Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes in the number and sizes of membrane-associated particles have been quantitated in the protoplasmic (P) and exoplasmic (E) fracture faces of the outer membrane of nuclei isolated from the inner cortex following renal ischemia and reflow in the rat. No changes were observed in the inner nuclear membrane. After 20-min ischemia, the number of particles in both fracture faces decreased. With reflow, the total number of particles decreased after both 20- and 60-min ischemia. The partition coefficient (Kp = CPF/CEF) increased from 10 to 11 and 17 at 20- and 60-min ischemia then fell below control values to a Kp of 7 after 120 min. After reflow, Kp steadily decreased except after 20-min ischemia followed by 240-min reflow when Kp began to rise. The sizes of particles were predominantly 60 A in the P face of control outer membranes but became larger after ischemia. After 20- and 60-min ischemia with reflow, the size distribution became more normal. The shifts in particle numbers and sizes seem to indicate modifications within the membrane resulting from ischemia.
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PMID:Quantitation of particles in the freeze-fractured nuclear membrane after renal ischemia. 9 7

The effect of transient renal ischemia on renal concentration and distribution of 99mTc-HEDP, 99mTc-DMSA, and 99mTc-DTPA was compared in rabbits with acute tubular necrosis. Scintigrams were obtained after injection in normal rabbits or ones with unilateral or bilateral ischemia. 99mTc-HEDP concentration in ischemic tissue was 8 to 18 times normal 1--4 hours after injection, and the resulting images delineated the morphological changes in the ischemic kidneys more accurately than those obtained with DMSA or DTPA. Calcium concentration in the ischemic kidneys increased sixfold. 99mTc-HEDP may be useful in evaluation of renal failure secondary to tubular injury.
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PMID:Renal hyperconcentration of 99mTc-HEDP in experimental acute tubular necrosis. 22 Jun 70

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

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

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

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

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

Renal prostaglandins have several potential functions in renal physiology. Perhaps their best documented role is the maintenance of renal blood flow during renal ischemia, although they are apparently not essential to blood flow autoregulation in the absence of ischemia. Alterations in sodium excretion parallel the hemodynamic changes induced by prostaglandin infusions and prostaglandin inhibition with indomethacin. A direct action on sodium balance is unproven. Numerous studies, in vivo and in vitro, have convincingly demonstrated that prostaglandins or their precursors stimulate renin release and prostaglandin inhibition blunts renin release independent of hemodynamic and electrolyte balance. These functions of prostaglandins have implicated them in the manifestations of Bartter's syndrome, the nephropathy of liver cirrhosis, renovascular hypertension, and other nephropathies.
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PMID:Prostaglandins: renin release and renal function. 72 86

Renal phospholipid metabolism was studied after ischemia was induced by occlusion of the left renal artery in the rat. There was no change in the rate of cellular [14C]choline uptake after 25 or 60 minutes of ischemia. However, [14C]choline incorporation into phospholipid was two to three times greater in slices from the ischemic kidney than in slices from the contralateral control kidney. The increase occurred after 25 minutes of ischemia plus 15 minutes of reflow, and after 60 minutes of ischemia with or without reflow. When [14C]choline was injected into rats after a 60-minute period of renal ischemia, the rate of incorporation into phospholipid in the ischemic kidney was almost twice that of the control kidney. These results were similar to those of the in vitro experiments. Since virtually all of the cellular phospholipids of the kidney are present in cellular membranes, renal ischemia affects membrane metabolism. The mean distribution ratio of alpha-aminoisobutyric acid in slices of kidneys ischemic for 60 minutes was similar to that of control slices: 4.11 +/- 0.2 (SEM) vs. 4.30 +/- 0.30. The normal uptake of alpha-aminoisobutyric acid indicates that the increased incorporation of choline is associated with functional integrity of the membrane.
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PMID:Choline uptake into renal phospholipids following renal ischemia in rats. 75 33


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