx are either lost or inactivated, so that reperfusion-induced changes are governed solely by the driving force favoring calcium influx. The occurrence of Ca2+ overload under this condition has been implicated in the irreversible damage to myocardium and contractile failure.
176 citations
171 citations
TL;DR: It is demonstrated that adaptive changes in the cardiovascular and sympatho-adrenal medullary systems of repeatedly immobilized rats are greater in SHR than in WKY rats.
Abstract: Blood pressure, heart rate, and circulating levels of norepinephrine, epinephrine, and corticosterone were measured before and during the first or seventh period of immobilization stress (150 min per day) in spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) normotensive male rats. A catheter was inserted into the tail artery of each rat to permit direct measurement of blood pressure and heart rate and serial sampling of blood in conscious, unhandled animals. During the first immobilization, SHR rats had significantly higher circulating levels of norepinephrine, epinephrine, and corticosterone than did WKY rats. One day after the sixth immobilization, basal levels of norepinephrine and epinephrine were significantly higher and mean blood pressure was significantly lower in repeatedly stressed SHRs compared to unstressed SHRs. In addition, adaptation to the repeated stress in SHRs was attended by reduced adrenomedullary secretion and an increased blood pressure response. These results demonstrate that adaptive changes in the cardiovascular and sympatho-adrenal medullary systems of repeatedly immobilized rats are greater in SHR than in WKY rats.
132 citations
TL;DR: Using the resting lamb as a model, the mechanisms that are called into play during this period to maintain oxygen delivery are studied, finding that at rest cardiac output varies as a result of the changing need for oxygen.
Abstract: After birth a decrease in hemoglobin concentration occurs while high metabolic demands are imposed on the infant by the extrauterine environment. Using the resting lamb as a model, we studied the mechanisms that are called into play during this period to maintain oxygen delivery. Measurements were made of oxygen consumption, arterial and mixed venous blood oxygen contents, cardiac output, hemoglobin concentration, percent fetal hemoglobin, 2,3-diphosphoglycerate, and hemoglobin oxygen affinity during the first two postnatal months. There was a rapid decrease in hemoglobin concentration after birth and concomitant decrease in hemoglobin oxygen affinity, changes similar to those described in humans. Cardiac output and oxygen consumption were both very high immediately after birth and declined in parallel, so that arteriovenous oxygen content difference was constant. Thus at rest cardiac output varies as a result of the changing need for oxygen. This relationship is independent of hemoglobin concentration or oxygen affinity within the normal range. If, however, oxygen demands were increased, oxygen delivery might be compromised by a limited ability to increase oxygen extraction during the immediate newborn period or when hemoglobin concentration is lowest.
127 citations
TL;DR: An intact sympathetic nervous system plays an essential role in the development of salt-induced increase in blood pressure in Dahl S rats and the hypothesis that "chemical sympathectomy" with 6-hydroxydopamine (6-OHDA) prevents salt- induced hypertension and increased vascular resistance in S rats is examined.
Abstract: Salt-induced hypertension in Dahl's genetically hypertensive rat has been attributed to humoral or renal factors. However, a recent study from our laboratory suggested that neurogenic mechanisms co...
112 citations
TL;DR: Sympathetic stimulation in pithed rats elicits increases in blood pressure and plasma levels of catecholamines, but the NE at sympathetic nerve endings is responsible for the increase in BP.
Abstract: Sympathetic stimulation in pithed rats elicits increases in blood pressure (BP) and plasma levels of catecholamines. The BP is proportional to the logarithm of the plasma norepinephrine (NE) concentration. Adrenal medullectomy diminishes slightly only the initial phase of the BP responses, whereas bretylium blocks completely the BP response and diminishes by about 70% the increase in plasma NE. Adrenal medullectomy completely prevents the increase in plasma epinephrine (Epi) and diminishes by 30% plasma NE. Plasma levels of NE appear to reflect sympathetic neuronal activity, but the NE at sympathetic nerve endings is responsible for the increase in BP. Epi released from the adrenal medulla may enhance and accelerate the initial BP response, but plays only a minor role after the first 15 s.
TL;DR: Tissue analysis indicated altered circulatory status secondary to HCO in liver, kidney, spleen, and lung, and plasma epinephrine and norepinephrine levels were significantly elevated in HCO suggesting enhanced sympathetic as well as adrenal catecholamine release.
