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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Histologic evidence of intrarenal vasomotor changes were observed in the rat in the course of acute renal failure caused by the injection of HgCl2. Male Wistar rats injected s.c. with 2.5 or 4.7 mg HgCl2 per kg b. wt. developed fibrinoid damage in the media segments of preglomerular renal vessels, mostly in the arcuate and interlobular arteries. The lesions were patchy and irregularly scattered throughout the kidneys. 24 h post-injection the lesions were very rare and of only mild degree, whereas they were fully developed and regularly seen 48 h post-injection. A high percentage of similar changes was found in certain extrarenal vascular areas especially in the mesentery and pancreas. The damaged vascular segments were usually dilated. The results of various thichrome stains and histochemical reactions suggested edema of vascular smooth muscle cells and imbibition of the media by blood plasma substances, sometimes reaching the degree of fibrinoid necrosis. These findings were confirmed by electron microscopy. The imbibition of the smooth muscle cells by blood plasma material was clearly evidenced by the demonstration of intracellular fibrin precipitations. In connection with the degeneration of smooth muscle cells, accumulations of crystal-like fibrin formations could often be shown. Subendothelial fibrin formations were not observed. 96 h after the 2.5 mg injection the changes were already regressing, but edema of the vascular wall and signs of disturbed vasotonia persisted for several days. The maximum of the vascular changes usually coincided with the maximum of azotemia and the formation of debris cylinders in the renal tubules. However, no clear relationship was recognizable in individual cases between vascular damage, extent of tubular necrosis and renal function. The pathogenesis of the vascular changes is obscure, but neurogenic factors, increased release of catecholamines and/or vasoactive agents of renal origin in connection with other factors might play a decisive role. Arterial hypertension was absent. It is assumed that the structural damage of the vascular media is mainly brought about by prolonged or recurring vasospasms, or by alternating spasm and vasodilatation with local ischemia and increased tension of the vascular wall in the dilated segments. The altered function and structure of the vascular wall might, to a certain extent, contribute to renal insufficiency.
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PMID:Intra- and extrarenal vascular changes in the acute renal failure of the rat caused by mercury chloride. 13 13

Regional and single glomerular blood flow conditions in the transplanted rat kidney after various periods of cold ischemia were investigated with use of the microsphere method. Intravascular injection of a silicon rubber compound (Microfil) allowed identification and sampling of single glomeruli. The periods of ischemia were two hours (minor damage), 12 hr (intermediate damage), and 16 hr (severe damage). After two hours of cold ischemia, the regional and total renal blood flows were fairly normal. After 12 hr and 16 hr of cold ischemia, the total and regional blood flows were reduced five minutes after recirculation, the reduction being pronounced in the deep cortex and juxtamedullary glomeruli. In the 12-hr group, the blood flow showed complete restitution after 65 min, whereas in the 16-hr group, the blood flow in the inner cortex and juxtamedullary glomeruli remained decreased. An impairment of medullary circulation would seem to be an important component in the pathophysiology of acute renal failure in this model.
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PMID:Intrarenal hemodynamics in the transplanted rat kidney. 35 4

The volume velocity-relation of renal blood flow was examined in transplanted dog kidneys during the oliguanuric phase of the acute renal failure (ARF). Under these circumstances it is possible to separate the ARF in consequence of ischemia or hypoxia of the transplant or in consequence of rejection. A significant relation between the total blood flow and the mean flow correlation exists in the acute functional failure of ischemically injured autotransplants as in the case of autochthonous kidneys. This velocity is also kept in the acute insufficiency of autotransplants induced by shock although there exists a stronger redistribution of cortex circulation than after the ischemic insultus. Extreme low or high circulatory velocities without a relation to the blood flow originate from the deficiency of extensive vascular regions and the formation of arteriovenous shunts in acutely failing rejected homotransplants.
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PMID:[Flow volume-velocity relationship in the circulation of acutely failing kidney transplants (experimental study)]. 39 1

Acute renal failure in man can best be simulated in model experiments by using either temporary occlusion of the renal artery or perfusions of noradrenaline into the renal artery. The kidney of the Tupaia belangeri, a primitive primate, is more resistant to temporary occlusion of the renal artery than of the rat. In Tupaia as in rats, anuria developing 48 hours after temporary ischemia is brought about by intratubular proteinaceous casts blocking the flow of urinary filtrate, most likely at Henle's loop. As proof that the proteinaceous casts block the tubular lumina, we found that when two micropipettes are inserted into the same nephron and that nephron perfused, the intratubular pressures rise, approaching systolic pressures.
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PMID:Acute renal failure in Tupaia belangeri and rats. 49 47

Three cases of rhabdomyolysis, two with acute renal failure, seen in a short period of time in an emergency department illustrate this increasingly recognized entity. Myoglobinuria may result from muscle trauma, ischemia, metabolic causes, drug-induced injury or intrinsic muscle disorders. The diagnosis is easily made by the presence of an elevated creatine phosphokinase, positive orthotoluidine in the urine and pigmented urine casts. Failure to diagnose rhabdomyolysis early will result in increased morbility and mortality from subsequent hyperkalemia, acute renal failure and hypocalcemia. These three cases illustrate the difficulty in predicting the eventual degree of renal failure from the initial assessment.
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PMID:Rhabdomyolysis and acute renal failure. 63 72

