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

Mannitol may be useful clinically both as a diuretic and as an obligate extracellular solute. As a diuretic it can be used to treat patients with intractable edema states, to increase urine flow and flush out debris from the renal tubules in patients with acute tubular necrosis, and to increase toxin excretion in patients with barbiturate, salicylate or bromide intoxication. As an obligate extracellular solute it may be useful to ameliorate symptoms of the dialysis disequilibrium syndrome, to decrease cerebral edema following trauma or cerebrovascular accident, and to prevent cell swelling related to renal ischemia following cross-clamping of the aorta. Largely unexplored uses for mannitol include its use as an osmotic agent in place of dextrose in peritoneal dialysis solutions, its use to maintain urine output in patients newly begun on hemodialysis, and its use to limit infarct size following acute myocardial infarction.
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PMID:Mannitol. 38 67

Rats were anesthetized and their lift kidneys were made ischemic for 1 h by clamping of the aorta just above the left renal artery. Mannitol (2.5 g/kg), Dextran 70 (0.6 g/kg), methylprednisolone (50 and 100 mg/kg), and allopurinol (100 mg/kg body weight) were administered before, during, or after the ischemia period in order to test the effect of each of these drugs upon this model of renal injury. At 24 h after the release of the aortic clamp the left kidneys of the drug treated animals wwere perfusion fixed and processed for light and electron microscopy. Dextran administration to animals with ischemic kidneys gave rise to a pronounced vacuolization ("osmotic nephrosis"), in the entire proximal tubule and especially in the pars recta. This was in contrast to dextran administration to rats with nonischemic kidenys, which showed no or very mild "osmotic nephrosis." This demonstrates that ischemia makes rat kidneys more susceptible to the development of "osmotic nephrosis." In controls (no drug treatment) one hour of renal ischemia gave partial necrosis of pars recta of the proximal tubule, while the pars convoluta tubule survived. Mannitol treatment significantly reduced the amount of necrosis of the pars recta, whereas dextran, methylprednisolone, and allopurinol had no or a negative effect on the survival of the cells of the pars recta segment. It is suggested that mannitol protects against the development of necrosis by increasing medullary blood flow in combination with a counteractive influence on the cellular swelling, which is known to occur in ischemia.
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PMID:Effect of mannitol, dextran (macrodex), allopurinol, and methylprednisolone on the morphology of the proximal tubule of the rat kidney made ischemic in vivo. 40 53

The delayed onset of anuria/oliguria in acute tubular necrosis has been theorized to represent a complicating compartment syndrome, i.e., parenchymal swelling within an unyielding capsule. To test this proposition, 12 monkeys had suprarenal aortic cross-clamping, followed by unilateral renal decapsulation to create an experimental as well as a control kidney unit in the same animal. Histologic examination uniformly confirmed tubular necrosis at death or sacrifice. Subsequent split renal function studies (creatinine, urea, and free water clearances) indicated significantly greater maintenance of renal function by the decapsulated kidney than by its paired control. Clinical evaluation in 21 hemorrhagic shock patients, with the capsule of one kidney stripped, revealed on follow-up that 15 developed a renal failure consistent with acute tubular necrosis. Although three patients with polyuric failure died before split studies could be run and two others have been too recent for computer analysis to have been completed, nine of the remaining ten had significantly greater renal plasma flows (194 versus 121 ml/min M(2), p < .01) and significantly greater urine flows (.99 versus .18 ml/min M(2), p < .01) on the decapsulated side than on the control, as determined by differential renal scans. No significant difference in these same lateralized renal functions was noted in the tenth patient with renal failure and in the six survivors without renal failure. Renal decapsulation as prophylaxis reduced the anticipated incidence of oliguria/anuria from an expected 75% to 7% (p < .01) in these 21 shock patients. Such data suggest that delayed renal ischemia, possibly based on a compartment syndrome, may be the cause for a progression of acute tubular necrosis from polyuria to oliguria and then to anuria.
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PMID:Renal decapsulation in the prevention of post-ischemic oliguria. 40 54

The excretory urograms of 14 children with ureteral notching were reviewed. In 10 of 14 cases the vascular impressions on the ureters were due to either venous obstruction and dilated collaterals or to dilated noncollateral veins. In two cases the notching was associated with arterial collaterals in renal ischemia and in two with dilated lymphatic channels. The implications of notching in children and the differences and similarities of this urographic sign between children and adults are discussed.
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PMID:Notching of the ureter and renal pelvis in children. 41 Feb 47

Acceptor control index, P/O ratio and inner membrane permeability were examined in isolated mitochondria following periods of renal ischemia for 15, 30, 60, 120, and 240 min. It was noted that the P/O ratio remained unchanged until 1-2 h after the onset of ischemia. A similar change was noted in the contraction rate of isolated ischemic mitochondria after swelling in KCl and addition of ATP+Mg2+. Both changes are probably indications of a basic membrane alteration which correlates with the occurrence of irreversibility of cell injury. In contrast, the swelling rate in KCl and the acceptor control index are altered almost simultaneously with the onset of ischemia. Therefore, acceptor control index and the rate of swelling are affected prior to the point of irreversible cell injury. They are not, therefore, good as indicators of irreversible changes in the inner membrane of mitochondria leading to the "point-of-no-return."
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PMID:Studies on the pathogenesis of ischemic cell injury. XI. P/O ratio and acceptor control. 41 34

