ISSN:0009-7330    

出版商:OVID    

年代:1978

数据来源: OVID

ISSN:0009-7330    

出版商:OVID    

年代:1978

数据来源: OVID

ISSN:0009-7330    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

Male Sprague-Dawley rats with unilateral renal artery stenosis and a contralateral untouched kidney develop a malignant hypertension (MH) which is characterized by high blood pressures, sodium and water depletion, and subsequent activation of the renin-angiotensin system. In the present studies we found plasma arginine vasopressin (AVP) concentrations 3-fold higher than those in rats with benign renal hypertension, and 4- to 5-fold higher than those in normotensive control rats. Analysis of individual values showed considerable scatter; about 50% of the values fell in the range of benign hypertensive or control rats. When a specific AVP antiserum was injected, iv, into eight conscious unrestrained MH rats, BP transiently fell toward control values in four; in one, BP fell by only 10 mm Hg, and three other MH rats showed no response. In the same rats, injection of a specific angiotensin II antiserum always induced a transient fall in BP. On the basis of these and previously reported observations, we conclude that, subsequent to sodium and water loss and activation of the renin-angiotensin system, vasopressin release is stimulated in a significant number of MH rats and that, in these rats, vasopressin may cause significant systemic vasoconstriction. Thereby vasopressin may contribute to the development of malignant renal hypertension in rats.

ISSN:0009-7330    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

We previously have shown that chronic sodium chloride (NaCI) loading protects against HgCI2-induced acute renal failure (ARF) in dogs. To determine whether NaCI loading protects against an ischemic model of ARF, unilateral oliguric renal failure was produced by the infusion of norepinephrine (NE) into the renal artery of both saline-expanded (SE) and water-drinking (WD) dogs (n = 7). The renal renin content (30 U/g kidney) of SE dogs was suppressed (P< 0.001) compared to that of WD dogs (132 ± 18). Forty-eight hours after infusion of NE (1.5 fig/kg per min x 100 min), inulin clearances from the infused kidney of SE (6 ml/min ± 2) and WD dogs (7 ± 2) did not differ; in both groups, respective clearances from the noninfused kidney (43 ml/min ± 3) and (36 ± 5) also did not differ from each other. The percent fall in renal blood flow to the infused kidney 48 hours after NE in SE (44%) and WD dogs (38%) did not differ. Because of failure to demonstrate protection, a lower dose of NE (0.75μg/kg Per m+- n x 40 min) was infused into SE and WD animals (n = 6). Forty-eight hours after low dose NE, inulin clearances of the infused kidney of SE (17 ml/min ± 5) and WD dogs (17 ± 4) did not differ. Respective clearances in the noninfused kidney of SE (46 ml/min ± 6) and WD dogs (35 ± 4) did not differ. Therefore, despite suppression of renal renin content, NaCI loading failed to protect against this ischemic model of ARF. In conclusion, unlike HgCI2-induced ARF, it is unlikely that the renin angiotensin system contributes to the pathogenesis of this ischemic model of ARF.

ISSN:0009-7330    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

Thin sections of canine right and left ventricular endocardium and myocardium were studied in a tissue bath to compare conduction properties of intraventricular specialized conducting tissue [Purkinje fibers (PF)], the superficial layers of subendocardial ventricular muscle (SVM), and the deeper ventricular muscle (DVM) below this level. The study was carried out because of observations that some areas of the endocardium, which are devoid of either specialized conducting tissue or of PF-VM junctions between specialized conducting tissue and ventricular muscle, conduct relatively rapidly, favoring specific orientations of propagation. Preparations containing PF, SVM, and DVM were studied electrophysiologically and histologically. A technique of stripping limited areas of endocardium was used to expose DVM in order to determine its intrinsic calculated conduction velocity. In 12 preparations, the average calculated conduction velocity in PF was 1.62 m/sec, and the average in DVM was 0.26 m/sec. The SVM conduction velocity was intermediate between the two, averaging 0.98 m/sec when propagation was parallel to SVM fiber orientation. Conduction velocity transverse to SVM fiber orientation was not significantly different from DVM conduction velocity. Histologically, the most superficial layers of VM were oriented uniformly in the direction of rapid subendocardial conduction, in contrast to DVM fibers in which orientation varied. It is concluded that the geometric arrangement of SVM fibers may provide a means for rapid subendocardial conduction and impulse distribution at a conduction velocity intermediate between PF and DVM in areas devoid of specialized conducting tissue.