Abstract: A model for high output heart failure (HCO) was developed in male, Sprague-Dawley rats using an abdominal aortocaval shunt equal to 50% of total cardiac output (CO) with 2 mo of postsurgical recove...
TL;DR: To determine the possible role that endogenously produced prostaglandins may play in the regulation of cerebral blood flow, the responses of cerebral precapillary vessels to prostag landins were studied in cats equipped with cranial windows for direct observation of the microvasculature.
Abstract: To determine the possible role that endogenously produced prostaglandins may play in the regulation of cerebral blood flow, the responses of cerebral precapillary vessels to prostaglandins (PG) D2, E2, G2, and I2 (8.1 X 10(-8) to 2.7 X 10(-5) M) were studied in cats equipped with cranial windows for direct observation of the microvasculature. Local application of PGs induced a dose-dependent dilation of large (greater than or equal to 100 microns) and small (less than 100 microns) arterioles with no effect on arterial blood pressure. The relative vasodilator potency was PGG2 greater than PGE2 greater than PGI2 greater than PGD2. With all PGs, except D2, the percent dilation of small arterioles was greater than the dilation of large arterioles. After application of prostaglandins in a concentration of 2.7 X 10(-5) M, the mean +/- standard error of the percent dilation of large and small arterioles was, respectively, 47.6 +/- 2.7 and 65.3 +/- 6.1 for G2, 34.1 +/- 2.0, and 53.6 +/- 5.5 for E2, 25.4 +/- 1.8, and 40.2 +/- 4.6 for I2, and 20.3 +/- 2.5 and 11.0 +/- 2.2 for D2. Because brain arterioles are strongly responsive to prostaglandins and the brain can synthesize prostaglandins from its large endogenous pool of prostaglandin precursor, prostaglandins may be important mediators of changes in cerebral blood flow under normal and abnormal conditions.
TL;DR: The isolated perfused rat heart was utilized to determine the maximum rate of adenosine incorporation into adenine nucleotides and the effect of ischemia on this rate, which appeared to represent ATP turnover in aerobic and postischemic hearts.
Abstract: The isolated perfused rat heart was utilized to determine the maximum rate of adenosine incorporation into adenine nucleotides and the effect of ischemia on this rate. In aerobic hearts, the rates of [8-14C]adenosine incorporation into nucleotides in nanomoles/minute per gram dry tissue were ATP 34 +/- 2, ADP 6 +/- 0.4, AMP 3 +/- 0.3, and IMP, 1 +/- 0.2. Following ischemia these values were not significantly different except for the rate of incorporation into IMP, which doubled. The extent of adenosine deamination with one pass through the coronary vasculature was the same in aerobic and postischemic hearts: 2% and 7% of the perfusate adenosine was converted to hypoxanthine and inosine, respectively. These percentages were similar at 50, 100, and 200 micron adenosine. Perfusion of aerobic hearts for 5 h with adenosine did not change ATP concentrations. Therefore, [8-14C]adenosine incorporation into ATP in these hearts appeared to represent ATP turnover. In contrast, 5 h perfusion of postischemic hearts with adenosine restored ATP concentrations to control values. The synthesis rate calculated from the increase in ATP concentration was comparable to the synthesis rate calculated from [8-14C]adenosine incorporation. Thus, incorporation of [8-14C]adenosine into ATP in postischemic hearts represented net ATP synthesis.
TL;DR: Bone and marrow vessels respond actively to physiological stresses and to several humoral and neurogenic stimuli, indicating that as much as 11% of cardiac output is directed to the skeleton.
Abstract: We used labeled microspheres to measure bone and marrow blood flow under control conditions and during several interventions. In dogs, blood flow to compact cortical bone (femoral diaphysis) was 2 +/- 0.1 ml.min-1. 100 g-1, and in hematopoietic marrow (femur), flow was 24 +/- 5 ml.min-1. 100 g-1. Hematopoietic cancellous bones (sternum, ilium) received substantial blood flow. We estimate that as much as 11% of cardiac output is directed to the skeleton. Bone and marrow vessels were responsive to several stimuli. During exercise, vascular resistance in bone increased two- to fourfold, in contrast to profound vasodilation in adjacent skeletal muscle. Hemmorrhage also increased bone vascular resistance. Bone and marrow vessels responded to humoral stimuli: norepinephrine increased vascular resistance and adenosine decreased resistance. Bone vessels also responded to neural stimuli: stimulation of carotid baroreceptors decreased vascular resistance, and activation of sympathetic pathways by baroreceptor deafferentation in cats increased vascular resistance. These studies indicate that bone and marrow vessels respond actively to physiological stresses and to several humoral and neurogenic stimuli
TL;DR: It is proposed that the P-V area as defined above may be a good index of ventricular oxygen consumption under a given inotropic background.
