ISSN:0009-7330    

出版商:OVID    

年代:1974

数据来源: OVID

摘要:

During reactive hyperemia following a brief coronary artery occlusion, excess arterial inflow exceeds the blood flow debt incurred during occlusion by 300–600%. The present study was performed to determine whether this marked reactive hyperemia is essential for restoration of coronary vascular tone. Coronary blood flow was measured in unanesthetized dogs with electromagnetic flowmeters and hydraulic occluders chronically implanted on their left circumflex coronary arteries. When 10-second coronary artery occlusions were performed in pairs separated by a brief interval during which excess arterial inflow equaled the blood flow debt incurred during the first occlusion, reactive hyperemia following the second occlusion was no greater than that following an isolated control occlusion. Thus, approximately 100% repayment of the blood flow debt resulted in restoration of normal reactivity to a second occlusion. To further ascertain whether coronary vascular tone could be regained without the usual excess inflow, the reactive hyperemia following a 10-second occlusion was mechanically limited by partial inflation of the occluder. When reactive hyperemia equal to 115 ± 10% repayment of the blood flow debt was allowed, final complete release of the occluder was followed by no additional hyperemia. These studies demonstrated that the markedly excess arterial inflow which occurs during coronary reactive hyperemia is not essential for restoration of coronary vascular tone.

ISSN:0009-7330    

出版商:OVID    

年代:1974

数据来源: OVID

摘要:

The effects of isoproterenol, propranolol, and compound D600 (α-isopropyl-α-[(N-methyl-N-homoveratryl)-γ-aminopropyl1–3, 4, 5-trimethoxyphenylacetonitrile) on myocardial adenine nucleotide metabolism were studied in rat hearts in situ. Isoproterenol in doses between 0.1 and 25 mg/kg induced an increase in heart rate concomitant with a significant acceleration in the de novo synthesis of adenine nucleotides (ATP, ADP, and AMP) and a diminution in their concentration. The effects of isoproterenol were antagonized by propranolol (1 and 50 mg/kg), which alone caused a reduction in the de novo synthesis of adenine nucleotides without inducing a change in their concentration. Compound D600 (10 mg/kg) brought about a slight elevation in the concentration of adenine nucleotides but did not influence the rate of de novo synthesis. The isoproterenol-induced diminution in adenine nucleotide concentration was prevented by D600; under these conditions, the acceleration of de novo synthesis was attenuated. These findings indicate that de novo synthesis of myocardial adenine nucleotides in the normal and the isoproterenol-stimulated heart is regulated not only by a feedback mechanism dependent on the concentration of adenine nucleotides but also by β-receptor-mediated alterations in carbohydrate metabolism which can cause changes in the size of the available pool of 5-phosphoribosyl-1-pyrophosphate.

ISSN:0009-7330    

出版商:OVID    

年代:1974

数据来源: OVID

摘要:

The metabolic turnover rate and the transcapillary escape rate of albumin were studied using131I-labeled human albumin in nine untreated subjects suffering from essential hypertension. The average mean arterial blood pressure of these subjects was 162/109 mm Hg; seven subjects had grade I–II funduscopic changes. Plasma albumin concentration was normal, but plasma volume was reduced (P< 0.05) in these subjects. Thus, the previously reported moderate decrease in the intravascular albumin mass of hypertensive subjects was confirmed; the average value for intravascular albumin mass in the present study was 62.8 g/m2 surface area compared with a normal value of 70.6 g/m2(−11%,P< 0.05). A surprising finding was a marked enhancement of albumin metabolic rate in essential hypertension. The fraction of intravascular albumin mass metabolized per 24-hour period was on the average 14.4% compared with a normal value of 8.4% (+72%,P< 0.001). The rate of synthesis was 9.1 g/24 hours m−2compared with a normal value of 5.9 g/24 hours m−2(+54%,P< 0.001). Total body albumin mass was decreased proportionally to intravascular albumin mass. Confirming a previous observation, we found an increase in the transcapillary escape rate of albumin (fraction of intravascular mass passing to the extravascular space per unit time) from a normal average of 5.6%/hour to 7.5%/hour (+34%,P< 0.001). There was a statistically significant positive correlation between the transcapillary escape rate of albumin and blood pressure (P< 0.05). These findings can best be explained by increased filtration due to the high arterial blood pressure. There was also a positive correlation between the transcapillary escape rate and the fractional catabolic rate of albumin (P< 0.05). This finding supports the concept that albumin is catabolized in connection with its permeation through the capillary endothelium.

