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

This study tested the ability of the converting enzyme inhibitor, captopril, to lessen the severity of acute renal failure following temporary occlusion of the renal artery. In the control group, 11 dogs were anesthetized with halothane, and the left kidney was isolated through a midline incision. The renal artery, vein, and ureter were then clamped for 120 min. Immediately after occlusion, the kidney was flushed with 40 ml of saline at 34 degrees C. When the clamp was released, a contralateral nephrectomy was performed and the animal allowed to recover. Serum creatinine and blood urea nitrogen levels were followed on a daily basis thereafter. Thirteen captopril-treated dogs were treated in the same fashion except that captopril (1.25 ml/kg, i.v.) was given prior to the 120-min period of renal ischemia. Three of 11 (27%) control dogs survived, whereas 10 of 13 (77%) captopril-treated animals survived (P less than 0.05). Serum creatinine (5.4 +/- 2.5 mg/dl) and serum urea nitrogen (96 +/- 33 mg/dl) peaked on day 8 in the captopril-treated group and were consistently lower than in the untreated group. These observations suggest that captopril is useful when temporary interruption of the renal circulation is encountered, such as in renal autotransplantation, cadaveric renal transplantation, and renal revascularization. These data also suggest that inhibition of the renin-angiotensin system may lessen the severity of acute renal failure following renal ischemia.
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PMID:Enhancement of recovery in postischemic acute renal failure with captopril. 637 20

Studies of the renin-angiotension system and the effects of pharmacologic blockade have enhanced our understanding of renovascular hypertension. A critical degree of arterial stenosis produces kidney ischemia sufficient to activate this hormonal system, whose actions include vasoconstriction and sodium retention. Accurate clinical evaluation may depend upon recognizing the differences in pathophysiology between "one-kidney" and "two-kidney" forms and the dynamic nature of this condition.
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PMID:Pathophysiology of renovascular hypertension. 638 77

The juxtaglomerular (JG) complex was studied at different times after 90 min of warm kidney ischemia: 2 h, 24 h, 3 days, 10 and 30 days following the ischemia. The ischemic injury was performed on the left kidney, under two experimental conditions: with and without previous nephrectomy of the contralateral nonischemic kidney. The activity of the JG complex was evaluated by assessing the JG index and by determination of plasma renin activity. Results show that, under given experimental conditions, fate of the particular JG complex depends on the fate of its own nephron. In the presence of the contralateral intact kidney most nephrons of the ischemic kidney underwent gradual degeneration and their JG complexes degenerated too. When ischemic kidney was the sole kidney, the majority of nephron units regenerated and their JG complexes recovered both morphologically and functionally.
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PMID:Fate of the juxtaglomerular complex after ischemic injury. 638 Jan 89

Aortic ligation between the origins of the renal arteries in the rat produces a left renal ischemia, renin-dependent hypertension, and a transitory hindlimb paralysis of less than 2 h. Removal of the left ischemic kidney at the time of aortic ligation curtails the rise of blood pressure, plasma renin activity is normal, and paralysis is still present 24 h after surgery. Administration of an angiotensin-converting enzyme inhibitor or saralasin also prevents recuperation from paralysis after aortic ligation. Independent manipulation of the mean arterial pressure or plasma renin activity by pretreatment with reserpine or deoxycorticosterone before surgery shows that the presence or absence of paralysis is dependent on the plasma renin activity and not on the high blood pressure. Blood flow measurements show that paralysis is due to a persistent impairment of blood supply to the hindlimb muscle and not to ischemia of the spinal cord. Infusion of angiotensin II to aortic-ligated, left-renoprival animals tends to restore blood flow to muscle. It is concluded that after renal ischemia the renin-angiotensin system, independent of its hypertensive effect, restores blood flow by stimulating the development of collateral circulation.
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PMID:Renin-angiotensin and development of collateral circulation after renal ischemia. 675 70

The objective of the present work was to study the changes in the brain and renal renin-angiotensin system (RAS) during their simultaneous stimulation by ischemia. Experiments were carried out on the following groups of male normotensive Wistar rats: intact, with brain ischemia, with renal ischemia, with combined brain and renal ischemia. The three ischemic groups of animals had some arterial pressure elevation without reaching hypertensive values. In animals with combined brain and renal ischemia brain renin concentration (BRC) was raised, while plasma renin activity (PRA) was reduced relative to the intact controls, i.e. as in animals with brain ischemia alone. Renal renin concentration (RRC) in the ischemic kidney was at the level of the one in intact animals and in animals with brain ischemia. In the intact contralateral kidney of rats with combined ischemia RRC was reduced relative to the intact kidney of animals with renal ischemia and statistically insignificantly reduced relative to the RRC in intact controls and in animals with brain ischemia. The results of this study showed that inverse ratio between renal and brain RAS exists also in the single clamped--birenal model of hypertension. Interaction between the two RAS is manifested when they both are simultaneously stimulated, with prevalence of the effect of brain RAS, which affects renin secretion in the kidney.
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PMID:[Brain and kidney renin-angiotensin system in rats with simultaneously induced cerebral and renal ischemia]. 699 Dec 47