Abstract: In 13 excised, cross-circulated canine hearts, we studied the correlation between left ventricular oxygen consumption per beat (MVO2) and the magnitude of a specific pressure-volume (P-V) area circumscribed by the end-systolic and end-diastolic P-V relationship curves and the systolic segment of the P-V trajectory of a left ventricular contraction. The pressure and volume load of the ventricle were changed with a volume servo pump in order to alter the P-V area, and MVO2 was measured (after each change in the pressure and volume load). In the data collected from both isovolumic and ejecting contractions of each left ventricle contracting with a stable inotropic background, we found a linear correlation between MVO2 and the P-V area. The average correlation coefficient was 0.92 +/- 0.016 (SE). Linear regression analysis yielded the formula: MVO2 (ml/beat) = alpha[P-V area (mmHg.ml/beat)] + b, where alpha, the slope coefficient, was (1.53 +/- 0.14) x 10(-5) and b, which probably represents the basal O2 consumption, was 0.019 +/- 0.003 ml/beta. We propose that the P-V area as defined above may be a good index of ventricular oxygen consumption under a given inotropic background.
TL;DR: Diastolic pressures should be measured at the same level as dimensions when assessing left ventricular diastolic mechanics, because of regional differences in pressures and dimensions.
Abstract: In eight chronically instrumented conscious dogs, apical and middle left ventricular transverse diameters were measured with pulse-transit ultrasonic dimension transducers. Intracavitary apical and...
TL;DR: The data demonstrate that the defect in cardiac performance with increased work loads associated with acute insulin deficiency is due to the relative inability of the heart to utilize physiologic concentrations of glucose as substrate for energy production.
Abstract: Acute alloxan diabetes (3 days) in the rat resulted in a decreased ability of the isolated perfused working heart to respond to increased atrial filling pressure with normal systolic (aortic) press...
TL;DR: It is concluded, contrary to the deductions of common dimensional arguments, that cardiac energy expenditure across species is not directly proportional to heart rate.
Abstract: The energy flux of rat, guinea pig, and cat papillary muscles was measured myothermically under resting, isometric, and isotonic conditions at 27 degrees C. Resting heat rate was highest in the sma...
TL;DR: Data indicate arteriolar closure occurs with higher incidence in SHR than WKY and is mediated by hyperresponsiveness of arterioles to norepinephrine.
Abstract: This study was designed to determine if a mechanism exists to cause abnormally large number of arterioles to be closed to blood flow in spontaneously hypertensive rats (SHR). The contributions to vessel closure by neural control and constrictor response to norepinephrine were investigated. Normal rats (WKY) and SHR were studied at age 18--20 wk. Their respective mean arterial blood pressures were 100 +/- 4 (SE) and 154 +/- 7 mmHg when anesthetized with 10% urethan and 2% alpha-chloralose (0.6 mg/100 g ip). The number of arterioles open to blood flow was counted in a large portion of the cremasteric muscle before and after denervation. The percent change in control diameter of denervated arterioles was measured during iontophoretic application (2 min) of norepinephrine at dose currents of 10--300 nA. Following denervation, a 22.2 +/- 6.3% (SE) and 61.8 +/- 12 increase in the number of third-order arterioles open to flow occurred in WKY and SHR. The diameters, wall thicknesses, and cross-sectional areas of vessel walls were not significantly (P less than 0.05) different for comparable types of denervated arterioles in WKY and SHR. The percent changes in diameters of arterioles in SHR were 3--5 times greater at all dose currents than for vessels of WKY. These data indicate arteriolar closure occurs with higher incidence in SHR than WKY and is mediated by hyperresponsiveness of arterioles to norepinephrine.
TL;DR: Data suggest an intimate link between parenchymal activity and local flow control in the small intestine and superregulation of intestinal flow was not observed in any of the fasted animals.
Abstract: Pressure-flow relations in the intestinal vasculature were obtained by producing stepwise reductions of intestinal perfusion pressure with an adjustable metal clamp placed upon the descending thora...