ISSN:0009-7330    

出版商:OVID    

年代:1974

数据来源: OVID

摘要:

The vasoconstrictor response of perfused rat mesenteric arteries to stimulation of sympathetic nerve fibers is markedly potentiated by glucose deprivation; this potentiation is abolished or reduced when glucose or other sugars are added. The augmentation of the vasoconstrictor response to nerve stimulation produced by glucose deprivation presumably results from an increased release of the adrenergic transmitter, since (1) the response to injected norepinephrine is much less affected by glucose deprivation and (2) the increase in the vasoconstrictor response to either adrenergic stimulus produced by inhibition of neuronal reuptake by cocaine is unaltered by glucose deprivation. The inhibitory effect of glucose may involve its metabolite(s). Pyruvic and lactic acids inhibit the vasoconstrictor response to nerve stimulation previously augmented by glucose deprivation but do not affect adrenergic transmission in the presence of glucose. Also, the inhibitory effect of glucose on the potentiated response is abolished by the simultaneous infusion of 2-deoxy-D-glucose or iodoacetic acid, inhibitors of glucose metabolism. The inhibitory effect of glucose and its metabolite(s) on adrenergic transmission may also involve changes in the ionic permeability of the nerve terminal. In the absence of glucose, raising the Na+and K+concentrations affects the vasoconstrictor response differently, namely, Na+potentiates and K+attenuates the response. These effects are abolished by addition of glucose. In contrast, the effects of increased concentrations of either Ca2+(facilitation) or Mg2+(inhibition) on neurotransmission are unaffected by removal or restoration of glucose. We conclude that glucose deprivation does not affect adrenergic transmission by acting directly through Ca2+. Rather, glucose deprivation decreases pyruvate and possibly other products of glucose metabolism, and these decreases, in turn, alter the concentrations of Na+and K+within the neuron. These latter changes then enhance the availability of Ca2+and, thereby, increase the release of the adrenergic transmitter.

ISSN:0009-7330    

出版商:OVID    

年代:1974

数据来源: OVID

摘要:

The effects of norepinephrine, theophylline, and adrenergic blocking drugs on renin release from rat kidney slices were studied in vitro.l-Norepinephrine increased renin release into the incubation medium; this increase was accompanied by an increase in the renin content of the slices. Statistically significant increases in renin release were produced by 10−5M and 2 × 10−5Ml-norepinephrine.d-Norepinephrine in the same doses was ineffective. Theophylline (10−3M) had no effect by itself, but it potentiated the effect ofl-norepinephrine on renin release. The response tol-norepinephrine was markedly suppressed byl-propranolol (10−4M) but not byd-propranolol (10−4M). The α-receptor blocking agents phentolamine (10−4M) and phenoxybenzamine (10−4M) increased rather than decreased the effect ofl-norepinephrine. These results are consistent with a direct intrarenal effect of norepinephrine on renin release; this effect appears to be mediated by a β-adrenergic mechanism.

ISSN:0009-7330    

出版商:OVID    

年代:1974

数据来源: OVID

摘要:

The indicator-dilution method was used to investigate blood flow in the microvascular network of the mesenteric membrane of the cat by replacing the normal blood flow into the mesenteric artery with a dextran-saline solution for a finite period of time. The dilution of the dextran-saline bolus as it flowed downstream was measured in a selected arteriole and its adjacent venule with a microphotometric system. Based on an in vitro calibration study done on glass capillary tubes, the measured optical density was converted to the hematocrit. The dilution curve for a finite injection and for a step injection, the mean transit time (MTT), and the appearance time for the arteriole and the venule were computed. The dispersion found in the arterial system, a network of diverging branches, was reasonably well simulated by the dispersion in a parabolic flow system. However, the dispersion found in the venules, where the irregular capillary blood flow converges, was considerably skewed from that in a parabolic system. A wide distribution of MTT was found for the arterioles and the venules, and there was considerable overlap in the MTT distribution for these two groups. This finding cannot be simulated by a network with a parallel arrangement. The difference in MTT for pairs of arterioles and venules was distributed over a narrow range, probably indicating shunt flow in the mesenteric microvascular network.

