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

The influence of temporary ischemia followed by recirculation on the ultrastructure of glomerular capillaries and some portions of the nephron was studied in 20 albino rats which were subjected to compression of the vascular bundle of the left kidney for 30 min., 1, 2 and 3 hours followed by recovery of the blood stream in the ischemic organ for 3 hours (with a simultaneous nephrectomy of the right kidney). The electron microscopic analysis has established that the amount of micropinocytic vesicles become markedly increased within 3 hours following 30-min. ischemia of the kidney with the recovery of blood circulation in the cytoplasm of endotheliocytes of glomerular blood capillaries. With increased terms of the left kidney ischemia (1, 2, 3 hs) the ultrastructural changes in endotheliocytes increased. There appeared microclasmatosis of the internal plasmalemma of endotheliocytes, the flattened peripheral part of the cytoplasm underwent considerable destruction. Swelling of microvilli of the brush border and vacuolization of the cytoplasm were observed in nephrocytes of the proximal part of the nephron in short-term ischemia (30 min) followed by the recovery of circulation for 3 hours. Longer periods of ischemia (1, 2, 3 hs) casued destruction of the brush border. There appeared secondary lysosomes, in mitochondria there occurred discomplexation and lysis of cristae.
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PMID:[Effect of temporary ischemia with subsequent recirculation on the ultrastructure of glomerular capillaries and nephrons]. 98 9

A new technique for in vivo renal perfusion is described which eliminates the need for autotransplantation. In short term ischemia studies using three solutions, Sacks' solution was found to provide the optimal renal ischemia protection.
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PMID:A technique for isolated in vivo renal perfusion. 99 69

The role of some mechanisms in the development of hypertension due to unilateral renal artery stenosis is influenced by the presence or absence of the intact opposite kidney. In this paper: a) the cardiovascular reactivity (CR) to norepinephrine (NE) and b) the effect of a ganglionic blocker (pentolinium, P) during the early (first two weeks) and later periods (ten weeks) of hypertension elicited by unilateral renal ischemia in the presence of the untouched contralateral kidney in the rat have been reported. Neither the threshold doses nor the dose-pressor response curves have shown a greater reactivity of the cardiovascular system to NE in this specific type of renovascular hypertension. An increase in the activity of the nervous system apparently contributes in early and late periods to the fuller development of high arterial pressure (AP).
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PMID:Cardiovascular reactivity and neurogenic tone in unilateral renovascular hypertension in the rat. 103 58

Hyperacute renal allograft rejection is initiated by primary immune injury to vascular endothelium and is propagated by secondary vasoconstriction, platelet aggregation and intravascular coagulation. Previous dissociation of these primary and secondary events, with graft survival in one human, suggested that the more usual graft failure was due to secondary injury. As a basis for further modification studies, this primate model most closely resembled its counterpart in man, as the onset and intensity of functional, morphologic and biochemical alterations were similar. Unmodified allografts failed within 5 minutes. The earliest and most abnormal finding was marked reduction in renal blood flow affecting all compartments. By 5 minutes, histologic changes of hyperacute rejection as well as antibody and faint C3 deposits were noted, but biopsies suggested that the initial flow reduction was more likely due to vasoconstriction, which was then followed by vascular obstruction. Glomeruli appeared most damaged, but at the highest antibody titer arterial injury was more prominent. Early red cell sequestration and stasis was marked, followed by progressive platelet clumping and neutrophil infiltration. While the decline in renal venous C3 levels was prompt, as in man, early intrarenal activation of the coagulation, fibrinolytic and kinin-forming systems could not be demonstrated, and fibrin formation was sparse by light and fluorescence microscopy. Qualitatively similar histologic and functional alterations were noted in autograft controls. While the initiating event was unclear and may have been accentuated by the arteriovenous shunts utilized, the final mechanism was probably marked vasoconstriction with renal ischemia. Intrarenal C3 consumption was an important finding and was not associated with tissue deposits of antibody or complement; it may provide a parallel with the progressive complement-mediated injury associated with acute myocardial ischemia noted by others. Endothelial injury was not seen in arteries, and all alterations were delayed in onset and progressed more slowly than in allografts. These findings may elucidate the mechanism of early malfunction of most autografts. Treatment of additional autografts with increasing doses of heparin progressively reversed these changes and even prevented the initial reduction in blood flow. Therefore, many alterations consistent with hyperacute rejection which are probably immediately responsible for graft failure can also be initiated by nonspecific, nonimmunologic events and, where injury is less intense, can be prevented pharmacologically. This model provides a means of dissecting the injurious events and subsequent evaluation of the effectiveness and interaction of various agents on the damaging secondary alterations which occur during hyperacute rejection.
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PMID:A primate model of hyperacute renal allograft rejection. 109 89