TL;DR: In dogs reflections were studied by inducing during diastole a pressure pulse in the aorta and measuring pressure and volume flow proximal to and pressure distal to a segment of the LADC at various levels of the coronary peripheral resistance, allowing application of the above-mentioned method for measuring the wave-front velocity, which is insensitive to low-frequency reflection.
Abstract: In this study the pressure wave velocity in the anterior descending branch of the left coronary artery (LADC) of the dog was measured by determining the delay time between pressure pulses along this artery. This method can only be applied if reflections of the pressure wave distal to the sites of pressure measurement are insignificant. From araldite casts of the coronary arteries the following relation between the diameter proximal to (dprox) and distal to (ddist 1, ddist 2) a bifurcation was found: dprox2.55 = ddist12.55 + ddist 22.55, indicating that reflections at a bifurcation areminimal. In dogs reflections were studied by inducing during diastole a pressure pulse in the aorta and measuring pressure and volume flow proximal to and pressure distal to a segment of the LADC at various levels of the coronary peripheral resistance. Reflection of high-frequency components (greater than 7 Hz) was found to be insignificant, allowing application of the above-mentioned method for measuring the wave-front velocity, which is insensitive to low-frequency reflection. At a pressure in the LADC of 13.3 kPa this velocity was 8.6 +/- 1.4 m.s-1 (mean +/- SD). The calculated dynamic cross-sectional stiffness (deltaP/(deltaA/A)) of the LADC was 97 +/- 11 kPa (mean +/- SE) at an arterial pressure of 13.3 kPa.
TL;DR: The number of bradykinin-induced venular fluorescent dextran leakage sites could be greatly reduced by the simultaneous topical application of isoproterenol, and this antagonism of the increase in macromolecular permeability could be prevented by pretreatment with propranolol.
Abstract: Bradykinin applied topically for 4 min produced marked dose-related increases in the number of fluorescent dextran (mol wt 145,000) vascular leakage sites exclusively from small postcapillary venules--evidence for an increase in macromolecular permeability. The increase in macromolecular permeability was short-lived, making repeated applications possible. The number of bradykinin-induced venular fluorescent dextran leakage sites could be greatly reduced by the simultaneous topical application of isoproterenol, and this antagonism of the increase in macromolecular permeability could be prevented by pretreatment with propranolol. The topical application of papaverine failed to antagonize the increase in the number of venular leakage sites of fluorescent dextran by bradykinin. A continuous 90-min superfusion of bradykinin elicited an initial marked increase in the number of fluorescent dextran venular leakage sites, which then waned after 20-30 min, returning to near control despite the continued superfusion with bradykinin. In canine forelimbs the bradykinin-induced increase in protein efflux, total protein transport, and lymph flow also peaked in approximately 30 min and then waned markedly despite continued local intra-arterial infusions of this agent for prolonged periods. The morphological data from the cheek pouch agrees well with the physiological data from the forelimb, suggesting that an increase in protein efflux in the canine forelimb could be readily explained by an increase in the number of large pores.
TL;DR: These results confirm and extend recent suggestions that high levels of PEEP depress left ventricular function in dogs, accounting for about half of the reduction in cardiac output before and during acute pulmonary edema.
Abstract: Artificial ventilation with positive end-expiratory pressure (PEEP) reduces venous return by raising intrathoracic pressure. To determine whether PEEP decreases cardiac output further by depressing myocardial function, we constructed Starling curves, using rapid dextran infusion in 7 anesthetized dogs ventilated with zero (ZEEP) and 20 cm PEEP. The changes in stroke volume and in left ventricular stroke work (LVSW) when PEEP was added or removed were significantly greater than could be attributed to the corresponding change in transmural left ventricular end-diastolic pressure (LVEDPTM) on these Starling curves. To the extent that PEEP did not alter left ventricular diastolic volume-pressure characteristics, these data indicated PEEP depressed ventricular function. Identical changes with PEEP in cardiac output (-30%), esophageal pressure (+10 cmH2O), and left ventricular function were observed after pulmonary edema was induced with oleic acid. These results confirm and extend recent suggestions that high levels of PEEP depress left ventricular function in dogs, accounting for about half of the reduction in cardiac output before and during acute pulmonary edema.
TL;DR: Baboons show a generalized redistribution of BF during heat stress, so that increments in skin BF are provided without increases in CO, whereas man depends on changes in both; despite this latter difference between the baboons and man, the similarity in magnitude of the splanchnic and renal vasoconstriction between the two primates may indicate that the baboon would be a suitable animal model for investigations into mechanisms of changes in regional blood flow in man during heat Stress.
