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Query: UMLS:C0920646 (renal ischemia)
 2,515 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies have demonstrated that the fall in inulin clearance which occurs 3 hours after the intrarenal administration of norepinephrine can be markedly attenuated by the prior administration of intrarenal prostaglandin E2 (PGE). Since in the previous studies PGE led to a marked increase in both renal blood flow and solute excretion, we designed the present series of experiments to investigate whether an increase in renal blood flow, solute excretion, or other factors were responsible for the protective effect in the norepinephrine model. Two renal vasodilators, bradykinin and secretin, were evaluated initially. Bradykinin administration prior to norepinephrine administration had a protective effect similar to that previously found with PGE, whereas secretin did not. Both of these vasocilators increased renal blood flow to the same degree, but only bradykinin increased urine flow and solute excretion. The fall in inulin clearance 3 hours after the administration of norepinephrine was also attenuated by two diuretics (mannitol and furosemide) which tended to increase renal blood flow. In contrast, two natriuretic agents, which are also renal vasoconstrictors (chlorothiazide and benzolamide), had no protective effect. Further, chlorothiazide and benzolamide obviated the protective effect of bradykinin. These studies demonstrate that there are several types of pharmacologic agents which can modify the magnitude of renal functional impairment resulting from extreme renal ischemia. Although the mechanism of the protective effects remain unclear, the findings are compatible with the view that the protective effect noted with PGE, bradykinin, mannitol, and furosemide may be related to an increase in osmolar excretion which occurred with administration of each of these agents. This potentially salutory effect (increased osmolar excretion), however, could be overcome by an agent (e.g., chlorothiazide or benzolamide) which also increased renal resistance prior to the administration of norepinephrine.
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PMID:Study of factors which modify the development of norepinephrine-induced acute renal failure in the dog. 51 86

The intrarenal arterial and arteriolar changes in the kidneys of 80 patients with chronic renal insufficiency maintained on hemodialysis were studied semiquantitatively by light microscopy and histochemistry. Intimal proliferation was common and accounted for thickening of vessel walls and luminal narrowing. Fibrocollagenous and fibroelastotic intimal changes were located predominantly in the interlobular and arcuate arteries, whereas the fibromucinous intimal lesion was found mainly in the interlobar arteries. Thickening of the media was encountered in 25 per cent, and adventitial fibrosis in 20 per cent of the kidneys. Necrotizing arterial of arteriolar lesions were not seen. The significance of these alterations as a possible cause of renal ischemia and their role in the perpetuation of hypertension are discussed.
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PMID:Intrarenal vascular alterations in hemodialysis patients. A semiquantitative light microscopic study. 52 65

Renal ischaemia produced by clamping of the blood vessels in situ for periods of 10 to 150 minutes resulted in a progressive depletion of the total content of adenylates in the kidney tissue (sigma ATP, ADP, AMP). Initial dephosphorylation of ATP and ADP, resulting in further catabolism of AMP to hypoxanthine and xanthine, accumulated in the ischaemic tissue. The postischaemic ability of the kidney tissue to functional regeneration was in correlation with the ischaemic adenylate loss (r = +0.94, P less than 0.001) as well as the accumulation of hypoxanthine and xanthine (r = -0.90, P less than 0.001). The initial adenylate resynthesis rate was constant during recovery (0.5--0.8 mumol/g . h-1), independent of the duration of the preceding ischaemia. Determination of the postischaemic adenylate regeneration thus gave no additional prediction of the reversibility of the ischaemic parenchymal damages.
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PMID:The predictive value of 5'-adenine nucleotide depletion and replenishment in ischaemic rabbit kidney tissue. 53 81

Metabolism of serotonin was studied in duodenum of rabbits in acute kidney ischemia (from 15 min to 1 hr). Estimations of serotonin and 5-hydroxy indolacetic acid content and the activities of 5-hydroxytryptophane decarboxylase (5-HTD) and monoamine oxidase (MAO) using serotonin as a substrate were carried out. A complicated phase dynamics in the intestine of main patterns of serotonin metabolism was observed in acute kidney ischemia. Within the ischemic period content of serotonin and the MAO activity correlated with the activity of 5-HTD in the duodenal tissue. The alterations in the activity of MAO from intestine suggest that this enzyme was especially important in the serotonin metabolic conversions studied.
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PMID:Serotonin metabolism in duodenal tissue in acute renal ischemia in rabbits. 59 97

Renovascular hypertension (RVH) in the neonatal period is frequently associated with thromboembolic complications of umbilical artery catheterization. Seven newborn infants with RVH were studied by angiography and/or radionuclide examination. Aortography and, in one case, selective angiography showed variable degrees of renal artery occlusion or attenuation. Thromboembolic defects were frequently present in other vessels. Radionuclide flow studies, renograms, and computer analysis of data (ADAC) demonstrated defects in renal function, indicative of renal ischemia. There was a high degree of correlation between angiographic and radionuclide studies. Successful medical management suggests a more conservative alternative to nephrectomy in the hypertensive newborn.
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PMID:Renovascular hypertension as a complication of umbilical arterial catheterization. 62 52

