ISSN:0009-7330    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

The mechanism by which clonidine suppresses renin release was investigated in conscious rats. This suppression was studied by means of selected autonomic interventions in conjunction with changes in sodium balance. Serum renin activity and direct arterial pressure were monitored.Clonidine administration suppressed basal (by 68–85%), diuretic-induced (by 89%), and sympathetic nervous system-mediated (by 75–100%) renin release. Cholinergic, ganglionic, and peripheral sympathetic neuronal blockade did not prevent this inhibitory effect of clonidine. These results indicate a peripheral site of action for suppression of renin release by clonidine. The a-adrenergic blocking drug phentolamine prevented clonidine suppression of renin release in sodium-depleted rats and was partially effective in normal rats. Phentolamine blocked the decrease in renin caused by clonidine in ganglion-blocked rats. Clozapine, a new neuroleptic agent with α-adrenergic blocking activity, or phenoxybenzamine blocked the effect of clonidine on renin release in both sodium-depleted and normal rats. After ganglionic blockade in sodium-depleted rats, clonidine caused a significantly greater suppression of renin release than did an equipressor dose of methoxamine. These data, combined with hemodynamic correlates, suggest that clonidine inhibits renin release by activation of an intrarenal a-adrenergic receptor.

ISSN:0009-7330    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

SUMMARY The mean circulatory pressure (Pmc) in dogs anesthetized with chloralose-urethane was estimated from 0.5 to 150 minutes after hemorrhages of 0, 17, or 34 ml/kg, or that volume giving an arterial pressure (Pa) of 40 mm Hg. The Pmc was 'determined by fibrillating the heart and then rapidly pumping blood from aorta to vena cava until Pa = venous pressure (Pv) = Pmc. Within about 10 seconds, the heart was defibrillated. Vascular compliance was estimated as the ratio of a test blood volume change (0, ± 8.5, or 17 ml/kg) to the change in Pmc, determined 0.5 minute after the start of the test volume change. Erythrocyte and plasma volumes were measured by51Cr-erythrocyte and125l-albumin dilution. In response to prolonged hemorrhage: (1) the total vascular compliance apparently decreased; (2) most of the changes in capacity vessels occurred within 5 minutes, and indeed a large part of the response probably had occurred by the time of the first measurement at 30 seconds; (3) the progressive recovery in Pmc after 5 minutes was primarily from fluid shifting into the vasculature; (4) even after 2 hours of severe hemorrhagic hypotension, the venoconstriction was not lost; but (5) after an hour of severe hemorrhagic hypotension (arterial pressure of 40 mm Hg) there was water loss from the vasculature, because plasma protein and erythrocyte concentrations and plasma oncotic pressure increased.

ISSN:0009-7330    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

The response of 14 atrial receptors with nonmedullated vagal afferents to changes in atrial pressure was determined in anesthetized thoracotomized cats. Recordings were made from 11 single fibers and three two-fiber filaments. Mean conduction velocity was 0.9 m/sec (range, 0.35 to 2.2 m/sec). During the control period, either no activity was detected or there was a sparse discharge (mean, 1.4 impulses/sec), which occasionally was related to the a or v waves. As atrial pressure was increased by transfusion or by occlusion of the aortic, pulmonary arterial, mitral, and tricuspid orifices, an increased rate of firing occurred, often related to the atrial v wave. The threshold for individual receptors was between 2 and 3 mm Hg (mean pressure) in the right atrium, and 5 and 12 mm Hg in the left atrium. The maximal firing rate was 5–11 impulses/sec for right atrial and 10-20 impulses/sec for left atrial receptors. The receptors were localized by probing the opened heart, and were identified in both atria, in the interatrial septum, and in the atrial-venous junctions. Thus receptors connected to vagal C fibers are present throughout both atria and are activated by moderate changes in pressure.