Activation of the renin-angiotensin system has been implicated as one of the mechanisms involved in acute renal failure. Support of this hypothesis was forwarded by the finding that propranolol, a blocker of renin release, reduced the deleterious effect of ischemia on kidney function. The hypothesis was tested further in these experiments by studying renal blood flow after ischemic injury to rat kidneys with and without propranolol proection. Miniature electromagnetic flow probes measured blood flow after 70 min of total renal artery occlusion. Although brief infusion of propranolol reduced the degree of acute renal failure, it had no effect on renal blood reflow. The data do not support the hypothesis that the renin-angiotensin system plays a role in acute renal failure. Other explanations for the protective effect of propranolol are suggested.
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PMID:Propranolol protection in acute renal failure. 64 Aug 2

Rat experiments were conducted for comparative study of the effect of diuretics, injected into the organism in a single dose prior to two-and-a-half-hour ischemia of an only kidney and after it, on the extent of the kidney affection and survival of the animals. It was established that furosemid, etacryn acid and mannitol exert a preventive protective effect in ischemia of the kidneys and considerably increase the survival of rats as compared to the control-group. Analysis of the renal function in the first five days of the postischemic period testifies to the property of the above-mentioned diuretics for normalizing excretory processes on the 2nd-4th days of the action of the injuring agent, and for relieving or shortening the oligoanuric phase of acute renal failure. The significance of metabolic shifts, intratubular hydrodynamics and vascular microcirculation in the mechanism of the protective effect of diuretics in ischemia of the kidneys is discussed.
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PMID:[Anti-ischemic action of diuretics]. 64 32

The pars convoluta of the proximal tubules of the rat kidney was examined by means of light and electron microscopy after 15, 30, 60 and 120 min of complete ischemia produced by clamping of the aorta. The same ischemia periods were also examined after 24 hrs of blood reflow. It was found that the vast majority of the cells of pars convoluta survived 60 min of ischemia as seen after 24 hrs of reflow. The following pattern of changes were observed at time intervals up to 60 min: progressive clumping of chromatin, progressive distortion of microvilli with bleb formation, increasing dilatation and finally vesiculation of rough-surfaced endoplasmic reticulum and initially condensation and later high amplitude swelling of mitochondria. It is concluded that these subcellular changes are compatible with cell survival. Also tubule cells containing swollen mitochondria with small flocculent densities are potential candidates for survival. 120 min of ischemia was associated with marked mitochondrial swelling with large flocculent densities, severe cell damage and necrosis and was not compatible with cell survival. A working hypothesis is presented relative to the pathogenesis of acute renal failure caused by complete ischemia.
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PMID:Studies on the pathogenesis of ischemic cell injury. II. Morphological changes of the pars convoluta (P1 and P2) of the proximal tubule of the rat kidney made ischemic in vivo. 81 77

Renal cortical blood flow of rats with postischemic, myohemoglobinuric, and mercury-induced acute renal failure was measured by the hydrogen washout technique using implanted platinum electrodes. Total renal blood flow was determined by venous cannulation in separate series of rats. The values obtained with the two methods were in excellent qualitative agreement (r=0.99, P less than 0.001), although venous cannulation gave values that were constantly lower than those calculated for whole kidney from the cortical flow rate and assumed cortical mass. Myohemoglobinuria produced by glycerol injection caused cortical blood flow to fall from a control value of 7.37+/-0.23 (SEM) ml/min X g of cortex to approximately one-half that value for four hours after injection (P less than 0.001). Flow rates 12 and 24 hr after glycerol injection were 85% (P less than 0.001) and 90% (P less than 0.05) of control, respectively. Cortical flow was reduced to 5.49+/-0.39 (SEM) ml/min X g of cortex four hours after release of one hour's total bilateral renal arterial occlusion (P less than 0.001), but rose to normal within 24 hr. Poisoning with 4.7 mg/kg of body wt of mercuric chloride produced a cortical blood flow value that was 30% higher than control 24 hr after injection (P less than 0.01), while a 12 mg/kg of body wt dose gave a normal flow value. Inulin clearance was severely depressed in all models at all study times. Thus, in contrast to human acute renal failure, marked renal cortical ischemia is not an essential feature of these different forms of murine acute renal failure.
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PMID:Normal renocortical blood flow in experimental acute renal failure. 85 3

It is commonly assumed that the decrease in the effective circulatory volume (ECV) is the major event in acute renal failure (ARF) and the preferential ischemia of the cortex another major modification. Frusemide has been given to try to prevent this change in glycerol-induced ARF because of its effect in redistributing renal blood flow from medulla to cortex. Isontonic saline was also tried to avoid the ECV depletion. The pretreatment with frusemide not only fails to protect against the ARF but increases its severity. Isotonic saline adminstration and replacement of urinary losses almost prevent glycerol-induced ARF but when both isotonic saline frusemide are administered together their effect is only a slight increase in the excretion rate of urea and creatinine during the first days of the experiment. The importance of the changes in the ECV or a possible direct action of frusemide on the renin-angiotensin axis are discussed. There is a good correlation between plasma creatinine levels and interstitial oedema. The importance of the oedema in the maintenance of ARF is discussed.
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PMID:Negative effect of frusemide pretreatment in glycerol induced acute renal failure. 87 19


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