Information defining the renin-angiotensin-aldosterone axis as a control system concurrently regulating salt balance and blood pressure has been applied to examine the role of renin in the causation of experimental and clinical forms of renovascular and renal hypertension and thence to develop criteria for differentiating these entities. Experimantally there are two models of renovascular hypertension, one characterized by excess renin with reduced sodium (vasoconstrictor form) and the other by excess sodium with reduced renin (volume form). But with sodium depletion, the volume form switches to a vasoconstrictor form, illustrating how the two factors coordinate to maintain blood pressure. Human renovascular and renal hypertensions appear to be sustained by the same two mechanisms. Experimental and clinical studies both indicate that curable renal hypertension is in fact a renin-dependent vasoconstrictor hypertension. Three criteria, derived from four renin measurements, identify this situation: (1) Hypersecretion of renin is reflected by a high peripheral level when referenced against sodium excretion. (2) Lacteralization of renin secretion with contralateral suppression rules out occult bilateral disease. It is indicated by V-A = 0 from the uninvolved kidney. (3) A third criterion, (V-A)/A greater than 48 per cent from the ipsilat-eral kidney, identifies renal ischemia. These three criteria, when taken together in a combined scoring analysis, provide high precision in identifying the patient with the vasoconstrictor form of renal hypertension that is potentially reversible by appropriate surgery. Absence of these criteria identifies hypertension associated with either occult or overt bilateral renal disease. In these patients, the volume factor often predominates and is expressed by some suppression of plasma renin levels. Here, removal of renal tissue is contraindicated. Corroborative evidence to support these three criteria can be developed from the blood pressure response to angiotensin blocking drugs or to anti-renin therapy with propranolol. Thus in all of these renal hypertensions, the vasoconstrictor and volume factors can be identified using renin measurements and pharmacologic interventions.
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PMID:New concepts of the renin system and of vasoconstriction-volume mechanisms. Diagnosis and treatment of renovascular and renal hypertensions. 109 53

A case is reported of documented renovascular hypertension due to traumatic occlusion of the main renal artery in a double renal artery system. Emphasis is placed on the value of the oblique renal arteriogram in assessing segmental vasuclature prior to surgical intervention. Oblique arteriography may also aid in the preoperative evaluation of patients with segmental renal ischemia due to other causes.
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PMID:Renovascular hypertension. Secondary to traumatic occlusion of supplemental renal artery. 111 29

Renal blood flow (RBF) and the distribution of cortical blood flow (microspheres) were measured in the dog after 90 min of total unilateral renal ischemia. RBF was 21% greater than control 2 min after release of the renal artery occlusion, and returned toward control 60 min later. At 2 min after release there was a small but significant increment in deep cortical blood flow which reverted to control by 60 min. When renal artery occlusion was maintained for 180 min, return of blood flow was blunted at 2 min after release of the occlusion, but was not significantly different from control within 10 min after release. Clearance rates of inulin and para-aminohippurate (Cin and Cpah) were 81 and 82% below control after release of occlusion. These data demonstrate that in the dog there is prompt and complete return of blood flow to or above control levels after complete renal artery occlusion. There was no evidence for the "no-reflow" phenomenon.
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PMID:The effect of ischemia on renal blood flow in the dog. 112 63