ISSN:0009-7330    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

We tested a number of hypotheses concerning the mechanism of K+-induced vasodilation of the coronary vascular bed. Blood flow in the circumflex artery was measured in pentobarbital-anesthetized, open-chest dogs. Intracircumflex artery bolus injections of 40 μmol of isosmotic KCI produced decreases in coronary vascular resistance ranging from 34% to 48%, depending on the initial resistance of the vascular bed. K+ administration had no effect on heart rate and produced a 4 mm Hg decrease in mean arterial pressure. K+ injection caused a 0.2 vol% increase in coronary sinus O2content in a preparation in which left common coronary flow was held constant. The magnitude of K+-induced vasodilation was not significantly affected by the administration of propranolol, atropine, phentolamine, or lidocaine. K+-induced vasodilation was attenuated (50%) by ouabain plus lidocaine. Acerylcholineinduced vasodilation was not significantly diminished by ouabain plus lidocaine. We conclude that the mechanism of K+-induced vasodilation does not involve an increase in the metabolic activity of the heart or an interaction between K+ and tissue neural elements. Our data do support the hypothesis that K+-induced vasodilation is at least partly the result of an activation of the electrogenic Na+—K+- transport system of coronary smooth muscle.

ISSN:0009-7330    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

Sodium arachidonate, 10−g/kg per minute, was infused into the renal artery of a nonfiltering canine kidney in situ in order to determine the effects of enhanced prostaglandin synthesis on renal blood flow and its distribution in circumstances where prostaglandins produced in the medulla could not gain access to the cortex via tubular fluid. The contralateral normal kidney was also infused with sodium arachidonate and served as control. Radioactive microspheres were used to calculate the hemodynamic effects. In the nonfiltering kidney, the total renal blood flow increased after sodium arachidonate from a mean of 105 ml/min per 100 g to 146 ml/min per 100 g (P< 0.01). This increase was completely abolished by prior treatment with indomethacin, 8 mg/kg, intravenously. The normal kidney responded qualitatively the same as the nonfiltering side. In both kidneys, blood flow increased significantly to all cortical zones except the outermost (zone 1), but the fractional distribution of renal blood flow was significantly increased only in the innermost cortex (zone 4). Since the kidneys were nonfiltering, the increase of renal blood flow during infusion of arachidonic acid cannot be explained by prostaglandins being transported from renal medulla to the cortex through renal tubules. Most likely prostaglandins are produced locally in the cortex and have only local effects.

ISSN:0009-7330    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

Angiotensin II was infused at rates varying from 0.1 to 10 ng/kg per minute into 49 subjects with hypertension and 26 normotensive subjects and changes in blood pressure, plasma angiotensin II, and plasma renin activity (PRA) were determined after 20 and 30 minutes at each dose. Similar dose-related increases in angiotensin II and blood pressure occurred with a threshold of 1 ng/kg per minute in the normotensive and hypertensive subjects. Whereas angiotensin II induced a significant, dose-related decrement in renin activity in the normotensive subjects, with a threshold of 1.0 ng/kg per minute, no significant change in renin activity occurred in either the normal-renin or high-renin hypertensive subjects. In a separate study, nine normotensive and six hypertensive sodium-restricted subjects were given a converting enzyme inhibitor, SQ 20881, 30 pg/kg. Despite a significantly greater fall in blood pressure(P< 0.006) and angiotensin II concentration(P< 0.045) in the hypertensive subjects, they did not have a greater rise in plasma renin activity. We conclude that angiotensin II reduces renin release in normal man at infusion rates that yield plasma angiotensin II levels within the physiological range but has a strikingly reduced influence on renin release in hypertension. In high-renin hypertension due to renal artery stenosis or nephrosclerosis, renin release is presumed to be relatively autonomous because of a dominant, intrarenal mechanism. The mechanism in normal-renin essential hypertension is not clear, but the abnormality could well be related to the pathogenesis of the hypertension.

ISSN:0009-7330    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

After inhalation, CI5O2(T,= 2 minutes) rapidly diffuses into pulmonary blood and is cleared from the lungs within 10 seconds. The purpose of this study was to determine whether impaired clearance of inhaled C15O2from oligemic zones, distal to areas of obstructed pulmonary blood flow, could be detected by serial pulmonary imaging with a positron camera. Experimental obstruction of branches of the pulmonary artery was induced in 19 anesthetized dogs by inflation of balloon-tipped catheters (8-12 mm in diameter), injection of radiopaque silicone spheres (0.5-4.0 mm), and embolization with barium-impregnated autologous blood clots (1-5 mm) via the right external jugular vein. After a single bolus injection of 2 mCi of C15O2into the endotracheal tube, serial lung images ofIO activity were obtained over 60-180 seconds. Obstruction of pulmonary arterial branches resulted in visualization of discrete zones of impaired15O clearance which varied in area with catheter diameter. Location and size of these zones were confirmed by repeat imaging after direct injection ofl5O-labeled blood through the distal catheter lumen. In dogs receiving autologous clots (n = 8), similar zones of impaired "O clearance were consistently imaged, and single emboli as small as 2 mm in diameter produced regions of retained I5O activity. Zones of retained15O activity corresponded to the location of radiopaque emboli on chest radiographs. This study introduces a new technique of radionuclide imaging for detection of pulmonary emboli that is noninvasive, safe, sensitive, and repeatable at short intervals.

ISSN:0009-7330    

出版商:OVID    

年代:1978

数据来源: OVID