Unilateral renal ischemia was induced in rats by clamping the left renal artery for 20, 60, and 120 min, respectively. One hour after the arterial clamp was removed, renal handling of gentamicin and paraaminohippurate (PAH) was studied over the next 2 hours; the kidneys were removed at the end of the experiments for determination of gentamicin and PAH content. The ischemic damage was evidenced by morphologic and functional changes. The glomerular filtration was decreased in proportion to the severity of ischemic injury. The excretion of gentamicin was highly correlated with GFR in normal and postischemic kidneys. In the cortex, ischemic injury resulted in reduced concentrations of gentamicin but markedly augmented those of PAH. The finding is consistent with the hypothesis that gentamicin is reabsorbed by the epithelial cells through the luminal membrane, whereas PAH enters via the peritubular membrane. In contrast, medullary concentrations of both compounds were similar, with suppression of uptake seen only after 120 min of ischemia. Conclusion. Ischemic damage impairs urinary elimination of gentamicin and the ability of renal parenchyma to retain the drug. Difference in uptake between gentamicin and PAH were unmasked in the postischemic kidneys.
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PMID:Urinary excretion and tissue accumulation of gentamicin and paraaminohippurate in postischemic rat kidneys. 45 44

Partial ligation of the aorta between the renal arteries in the rat induces malignant hypertension, metaplasia of smooth-muscle cells of arterioles and arteries into juxtaglomerular cells, and a complex series of events in tubular cells at all levels of the ischemic kidney. The tubular cells of the outer cortex, particularly the proximal convoluted cells, show a very rapid and progressive simple atrophy. In contrast, necrosis of individual cells is followed by mitotic activity in atrophic tubular cells of the inner cortex, medulla, and papilla. Subsequently, polyploidy and hyperplasia occur in the inner cortex. At the same time, hypertrophy of the protein-synthesizing apparatus and an increase in protein, DNA, and RNA, followed by a decrease in the protein content, are seen in the tubular cells of the inner cortex. In the medulla and papilla, necrosis of individual cells proceeds side by side with waves of mitotic activity. These events take place, albeit to a lesser degree, even in cases of very mild renal ischemia. While they may by unrelated to hypertension, these changes are probably involved in the increase in hydrolytic enzyme activity characteristic of the ischemic renal cortex.
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PMID:Metaplastic and mitotic activity of the ischemic (endocrine) kidney in experimental renal hypertension. 47 9

To evaluate the effect of prostaglandin inhibition on the renal blood flow of the ischemic kidney, we administered indomethacin to 10 anesthetized dogs with renal artery stenosis and contralateral nephrectomy. Following the operation to produce renal ischemia, there was an increase of blood pressure associated with an increase of renin and the prostaglandins F1 (PGF1), and E (PGE). The administration of indomethacin to the intact, normotensive animals caused the anticipated decrease of prostaglandin E, renin, and renal blood flow. However, in the hypertensive dogs, indomethacin caused a paradoxical 45 per cent increase in the renal blood flow, despite a 44 per cent decrease of prostaglandin E. PGF1, PGE, renin, and erythropoietin exhibited the anticipated decreased levels. The study suggests that prostaglandins may not be the sole important factor in the regulation of renal blood flow in the presence of ischemia. Other important factors likely include the renin-sensitive angiotensin, the adrenergic, and the kallikrein-kinin systems.
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PMID:Paradoxical increase of renal blood flow in anesthetized hypertensive dog treated with indomethacin. 48

We report a serioangiographic method in rats which permits assessment of the course and dimensions of the renal arteries, the durations of the arterial and venous phases, and the intensity and uniformity of the renal parenchymal filling. The procedure was employed to study the mechanism by which administration of vasopressin to rats pretreated with estrin leads to renal cortical necrosis. The pathogenetic significance of the spasm localized on the larger renal arteries was proved directly; the possible role of the arteriovenous shunt in the development of the renal ischemia was excluded.
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PMID:Serioangiographic study of renal cortical necrosis induced by administration of estrin and vasopressin in rats. 48 69

The potential role of computed tomography (CT) in the detection of acute renal ischemia was assessed in nine mongrel dogs. Ischemia was produced by inflation of a balloon catheter in the main renal artery, with scans performed before, during, and after a 60-minute period of ischemia. A small but consistent increase in the attenuation value of ischemic renal parenchyma was observed. When intravenous contrast material was given, the ischemic kidney was markedly less enhanced than the contralateral, nonischemic kidney. By using the contralateral kidney for comparison, the ischemic kidney could be identified with or without the use of a contrast agent. Although calculations of mean pixel values were necessary when a contrast agent was not injected, the abnormal kidney could be easily recognized from the CT images themselves when intravenous contrast material was given. Because of the consistency with which the abnormalities were observed, we recommend a clinical trial of CT in suspected acute renal ischemia.
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PMID:Computed tomography of experimental acute renal ischemia. 50 Mar 7


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