ISSN:0009-7330    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

The possibility that the vascular muscle cell might contribute to the development of essential hypertension by being more responsive to norepinephrine because of an inherently lower membrane potential (Em) was investigated. Experiments were designed to test the hypothesis thatEmof arterial vascular muscle cells from spontaneously hypertensive rats (SHR) are less negative than those from matched Kyoto normotensive rats (KINK). The caudal artery, a muscular, densely innervated regulating artery 300–400&mgr;min outside diameter, which is activated by graded (nonspiking) depolarization to produce a maintained contraction, was studied. Vascular muscle cells from SHR always had less negativeEmthan those from KNR at 16°C, but not at 36°C, over a range of K+concentrations from 2.7 m.M to 150 mM. From the relationship betweenEmand K+concentration, intraccllular K+concentration (|K+l1) was estimated to be 150 mM for SHR and 170 mM for KNR. The caudal artery undergoes a large depolarization when K* is removed from the superfusing solution and a transient hyperpolarization that exceeds the calculatedEK(potassium equilibrium potential) when K+is replaced. The magnitude of the hyperpolarization on returning to 30 mM or 50 mM K+always was greater for vascular muscle of SHR than KNR. The apparently lower [K1], and more active (compensating) electrogenic ion transport in the SHR vascular muscle cells thus result in an unalteredEmat body temperature in the physiological range of K+concentrations. However, depolarization by norepinephrine was greater over the middle of the dose-response curve, and this greater depolarization caused the contractions of SHR arteries to be greater. The altered electrogenesis of the SHR vascular muscle cells is postulated to provide a mechanism for the increased reactivity of arteries to norepinephrine in hypertension.

ISSN:0009-7330    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

We studied the excitatory and inhibitory effects of overdrive on idioventricular pacemakers in anesthetized dogs with recently induced complete atrioventricular block. The following results were obtained: (1) a slow driving rate may induce a temporary rhythm which may be reinstituted with additional stimuli; (2) the induced rhythm may appear as coupled extrasystoles which, on interruption of the drive, are found to be self-sustaining; (3) during continued slow driving, extrasystoles may appear and disappear in a cyclical manner; (4) a short period of fast driving may be followed by a fast new rhythm, the rate and duration of which are a function of the rate and duration of drive; (5) fast driving may induce a new rhythm at a rate below predrive control; (6) after a long period fast driving, only suppression follows; and (7) intermittent periods of fast driving lead to a summation of inhibition with each successive period. These results suggest the following conclusions: (1) under certain conditions, electrical driving instead of inducing suppression may induce a rhythm ("overdrive excitation") at a rate similar to, faster than, or slower ("inhibited excitation") than control; (2) the duration of diastole and the number of driven beats are major factors in the induction of new rhythms; and (3) overdrive excitation is counteracted by overdrive inhibition, with development of the former requiring fewer beats than the latter.

ISSN:0009-7330    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

We examined the water, sodium, and potassium composition of the thoracic aorta, abdominal aorta (plus iliac arteries), and veins (vena cava and portal vein) from rats with aortic coarctation. The aortas of 10 rats (group A) were coarcted above the renal arteries to produce hypertension. Control groups consisted of 10 rats sham-coarcted above and 10 rats coarcted below the renal arteries. In group A rats heart weights and carotid artery pressures were elevated over controls (P< 0.01), whereas there were no significant differences in femoral arterial pressures. In group A rats both the hypertensive thoracic aorta and the normotensive abdominal aorta contained about 20% more water per unit of wet weight, and about 35% and 60% more sodium and potassium, respectively, per unit of dry weight than did the corresponding portions of aorta from control rats (P< 0.01). In group A rats water (P< 0.01), sodium (P< 0.02), and potassium (P< 0.05) contents of veins also were increased. There were no significant correlations between level of carotid arterial pressure and magnitude of changes in arterial and venous composition, nor were there significant differences between the magnitude of changes in the normotensive and hypertensive portions of the aorta. These results indicate that in rats abnormalities in vascular wall salt and water content are not necessarily a direct effect of the elevated pressure in hypertension.