Quinacrine (QC) binds with high affinity to the intracellular storage granules of juxtaglomerular cells (JG-cells) in the afferent arteriolus of the glomerulus of the kidney. The present study tests whether QC bound to JG-cells can be released. The cells were stimulated by renal ischemia and hemorrhagic shock combined with immobilization stress. 1 h after onset of renal ischemia QC-JGI (modified Hartroft & Hartroft 1953) in 14C-QC-treated rats had decreased to about 40% in the ischemic kidney compared to a not ligated control kidney. The 14C-contents in the ischemic kidney had decreased to 33% of that in the untouched control kidney. Hemorrhagic shock was obtained by bleeding into a reservoir for 15 min or 1 h. Rats who received QC or 14C-QC 1 h before onset of bleeding showed no change in QC-JGI (15 min shock) or 14C-contents (1 h shock) as compared to controls. This was probably due to formation of new QC-binding granules, which took up still circulating quinacrine thereby masking a release. If the time between the QC injection and the onset of shock was extended to about 15 h, when circulating amounts of QC are very low, a decrease of QC-JGI (about 30% of controls) was seen in the kidneys of the shocked rats. The results are compatible with the possibility that QC in vivo bound to granules of JG-cells could be released together with the content of the granules following stimuli known to induce renin release. Quinacrine-binding therefore possibly provides a new method to study endocrine cells in the way it has been used in the present study as a marker of JG-cell activity.
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PMID:Juxtaglomerular cell activity during hemorrhage and ischemia as revealed by quinacrine histofluorescence. 701 Sep 18

The high blood flow rate/gram of kidney tissue supplies mainly the renal cortex. The net effect of the interaction of the renin-angiotensin system, the kallikrein-kinin system and prostaglandins is to autoregulate renal blood flow within a narrow range. Drugs and neurogenic factors also influence renal hemodynamics. The renal circulation responds to changes in extracellular fluid volume, and in cardiac output. Renal ischemia occurs readily as these parameters decrease and prompt correction of circulatory dynamics can restore renal blood flow and prevent tubular necrosis. With hypovolemia or heart failure, angiotensin II is a mediator of efferent arteriolar constriction promoting a proportionately greater fall in renal plasma flow than in glomerular filtration rate, thereby augmenting sodium reabsorption. With renal failure, glomerulotubular balance is affected conversely promoting sodium loss. Appreciating these distinctions allows recognition of inappropriate sodium retention or loss. With such data, prognosis can be estimated more accurately and attempts to restore circulatory dynamics can be guided.
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PMID:Pathophysiology of renal hemodynamics. 726 10

The aims of this study were (1) to investigate the effect of R 75231, a nucleoside transport inhibitor, on renin-angiotensin release after renal ischemia-reperfusion and (2) to establish a possible protective effect of this drug on renal function. We used a canine model for auto- transplantation of kidneys that had been subjected to 30 min of warm ischemia and subsequently to 24h of cold storage in HTK preservation solution, with immediate contralateral nephrectomy. R 75231 was injected intravenously into six dogs in two equal portions of 0.05 mg/kg both 30 min and 10 min before reanastomosis was established. Another six dogs were used as a control group. At 2 weeks post-transplantation, five out of six dogs in the R 75231 group and one out of six in the control group were still alive. Starting on day 4, serum creatinine was lower in the R 75231 group than in the control group (p < 0.005). In contrast to the control group, an inversion of the median preischemia adenosine/inosine ratio was observed in the R 75231 group after reperfusion (0.4 preischemia vs 4.0 after 60 min of reperfusion). Reperfusion of the graft resulted in an immediate increase in renin, angiotensin I, and angiotensin II venous blood levels in the control group. In the R 75231 group, renin, angiotension I, and angiotensin II levels were significantly lower. We conclude that administration of R 75231 before reperfusion has a protective effect on post-transplant function of kidneys that have been subjected to prolonged warm ischemia. This effect may, at least in part, be ascribed to inhibition of the breakdown and disposal of endogenous adenosine which, in turn, inhibits the excessive stimulation of the renin-angiotensin system in the early phase of reperfusion.
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PMID:Protection of canine renal grafts by renin-angiotensin inhibition through nucleoside transport blockade. 762 81

Renal ischaemia, both unilateral or bilateral, is the cause of renin dependent hypertension but only at the beginning of kidney hypoperfusion. Long lasting renovascular hypertension is progressively becoming more and more independent from the renal renin-angiotensin (RA) system and finally mostly dependent from extrarenal hypertensinogenic factors. This is the reason, why assessment of the individual components of the renal RA system and anatomical or physiological methods of kidney imaging are becoming progressively less sensitive and less specific in the diagnosis of renovascular hypertension of long-term duration.
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PMID:[Renovascular hypertension--a persistently difficult diagnostic problem]. 767 27

Renovascular hypertension is one of the more common causes of secondary hypertension. The true prevalence of this condition is not known, because only a selected few with hypertension are considered for thorough diagnostic work-up. The higher incidence figures come from centers with a special interest in this disease. The ability of a clinician to detect renovascular hypertension has improved substantially, thanks to the advances in radiology. The predominant mechanism of blood pressure elevation from renal ischemia is activation of the renin-angiotensin system. Clinically, the pathological lesions that cause renal artery stenosis are atherosclerosis and fibromuscular dysplasia; the former is typically seen in older men, and the latter is typically found in young women. Suspicion of the presence of renovascular disease should prompt the physician to obtain appropriate screening and confirmatory tests. Once diagnosed, the management of patients with renovascular hypertension requires a carefully planned multidisciplinary approach to offer the patient a best possible therapeutic option, with surgical revascularization or balloon angioplasty, or chronic medical therapy. However, these options are not mutually exclusive. The best long-term results are obtained with surgical therapy. Although balloon angioplasty is being increasingly used perhaps as the preferred initial therapeutic procedure for many patients with renal artery stenosis, long-term results comparable with surgery are not yet available. The ideal rational therapy for patients with renal artery stenosis is reperfusion of the ischemic kidney either by surgical correction or by balloon dilation. The aim is not only to improve the blood pressure control, but also to prevent and at times to reverse renal failure. Although effective antihypertensive drugs have become available, the role of medical management of renovascular hypertension is shrinking and should be limited to patients who have contraindications to or unwilling to undergo corrective procedures to relieve renal ischemia.
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PMID:Renovascular hypertension. 777 25


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