Peripheral plasma renin activity (PRA) is not invariably elevated in patients whose ischemic renal lesion is causing hypertension. Infusions of an angiotensin II antagonist, 1-sar-8-ala-angiotensin II (P-113), have been used to determine whether the blood pressure responses might indicate angiotensin dependence in 221 consecutive hypertensive patients. In 32 patients P-113 infusion reversibly reduced blood pressure, and almost all of these "P-113 responders" had elevated renal vein and/or peripheral PRA levels, together with evidence of renal ischemia. Among the 189 "P-113 nonresponders," peripheral PRA was elevated in seven (3.8%), and renal vein PRA ratio was abnormal in two patients, who might represent exceptions to the otherwise successful record of the P-113 response in identifying "angiotensinoginic" hypertensives.
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PMID:Identification of angiotensinogenic hypertension in man using 1-sar-8-ala-angiotensin II (Saralasin, P-113). 113 74

Reaction constants of renin in juxtaglomerular apparatus and plasma renin activity after renal ischemia and hemorrhage. During and after total renal ischemia and acute hemorrhage, renin activity in plasma (PRA) and microdissected juxtaglomerular apparatus (JGA) of rabbits were investigated. In controls, the apparent Michaelis-Mentoen constant (MMC) of semipurified standard renin of rabbits was 1025 plus or minus 223 SD ng/ml. Plasma renin of normal rabbits showed similar values: 1062 plus or minus 138 SD ng/ml. Intrarenal JGA renin, however, showed a great scatter of MMC (920 to 4760 ng/ml) and a significantly higher mean value of 2572 plus or minus 1156 SD ng/ml (pis less than 0.001). After complete renal ischemia by clamping both renal arteries for a 90-min period, the following results wereobtained: 1) Sixty min after the beginning of ischemia, PRA decreased from 20.9 plus or minus 9.8 SD to 7.6 plus or minus 5.2 SD ng/ml-hr (P is less than 0.05) and increased to 103, 68 and 42 ng/ml-hr 10, 30 and 90 min after removal of the clamps, respectively (P is less than 0.05).
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PMID:Reaction constants of renin in juxtaglomerular apparatus and plasma renin activity after renal ischemia and hemorrhage. 113 98

In a series of 114 consecutive patients with acute renal failure, the over-all mortality rate was 60 per cent; 62 per cent of the patients had a documented episode of hypotension just prior to the development of acute renal failure. In 11 patients, a second episode of renal failure developed following recovery from the initial episode of acute renal failure; all of these patients died. The urine output rate during the course of acute renal failure was inversely related to the mortality rate in the series as a whole. The mean duration of acute renal failure in survivors of the present series was 11.0 plus or minus 1.4 days. Complications of renal failure in the order of their frequency included hemorrhagic hypotension, sepsis, sepsis with hypotension and consumption coagulopathies; only 12 per cent had no complications. Only six of 51 patients whose clinical course was complicated by sepsis with or without an episode of hypotension survived. By contrast, 30 of 53 patients who had hemorrhagic hypotension without sepsis survived. The date suggest that although acute renal failure has a high mortality rate, it is a benign disease that is potentially reversible. Regardless of age and sex, renal functional recovery will take place if the patient is maintained in good physiologic condition long enough without a continued stress, such as sepsis, hypotension or hypovolemia, all of which prolong renal ischemia. During the course of renal failure, extreme care is essential to maintain adequate circulating volume without extracellular fluid overload; a second hemodynamic insult may result in serious damage to the regenerating renal tubules. We conclude that early recognition of acute renal failure, aggressive management of sepsis, careful titration of fluid and electrolyte therapy, meticulous monitoring, maintenance of the circulation and judicious utilization of dialysis will aid in reduction of mortality in these critically ill patients.
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PMID:Clinical determinants of survival from postoperative renal failure. 114 2


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