ISSN:0009-7330    

出版商:OVID    

年代:1974

数据来源: OVID

摘要:

The 1-sarcosine-8-alanine analogue of angiotensin II (1-Sar-8-Ala-angiotensin II) was infused at 1 and 5 μg/kg min−1into conscious rabbits on normal or sodium-deficient diets. Blood pressures during the control period were comparable in both groups; plasma renin activity, angiotensin II concentration, and aldosterone concentration were higher in the rabbits on the sodium-deficient diet than they were in the rabbits on the normal diet. The analogue caused a 6-mm Hg fall in mean arterial blood pressure in sodium-depleted rabbits. Plasma renin activity increased in both groups to eight to ten times the control values with the higher rate of infusion. Angiotensin II concentration paralleled plasma renin activity. Plasma aldosterone concentration increased after infusion of the analogue at 1 μg/kg min−1to three to four times the control values but decreased from these high levels after an additional 90-minute infusion at 5 μg/kg min−1to only one to two times the control values in both groups. Infusion of angiotensin II during the administration of the analogue caused a clear-cut increase in aldosterone concentration without a change in blood pressure. The persistence of elevated aldosterone levels during inhibitor blockade in the sodium-depleted rabbits does not prove that factors other than angiotensin participate in the aldosterone response to sodium deprivation. However, the data do indicate that 1-Sar-8-Ala-angiotensin II is a less effective antagonist of angiotensin II at the adrenal receptors than it is at the vascular smooth muscle receptors and suggest that the pressor and adrenal receptors differ.

ISSN:0009-7330    

出版商:OVID    

年代:1974

数据来源: OVID

摘要:

A ouabain-sensitive, Mg2+-dependent, Na+, K+-stimulated adenosinetriphosphatase (ATPase) isolated from canine mesenteric arteries was activated by the following vasodilators: hydralazine, diazoxide, PGE1, PGE2, PGA2, and minoxidil. Epinephrine, norepinephrine, and isoproterenol also stimulated the ATPase, but PGF2αwas ineffective. Since these vasodilators activate the adenylate cyclase of vascular smooth muscle, the effects of cyclic adenosine monophosphate (AMP) and theophylline on the Na+, K+-ATPase were studied; both substances caused a concentration-dependent increase in enzymatic activity. Propranolol blocked the catecholamine-induced stimulation of Na+, K+-ATPase, and polyphloretin phosphate antagonized the effects of the prostaglandins. It is concluded that vasodilatation in response to these substances is associated with the stimulation of the Na+, K+-ATPase of vascular smooth muscle probably mediated through cyclic AMP.

ISSN:0009-7330    

出版商:OVID    

年代:1974

数据来源: OVID

摘要:

Turbulence is one of the hydraulic disturbances implicated in thrombus formation, even though absolute proof of its contributory effect is lacking. Because of the importance of a possible effect of turbulence on thrombus formation, the relation was studied in eight dogs. In each dog, two arteriovenous shunts were established, one from each femoral artery to the contralateral femoral vein. Only one shunt contained a turbulence-producing device; otherwise, the shunts were identical in shape, size, and material. The intensity of turbulence distal to the turbulence generator was quantified in vitro by measuring the relative magnitude of the randomly fluctuating velocities. In each of the eight dogs, more thrombi, by weight, accumulated in the turbulent shunt than in the laminar shunt (P< 0.001). Thrombi from the turbulent shunt weighed 180 ± 30 (SE) mg, whereas those from the laminar shunt weighed 0.9 ± 0.6 mg. The weight of thrombi that accumulated within the turbulent system appeared to be related to the intensity of turbulence. A linear relation was observed between the Reynolds number in the region of the turbulence-producing orifice and the weight of the thrombi within the turbulent shunt (r= 0.90). The relative intensity and the absolute intensity of turbulence distal to the turbulence generator were also linearly related to the Reynolds number (r= 0.97 and 0.90, respectively). The results of this study therefore indicate that turbulence is a characteristic of blood flow that can contribute to the formation of thrombi.

ISSN:0009-7330    

出版商:OVID    

年代:1974

数据来源: OVID