ISSN:0009-7330    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

We studied the effect of bilateral common carotid occlusion (implanted pneumatic cuffs) on renal blood flow (electromagnetic flowmeter) and renal function (implanted ureteral catheter) in nine chronically instrumented, conscious dogs on a high sodium diet (14 mmol/kg body weight per day). By means of suprarenal aortic constriction (pneumatic cuff) the influence of renal perfusion pressure was investigated. There was no change in renal blood flow or glomerular filtration rate (inulin clearance) with either reflexly increasing (+49.6%) or constant renal perfusion pressure. Carotid occlusion caused an increase of urine output by 80.5% and of sodium excretion by 85.3% due to a fall in fractional sodium reabsorption (−0.9%) when renal perfusion pressure was allowed to rise. Neither an increase of diuresis or sodium excretion nor an antinatriuresis was observed when renal perfusion pressure was kept constant during carotid occlusion. We conclude that, in conscious dogs at rest, the moderate sympathetic activation associated with carotid occlusion is too small to induce renal sympathetic vasoconstriction or antinatriuresis. The “carotid sinus polyuria” is a pressure-diuresis.

ISSN:0009-7330    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

We determined regional myocardial blood flow (MBF: 15 /im tracer microspheres) and hemodynamics in 12 unanesthetized normal calves and 10 unanesthetized calves with severe right ventricular hypertrophy (RVH). RVH was produced by banding the main pulmonary artery of 24- to 48-hour-old calves 25–30 weeks prior to the study. Measurements were made in six normal calves and seven calves with RVH at control (baseline), during isoproterenol infusion (0.2 μg/kg per min), and during acute volume overload produced before and after propranolol pretreatment. In six normal calves and three RVH calves, these parameters also were determined before and during maximal coronary vasodilation produced by intraventricular infusion of adenosine (4 μM/kg per min). In this model of RVH, right ventricular (RV) MBF was significantly increased whereas the left ventricular (LV) mass and LV MBF were normal. Minimal coronary vascular resistance per unit weight of the hypertrophied RV was identical to that in the normal RV myocardium. This suggested that, although functional cross-sectional area of the vascular bed supplying RV myocardium, hypertrophied from soon after birth, kept pace with increasing muscle mass, higher baseline perfusion in the hypertrophied RV myocardium occurred at the expense of decreased available coronary vascular reserve. Isoproterenol infusion resulted in subendocardial underperfusion in both ventricles of calves with RVH, but this did not occur in the normal RV myocardium. Acute volume expansion of a similar magnitude was perceived as a more severe stress in calves with RVH as reflected by a larger increase in their RV and LV MBF. Propranolol pretreatment significantly blunted these increments in MBF despite markedly higher ventricular filling pressures. Throughout the study, blood flow in right and left sides of the interventricular septum closely resembled that in RV and LV, respectively.

ISSN:0009-7330    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

The relaxation of isolated cardiac muscles from mammals was recently shown to be sensitive to the loading conditions because the time course of relaxation could be changed by changing the load. This effect apparently is related to the amount and functional status of the sarcoplasmic reticulum. The purpose of this study was to determine whether hypoxia affected the load sensitivity of papillary muscles isolated from both rats and cats. We used three mechanical tests to establish the presence of load-sensitive relaxation. First, we superimposed records of isotonic contractions at increasing afterloads up to isometric contraction. From these records we measured the ratio (tRi) which was the time from the initiation of the contraction to the initial decay of force at each isotonic afterload, divided by the time it took for the force of an isometric contraction to relax to that same afterload. If the tRi was less than 1.0, then the muscle was load sensitive. Hypoxia caused the loss of load-sensitive relaxation in isotonically contracting rat papillary muscles since the tRi ratios were not significantly different from 1.0 at all afterloads. Both hypoxia and caffeine were required to make cat papillary muscles load insensitive. Second, during hypoxia, loads added in midcontraction did not induce early relaxation in rat papillary muscles, but still did so in cat muscles. Hypoxia plus caffeine eliminated this load-induced early relaxation in cat papillary muscles. Third, physiologically contracting muscles made hypoxic did not lengthen earlier in response to an additional load. This decrease of load sensitivity under hypoxic conditions could contribute to the relaxation abnormalities observed during regional wall motion studies.