Abstract: Radioactive microspheres (containing six different nuclide labels) were used to measure blood flow (BF) to most major organs of eight conscious baboons during heat stress. Cardiac output (CO), arterial mean pressure, and arterial PO2, PCO2, and pH did not change, but heart rate increased and stroke volume fell as body temperature increased by as much as 2.56 degrees C. Skin BF increased in all regions sampled so that the fraction of CO distributed to skin (not including feet and hands) increased from 3% (control) to 14%. Increased skin BF was compensated for by decreases in splanchnic (intestines, stomach, pancreas, and spleen) (35%), renal (27%), and possibly muscle BF. There was no change in BF to the brain, spinal cord, coronary, or subcutaneous adipose tissue during heating. Therefore, baboons show a generalized redistribution of BF during heat stress, so that increments in skin BF are provided without increases in CO, whereas man depends on changes in both; despite this latter difference between the baboon and man, the similarity in magnitude of the splanchnic and renal vasoconstriction between the two primates may indicate that the baboon would be a suitable animal model for investigations into mechanisms of changes in regional blood flow in man during heat stress.
TL;DR: It is shown that retardation of blood flow may cause a significant increase in precapillary oxygen losses, and theoretical prediction of transmural and longitudinal oxygen tension (PO2) gradients is in qualitative agreement with available experimental data.
Abstract: A mathematical model of oxygen transport in the precapillary microcirculation is presented. The theory is then used to simulate oxygen distribution in the arteriolar network of the hamster cheek pouch. Theoretical prediction of transmural and longitudinal oxygen tension (PO2) gradients is in qualitative agreement with available experimental data. The effect of the variation of inlet network PO2, blood flow rate, blood hematocrit, and other parameters on the transport characteristics is studied. The calculations predict that the luminal PO2 in small arterioles is practically independent of the inlet network PO2 leve if the latter is sufficiently high; when this inlet PO2 level is low, then the longitudinal gradients of luminal PO2 vanish. It is further shown that retardation of blood flow may cause a significant increase in precapillary oxygen losses.
TL;DR: The preparation avoids intrinsic limitations encountered with buffer-perfused hearts and should prove useful for characterization of cardiac metabolism with radiolabeled tracers relevant to positron emission transaxial tomography.
Abstract: To facilitate characterization of myocardial metabolism with the use of positron-emitting tracers, we developed an isolated heart preparation designed to simulate physiological levels of flow and substrate extraction. Isovolumically beating hearts were perfused retrograde at 60 mmHg with modified non-recirculating Krebs-Henseleit (KH) solution with or without washed sheep red blood cells at a hematocrit of 25 or 40 (KH-RBC25, KH-RBC40). Left ventricular (LV) systolic pressure averaged 63 mmHg with KH alone, 78 with KH-RBC25, and 98 with KH-RBC40. LV dP/dt, pressure-time index, and oxygen consumption increased in an analogous fashion. Fatty acid extraction increased from 1.5% with KH to 11.8% in hearts perfused with KH-RBC40, although net uptake was not increased markedly because of the associated differences in flow (4.6 ml.g-1.min-1 with KH and 1.5 with KH-RBC40). Hearts perfused with erythrocyte-rich media exhibited functional and metabolic stability and less edema. The preparation avoids intrinsic limitations encountered with buffer-perfused hearts and should prove useful for characterization of cardiac metabolism with radiolabeled tracers relevant to positron emission transaxial tomography.
TL;DR: The appearance of load dependence during relaxation in cardiac muscle thus emphasizes the presence of an effective sarcoplasmic reticulum.
Abstract: Relaxation of spontaneously contracting single rat cardiac cells with an effective sarcoplasmic reticulum was shown to be sensitive to load, as previously described for intact mammalian ventricular cardiac muscle. Caffeine and tetanic stimulation could modify load-dependent relaxation in intact papillary muscle from cat or rat into a load-insensitive relaxation. Although such load dependence was demonstrated to be normally absent in frog ventricular cardiac muscle, in the present study it could also be made moderately manifest under specific conditions, e.g., high calcium, low sodium, or ouabain. The appearance of load dependence during relaxation in cardiac muscle thus emphasizes the presence of an effective sarcoplasmic reticulum.