ISSN:0009-7330    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

The effects of reduction in perfusion pressure, arterial hypoxia, muscle contraction, and adrenergic stimulation on the hindlimb muscle circulation were studied. Under normal conditions (venous Po2≤ 40 mm Hg), oxygen delivery to the muscle was maintained mainly by large increases in the capillary exchange capacity and the oxygen extraction ratio in accord with tissue demand following the application of the above stresses. The participation of the resistance vessels under these conditions was minimal. The prevailing venous oxygen tension then was reduced by several means and the response of vascular resistance and capillary exchange capacity to the same stresses was reexamined. At the lower prevailing venous Po2, the sensitivity of the resistance vessels to metabolic and hemodynamic disturbances was greatly increased. Consequently, blood flow autoregulation, functional hyperemia, and hypoxic hyper-emia were more intense when venous oxygen tension was low. In contrast, the contribution of exchange capacity was diminished, probably owing to the fact that most of the capillaries already are open at low venous Po2. These data suggest that the locus of local microvascular control of muscle oxygenation shifts from the normally more sensitive precapillary sphincters to the proximal flow-controlling arterioles as the prevailing venous oxygen tension falls. Yet, although the relative contribution of the resistance and exchange vessels to intrinsic regulation of tissue oxygenation is related to the prevailing venous oxygen tension, the two compensatory mechanisms operating in concert maintain tissue Po2above the critical level over a wide range of stresses.

ISSN:0009-7330    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

Isopotential maps based on 192–200 body surface electrocardiograms were obtained for 20 dogs during multiple patterns of ventricular activation. The purposes of the study were to determine whether the cardiac location of events responsible for surface potentials had a recognizable influence on surface potential patterns and to examine the influence of electrical events occurring simultaneously in multiple cardiac regions. Substantially different effects of electrical activity in various cardiac regions on body surface potentials were evidenced by the body surface location of potential maxima and minima and by patterns of isopotential lines during early portions of ventricular excitation initiated at different ventricular sites. Simultaneous stimulation at some sites gave surface potential distributions with multiple extrema. These were demonstrated to be due to effects of the different cardiac regions, because addition of potentials due to stimulation of the individual sites duplicated those associated with simultaneous stimulation of the same sites. It was also shown that body surface locations of maxima and minima are not related in the same manner to the cardiac location of the responsible events when these events are present in single and multiple regions. Slopes of potentials due to events in single cardiac regions were shown to combine with slopes produced by events in other regions to yield maxima or minima at new body surface locations. Results of the study support the possibility of regional cardiac examination by electrocardiograph) but suggest that this will require quantitative descriptions of the details of potential patterns in addition to the location of potential peaks.

ISSN:0009-7330    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

Hypobaric hypoxia causes hypocapnia and alkalosis, hemoconcentration and increased hematocrit, and a decreased cardiac stroke volume. To assess the role of the hypocapnic alkalosis in causing these other changes, five men were exposed to hypobaric hypoxia at a barometric pressure (PB) of 440 torr with an alveolar O, tension of 55 torr for 5 days with 3.77% CO2added to the atmosphere to prevent alkalosis. They did not lose weight, and arterial CO2tension, pH, and cardiac stroke volume were unchanged. An unchanged hematocrit implied an unchanged plasma volume. During exercise to maximum, stroke volumes equaled sea level values but arterial hypoxemia was profound, the arterial O2tension being 39 torr. By contrast, three men at high altitude without CO2supplementation (PB= 455 torr; alveolar Po2= 56 torr) had weight loss, hypocapnia, alkalosis, and decreased stroke volume. Increased hematocrits suggested decreased plasma volumes. During exercise, arterial Po2(48 torr) was higher than in the group receiving CO2. Maximum oxygen uptakes were decreased to a similar degree in the two groups. Catecholamine excretion doubled in the group with CO2but in the group without CO2catechoamine excretion was unchanged. A normal pH at high altitude apparently maintained plasma volume, which, with the increased catecholamine excretion, may have prevented a decrease in stroke volume. However, the subjects with CO2added did not have enhanced oxygen transport, because their arterial oxygenation was impaired.

ISSN:0009-7330    

出版商:OVID    

年代:1976

数据来源: OVID