ISSN:0009-7330    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

Groups of littermate rabbits were treated for various periods up to 6 weeks with twice daily subcutaneous injections of saline, D-propranolol, DL-propranolol, or metoprolol, the latter two at doses equivalent to those used in clinical therapy. Investigations were made at a sufficient time (20–24 hours after the most recent dose) to ensure that the drugs would have been eliminated from the body, so that any observed changes would represent an adaptation to treatment, not effects due to the presence of the drugs. The ECG was recorded in vivo at regular intervals during treatment. After several days, Q-Tcwas prolonged by the /J-blockers, reaching a peak effect at about 3 weeks from the start of treatment, and returned to control values at 3 weeks after cessation of treatment. Action potential duration, measured in vitro by intracellular recording, was also prolonged uniformly in atria and ventricles over a similar time-course, unrelated to cardiac frequency, but shortened in distal Purkinje cells. Peak tension was not altered in propranolol-adapted papillary muscles, but the relationship of rate of rise of tension to peak tension was steeper. It is concluded that these effects represent a myocardial adaptation to prolonged β-blockade.

ISSN:0009-7330    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

We studied the effects of volume loading on left ventricular isovolumic relaxation rate in 16 intact anesthetized dogs. End-diastolic pressure, mean aortic systolic pressure, dp/dtmnx, and heart rate were measured at end expiration and end inspiration. Volume loading to approximately 5, 10, 15, and 20 mm Hg above initial end-diastolic pressure was performed. In nine dogs, simultaneous ventricular dimensions were measured with previously implanted tantalum screws using biplane cineangiography. Similar volume loading was done in open-chest and open-pericardium states. Relaxation rate was measured in 3413 beats using T, the time constant of exponential isovolumic pressure fall. T was calculated as reported previously by others and also from a linear regression of dp/dt against p, to eliminate the effects of extracavity pressure changes. T always increased significantly with volume loading, indicating slower relaxation. (For example, with the chest intact, mean T increased from 26 ± 2 (SEM) msec before volume loading to 41.5 ± 4 msec after volume loading.) Using multiple linear regression analysis, we found, in agreement with previous reports, that T decreased significantly as dp/dtMAX, and heart rate increased. In contrast to previous reports, we also found that T increased significantly as end-diastolic and mean aortic systolic pressure increased. These four variables taken together accurately predicted T [SEE (standard error of estimate) = 3.2 msec,R= 0.94,P< 0.001]. Geometric variables, including ventricular dimensions and ejection fraction, did not have a statistically significant effect on T independent of the hemodynamic variables. Opening the chest or pericardium did not have a consistent effect on T. Volume loading slows isovolumic relaxation rate in the intact canine heart. This effect appears to be a reflection of the dependence of relaxation on both end-diastolic and mean aortic systolic pressures.

ISSN:0009-7330    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

Our goal was to distinguish the circulatory changes due to acute hypervolemia caused by whole blood and colloid solution from those due to acute hemodilution caused by colloid solution in the conscious rabbit. In six rabbits, homologous whole blood, dextran solution, or modified gelatin solution, equal to 32% of blood volume, was infused over 22 minutes. In six rabbits, 42% of blood volume was exchanged with dextran solution over 34 minutes, at constant left atrial pressure. A similar exchange was performed over 28 minutes in a further six arterial baroreceptor-denervated rabbits. Withdrawn blood later was infused over 10–12 minutes. In all rabbits, the baroreceptor-heart rate reflex was characterized by infusion of phenylephrine and sodium nitroprusside. Whole blood hypervolemia caused stroke volume and blood pressure to rise, without a rise in heart rate. Colloid-solution hypervolemia caused stroke volume and heart rate to rise, with little change in blood pressure. The effects of hemodilution were the same as those of dextran-solution hypervolemia, and the fall in hematocrit was similar, but baroreceptor denervation eliminated the rise in heart rate. We conclude that in the conscious rabbit: (1) acute rise in central venous pressure causes tachycardia only when there is concomitant hemodilution; (2) the tachycardia of hemodilution with unchanged central venous pressure is largely baroreceptor-dependent; (3) the effects of hemodilution on systemic vascular conductance appear to be due to reduction in oxygen-carriage rather than in viscosity; (4) the rabbit can closely match increase in conductance by increase in output, which is largely baroreceptor-independent.

