ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

We investigated the effect of vasodilation and flow rate on derived estimates of capillary permeability surface (PS) product and interstitial space size in the in situ canine heart. We used the multiple indicator dilution technique, with labeled red cells and albumin as reference tracers, Na ion as an interstitial space marker, and tritium-enriched water as a substance entering both interstitial and sarcomeric spaces. The simultaneous outflow curves for these substances were analyzed with a model of the coronary microcirculation which contained unique parameters representative of capillary and sarcolemmal PS products, the ratio of myocyte to interstitial space sizes and the heterogeneity of capillary transit times. Parameter optimization was accomplished by an efficient algorithm based on frequency-domain representations of the model and the data. Vasodilation at constant flow rate with decreased perfusion pressure in the heart working at a constant basal level had no significant effect on the permeability and space size parameters, but the capillary transit time heterogeneity was reduced. Restoration of control perfusion pressure by increased flow (in the face of continuing vasodilation) caused an increase in both capillary PS product and relative interstitial space size, but no change occurred in the sarcolemmal PS product. We conclude that there is no significant recruitment of myocardial cells with increased flow rate and that, when capillary recruitment occurs, it is only an effect of increased flow rate and unrelated to vasodilation per se. At high flow rates, with normal perfusion pressures, a mild but significant degree of interstitial edema accumulation is found.Circ Res 47: 312-328, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

The kinetics underlying the uptake of tracer amounts of norepinephrine and isoproterenol by the heart were studied in a pentobarbital-anesthetized dog with the multiple indicator dilution technique. The circumflex coronary artery was perfused with blood from the femoral artery, with a pressure-dependent system. A small bolus containing labeled albumin (a tracer confined to the vascular space), labeled sucrose (which penetrates into the extracellular space in a barrier-limited fashion), and labeled norepinephrine or isoproterenol was injected into the artery and outflow dilution curves were obtained from the coronary sinus. Analysis of data enabled us to assess separately the myocardial capillary permeability for norepinephrine or isoproterenol, and their rate constants for uptake by the interstitial sympathetic fibers (the process is essentially unidirectional over the time of a single passage, because of the highly concentrative nature of the uptake). We found a major resistance to catecholamine transfer at the capillary surface (approximately half of the label emerged at the outflow without leaving the circulation) and a neuronal uptake process beyond the barrier large enough that, after steady infusion, it would be expected to reduce the tracer concentration of norepinephrine to a value the order of one-sixth that in the plasma space. The injection of desmethylimipramine selectively diminished the apparently unidirectional flux of labeled norepinephrine into the neuronal terminals, and this uptake was found to be significantly lower for isoproterenol than for norepinephrine. The capillary-intersti-tium-concentrative uptake mechanism, documented here, partially explains the quantitatively different cardiac responses to infused and locally released catecholamines.Circ Res 47: 329-338, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

We measured glucose metabolism in five dogs before and 3 weeks after cardiac dener-vation; after this time myocardial norepinephrine is depleted. The discharge by the myocardium, of14CO2from infused 14C-D-glucose (U), decreased following denervation (P= 0.05). The ratio of14CO to total CO2 production, which measured the proportion of glucose to total substrate oxidized, also decreased following denervation (P = 0.05). The inhibition of glucose oxidation by denervation was not due to an increase in arterial lactate concentration. There was an associated increase in myocardial content of fructose-6-phosphate in an additional seven dogs (P< 0.01). We postulate that myocardial tissue norepinephrine is one of the controllers of the activity of phosphofructokinase. Circ Res 47: 338-345, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

The possibility that vasopressin plays a role in cardiovascular control arouses increasing interest. We studied in unanesthetized dogs the hemodynamic consequences of 1-hour vasopressin infusions that modified plasma concentrations over a range similar to that found in physiological situations. We also examined the cardiovascular events following the stimulation of endogenous vasopressin release by an increase in plasma osmolality. In dogs with baroreceptor reflexes intact, vasopressin infusions which increased plasma vasopressin concentration by 2-20 fmol/ml did not affect mean arterial pressure. However, they significantly decreased cardiac output (measured by an electro-magnetic flowmeter) and increased total peripheral resistance. After baroreceptor denervation, vaso-pressin infusion rates as low as 40 fmol/kg per min (0.017 mU/kg per min) led to an increase in mean arterial pressure. Cardiac output was unaffected until much higher infusion rates were used. Changes in total peripheral resistance were very similar to those calculated in dogs with intact baroreceptors. The release of vasopressin following infusions of hypertonic solutions either intravenously or into a carotid artery induced detectable hemodynamic changes which appeared in many respects similar to those following low infusion rates of vasopressin. We conclude that physiological plasma concentra-tions of vasopressin have hemodynamic effects even though they do not normally modify arterial pressure, presumably because of some particular interaction of vasopressin with the baroreceptor reflex. Circ Res 47: 346-355, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

The effects of acute renovascular hypertension on the sympathetic nervous system, regional blood flow and cardiac function were studied in conscious dogs submitted to renal artery occlusion by inflation of a cuff implanted previously around one renal artery. We then compared the alterations in plasma renin and catecholamine levels and in the various hemodynamic parameters induced by those maneuvers in intact dogs, to those in dogs pretreated with α-and β-adrenergic receptor blockers. Subsequently, the converting enzyme inhibitor teprotide was administered to inhibit angiotensin formation in both experiments. Our results suggest that both the renin-angiotensin system and the sympathetic system contribute to the rise in blood pressure. The hemodynamic changes and alterations in regional blood flows accompanying this acute hypertension appear to be due mostly to the increase in plasma angiotensin, since prior adrenoceptor blockade only attenuated their magnitude but did not alter their direction. However, angiotensin-induced coronary vasoconstriction was observed only in adrenergically blocked but not intact animals, probably because of the protective effect of baroreceptor-mediated reflex sympathetic coronary vasodilation. Circ Res 47: 356-365, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