Renal ischemia and cooling may be achieved by intraluminal balloon occlusion and intermittent hypothermic perfusion using a double lumen, balloon-tipped catheter introduced into the renal artery percutaneously. This technique was used successfully in 26 of 31 extensive nephrolithotomies, eliminating the need for dissection and clamping of the renal artery and intricate surface cooling. Intrarenal operations could be performed as effectively as with clamp occlusion. Despite a mean ischemia time of 54 minutes the individual 131I-hippuran clearance of the operated kidneys was only reduced to a mean 78.4 per cent of the preoperative value 2 to 3 weeks postoperatively and increased to 92.2 per cent after 3 to 6 months, with a tendency toward further improvement.
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PMID:Simultaneous balloon occlusion of the renal artery and hypothermic perfusion in in situ surgery of the kidney. 65 Jul 44

Hypertension is a frequent complication of reflux nephropathy. The cause of this hypertension is unknown. Our study was undertaken to assess the possible role of the renin-angiotensin system in the hypertension associated with unilateral reflux nephropathy. We selected for study 17 normotensive and 12 hypertensive patients with strictly unilateral reflux nephropathy. There were 3 normotensive and 2 hypertensive patients with a renal vein renin ratio exceeding 1.5. Of these 3 normotensive patients 1 had evidence from divided renal function studies to suggest functional renal ischemia. No consistent evidence was obtained to support the concept that the renin-angiotensin system has a primary role in the non-malignant hypertension of unilateral reflux nephropathy.
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PMID:Renal vein renin concentration in the hypertension of unilateral reflux nephropathy. 67 98

Cardiac output (CO) and renal blood flow (RBF) were simultaneously evaluated (microsphere method) in awake rats, 3, 6, and 24 h after induction of acute renal failure by mercuric chloride (HgCl2; 4.7 mg/kg body weight). 3 h after injection of HgCl2, CO and RBF decreased to 77 and 72% of respective control values of 32.0 +/- 2.4 and 4.65 +/- 0.44 ml/min/100 g. Renal vascular resistance (RVR) and total peripheral resistance (TPR) were significantly increased compared to control at this time. Similar results were observed 6 h after administration of HgCl2. Volume expansion with plasma (2% of body weight) restored CO, RBF, TPR, and RVR to normal 3 h after injection of HgCl2. Despite significantly elevated blood urea nitrogen 24h after injection of HgCl2 (103.7 mg%), all hemodynamic parameters were within control range. Plasma volume was normal 3 h after HgCl2 but was significantly elevated compared to control 24 h after HgCl2 (4.73 vs. 3.92 ml/100 g, p less than 0.01). These findings indicate that factors other than preferential renal vasoconstriction may be involved in the transient renal ischemia of HgCl2-induced acute renal failure.
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PMID:Systemic hemodynamics in nephrotoxic acute renal failure. 67 89

We conducted experiments to determine (1) tissue, blood, and urine levels of adenosine produced by the ischemic kidney under conditions of renal artery occlusion, and (2) the site(s) of production and release of adenosine by the kidney. Concentrations of adenosine, inosine, and hypoxanthine in the dog urine were found to increase after 2 minutes of renal artery occlusion as were concentrations of these metabolites in renal tissue after 10 minutes of renal artery occlusion. Renal venous plasma levels of inosine and hypoxanthine also were elevated after 3 minutes of arterial occlusion. In modified stop-flow experiments, adenosine appeared in the urine in a peak that corresponded most closely with proximal tubule fluid. 5'-Nucleotidase, the enzyme which catalyzes the dephosphorylation of 5'-AMP or 5'-IMP to adenosine or inosine, respectively, was found to be located primarily on the external membranes and mitochondria of proximal tubule cells, but not in distal tubule or collecting duct cells. Since adenosine has been demonstrated to elicit renal vasoconstriction and is produced by the ischemic kidney, it is suggested that adenosine may be involved in the mediation of postocclusion renal ischemia.
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PMID:Adenosine production in the ischemic kidney. 67 22

There are afferent nerve fibers responsive to alterations of the kidney's chemical environment in the renal nerves of the rat. In anesthetized, artificially ventilated, male Sprague-Dawley rats, single unit recordings were prepared by dissection of the centrally cut nerves of the right kidney. The stimuli used included occlusion of the renal artery, systemic asphyxia, changes in renal arterial and venous pressures, changes in ureteral pressure, and cyanide infusion. We found a population of sensory nerve fibers whose endings are activated only during markedly impaired renal blood flow (produced by clamping the renal artery, severe hypotension below 40 mm Hg, and prolonged occlusion of the renal vein), and during systemic asphyxia. The same units are not responsive to increases and decreases in systemic arterial pressure (range: 40--190 mm Hg), to ureteral pressure (range: 0--50 mm Hg), or to changes in renal venous pressure. None of the 40 single units studied was spontaneously active; their pattern of activation during renal ischemia always was characterized by trains of impulses. These sensory units have functional properties distinctly different from those of known renal mechanoreceptors. They appear to be a homogeneous group of sensory elements, and we have termed them renal ("R") chemoreceptors. Evidence also is presented which is consistent with the concept that a chemical substance released by or accumulated within the kidney might be the agent activating these chemoreceptors during renal ischemia.
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PMID:Renal chemoreceptors in the rat. 68 56


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