ISSN:0009-7330    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

To determine the role of the prostaglandins on renal norepinephrine release, the effect of inhibition of prostaglandin synthesis was examined in anesthetized dogs during reflex activation of the renal adrenergic nerves. Hypotension increased the renal vein plasma concentrations of norepinephrine from 380 ± 59 to 608 ± 106 pg/ml (mean ± SEM;P< 0.01) and of PGE2from 55 ± 7 to 81 ± 14 pg/ml (P< 0.05). Subsequent administration of indomethacin or meclofenamate lowered the renal venous concentration of PGE2to 26 ± 3 pg/ml (P< 0.01), but had no significant effect on the norepinephrine concentration (620 ± 89 pg/ml). Administration of indomethacin or meclofenamate to dogs with sodium depletion lowered renal venin plasma concentration of PGE2from 108 ± 40 to 20 ± 3 pg/ml (0.05 <P< 0.1) but had no effect on the renal venous norepinephrine concentration (475 ± 50 vs. 397 ± 46 pg/ ml). In dogs fed a normal salt diet, inflation of a balloon placed in the thoracic inferior vena cava lowered cardiac output and increased the renal venous concentrations of norepinephrine from 212 ± 60 to 496 ± 112 pg/ml (P< 0.01) and of PGE2from 28 ± 5 to 96 ± 18 pg/ml (P< 0.01). Subsequent administration of indomethacin lowered the renal venous concentration of PGE2to 16 ± 5 pg/ml (P< 0.01), but had no significant effect on the concentration of norepinephrine (548 ± 91 pg/ml). During the three experimental conditions examined, renal blood flow was lowered by inhibition of prostaglandin synthesis. These results in the dog suggest that the attenuating effect that prostaglandins exert on the renal vascular action of the adrenergic nerves is not due to inhibition of norepinephrine release.

ISSN:0009-7330    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

The purpose of this study was to determine whether inhibitors of prostaglandin synthesis alter the peripheral vascular effects of the cardiac glycoside, ouabain. Ouabain (35 /»g/kg) was given to 12 mongrel dogs, six of which had been pretreated 1 hour previously with the non-steroidal anti- inflammatory drugs (NSAID), indomethacin or meclofenamate (6 mg/kg, iv, bolus followed by 1 mg/ min infusion). Hemodynamic variables were monitored for 30 minutes before and for 3 hours after ouabain administration. Mean arterial pressure was significantly increased in all dogs for 45 minutes after ouabain, and cardiac output was unchanged. In the animals that did not receive non-steroidal anti-inflammatory drugs, ouabain transiently (15 min) decreased renal blood flow and increased renal vascular resistance. Mesenteric blood flow was not altered by ouabain until 90 minutes, after which time it was significantly increased. In the dogs pretreated with NSAID, renal blood flow was reduced for 60 minutes after administration of ouabain. In addition, 30 minutes after ouabain, the mesenteric blood flow was reduced by 43 ± 17 ml/min from a baseline value of 192 ± 42 ml/min (P< 0.05), and this reduction persisted for the entire 3-hour observation period. Control animals that did not receive ouabain showed neither an increase in arterial pressure nor a decrease in renal or mesenteric blood flow over the period of the experiment. Thus, pretreatment with NSAID enhanced the duration of the renal vasoconstrictor effects of ouabain in the dog and converted late mesenteric vasodilation to early and persistent vasoconstriction. These data imply a potentially important role for vasodilating prostaglandins in modulating the mesenteric as well as the renal circulatory responses to ouabain.

ISSN:0009-7330    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

The ability of rabbit aorta to oxidize various substrates was studied to determine which of these compounds may be energy substrates for vascular smooth muscle (VSM). Glucose, ketone bodies, medium-chain length fatty acids, branched-chain amino acids, and glutamine all are oxidized at comparable rates on a molar basis. Some other amino acids, long chain fatty acids, pyruvate and glycerol also are oxidized, but at lower rates. The oxidation of 6 amino acids could not be detected. VSM was found to release ketone bodies when incubated in leucine /β-hydroxybutyrate or octanoate. This suggests that the acetoacetyl CoA and/or acetoacetate derived from these substrates is not completely oxidized. The oxidation rate of several substrates when measured individually is inhibited by 50–80% by the presence of a combination of other substrates in the medium. Under these conditions, glucose is a minor substrate for oxidative metabolism accounting for only 5% of O2consumption. The oxidation rate of all the exogenous substrates together is calculated to account for less than half of the oxygen consumption; this finding indicates that an endogenous substrate must also be utilized.

ISSN:0009-7330    

出版商:OVID    

年代:1981

数据来源: OVID