In anesthetized and vagotomized rats, an intense cerebral compression (CC) by intracra-nial placement of a space-occupying mass evoked systemic arterial hypertension (SAH), pulmonary venous hypertension (PVH), and pulmonary hemorrhagic edema (PHE) in 2-3 minutes. Observation of the regional weight changes revealed an acute increase in pulmonary blood volume with a decrease in the volume of the systemic vascular beds. With chronically instrumented flow probes, we demonstrated that the overall pattern of imbalance in right and left cardiac outputs was characterized by an immediate fall in aortic flow by 52% accompanying a slower decline pulmonary arterial flow. In 10 rats with a right heart bypass (venous return to reservoir and constant pulmonary inflow), CC produced severe PVH and PHE associated with SAH, reservoir volume reduction, and no significant change in pulmonary vascular resistance. The increases in left atrial pressure and lung index (lung: body weight x 100) were much greater than those obtained with natural circulation. In 20 left heart-bypassed rats (constant aortic flow either with or without a reservoir between the left atrium and roller pump), CC induced SAH, whereas no significant changes occurred in the lungs. The lung index was not different from the normal value. The results indicate that neurogenic constriction of the systemic capacitance vessels to favor venous return is not an important hemodynamic event in the centrogenic pulmonary pathology. Pulmonary volume loading leading to pulmonary hypertension and PHE is evoked princi-pally by a dramatic pulmonary hypertension decrease in left ventricular output due to ventricular strain in the face of an intense arteriolar constriction.Circ Res 47: 366-373, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Cultured human smooth muscle and adventitial cells were incubated with human serum and low density lipoprotein (LDL) to study the Uptake and accumulation of cholesterol ester from exogenous LDL. The cellular total cholesterol varied with the amount of LDL cholesterol in the medium. The cholesterol ester content increased 4-fold after 2 hours of incubation. A 6-fold rise occurred by 24 hours and continued to 72 hours. The cholesterol ester of the adventitial cells was markedly depleted by incubation with abetalipoproteinemic serum or with a lipid-depleted plasma fraction. By the use of14C-labeled LDL free cholesterol in the incubation medium, we calculated that some 70-80% of the total accumulated cholesterol ester after 24 hours of incubation was derived from LDL cholesterol ester, and only 20-30% was synthesized by the cells. These studies demonstrated conclusively that human cells greatly increase their cholesterol ester mass after incubation with LDL.Circ Res 47: 374-383, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

Pinocytotic vesicles are one of several anatomic factors relevant to the permeability for macromolecules of capillary endothelia. We quantified the number and distribution of pinocytotic vesicles present in the endothelium of pulmonary capillaries. Several similar studies have been reported in the past for endothelia of systemic capillaries, but the technical difficulties involved in this difficult application of morphometry never have been discussed. In the present work, an on-line microprocessor was used to assist with the processing of the point-counting data. The average figures from nine rabbit lungs for parameters thought to be relevant to characterize the population of vesicles are: thickness of the endothelium (TAUen), 0.192 fim; number of vesicles per volume unit of cell (Nv—), 131 vesicles//im3; vesicular load of each cell front (N/S)b, 196 vesicles//im2, and (N/S)i, 181 vesicles//im2. The number of vesicles per volume unit (Nvra) is smaller than that which has been described for systemic capillaries.Circ Res 47: 384-391, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

My objective was to observe if coronary vasodilator responses after bolus (0.2 ml) intracoronary injection of adenosine (1-5000 /IM) or after coronary artery occlusion (5-30 seconds) are modified over a range from mild to severe hypoxia [outflow oxygen tension (PO2V) = 119 ± 9 to 10 ± 2 (mean ± SEM) torr]. The vasculature of ten isolated, paced (240 beats/min), nonworking guinea pig hearts was perfused by the Langendorff technique with a fortified Krebs-Ringer solution at 37.5°C and at a constant pressure of 55 torr. Graded hypoxia was produced by randomly altering perfusate FO2 to one of five predetermined levels. Individually, maximal hypoxia, maximal adenosine injection, and 30-second occlusion increased vascular conductance by 98, 100, and 98%, respectively. At constant myocardial oxygen consumption (MVO2), PO2V was inversely proportional to baseline conductance (r= 0.42,P< 0.01); during normoxia (PO2v= 119 torr) both log-dose adenosine concentration and occlusion period were directly proportional to peak conductance (r= 0.78,P< 0.01;r= 0.73,P< 0.01). Low doses of adenosine or short occlusions significantly shifted the conductance intercept to higher values but did not change individual PO2V vs. conductance slopes. Similar results were found in the relationship between PO2vand overflow volume after adenosine injection or occlusion. Moreover, both the excess volume flow with low doses of adenosine and the volume of reactive hyperemia were unaffected by PO2V when MVO2 was unchanged. As hypoxia became more severe and MVO2 decreased, reactive hyperemia decreased and the flow debt increased. This study indicates that adenosine or coronary occlusion produces additive, noninteractive coronary vasodilation in the presence of tissue hypoxia. One possible explanation for these results is that as conductance rises, the common receptors for endogenous and exogenous adenosine become increasingly saturated.Circ Res 47: 392-399, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID