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)

We have shown previously that theophylline increases both renal plasma flow (RPF) and glomerular filtration rate (GFR) during the initiation phase of post-ischemic acute renal failure (ARF) in rats. The purpose of the present experiments was to determine the effects of theophylline during the maintenance phase of ARF, five days after initiation. Clearance techniques were used to measure renal function in a control group of pentobarbital anesthetized rats (group C) and in three experimental groups, five days after subjecting the left kidney to a thirty-minute period of complete ischemia. Group SS received saline during both the ischemic episode and the clearance measurements; group ST received saline during ischemia and theophylline, acutely, during the clearance measurements; group TS received theophylline during ischemia and saline during the clearance measurements. In comparison with the values for the control group (group C), RPF and GFR of the post-ischemic left kidneys of group SS were approximately half normal. In groups ST and TS, RPF and GFR of the left kidneys were higher than in group SS. Collectively, these results demonstrate that pretreatment with theophylline during the initiation phase of ischemia-induced ARF leads to increased RPF and GFR during the maintenance phase, and that acute theophylline treatment during the maintenance phase acutely increases RPF and GFR. Since increases in GFR were associated with increases in RPF, and since theophylline is an adenosine receptor antagonist, these results are consistent with the hypothesis that adenosine-mediated hemodynamic changes play a pathogenic role in ischemia-induced ARF in rats.
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PMID:Theophylline in rats during maintenance phase of post-ischemic acute renal failure. 335 58

The present work was performed on uninephrectomized rabbits recovering from ischemic acute renal failure (ARF) in an attempt to elucidate whether or not intraglomerular events are a determinant factor in the development of resistance to ARF. 14 days after a 2-hour clamping of the renal artery (the recovery phase), the animals did not show resistance to an additional ischemia. On the other hand, glomeruli derived from normal kidneys displayed a contractile response to angiotensin II, arginine vasopressin or norepinephrine in Eagle's minimum essential medium, whereas glomeruli from rabbits recovering from ischemic ARF were refractory to the vasoconstrictor agents. The findings suggest that glomerular refractoriness to contractile stimuli does not provide resistance to an additional renal ischemia in the ischemic model of ARF.
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PMID:Glomerular refractoriness to contractile stimuli in rabbits recovering from ischemic acute renal failure. 336 77

Functional and biochemical parameters, changes in renal morphology were studied in 122 dogs at different time of lower limb ischemia and revascularization. Two groups of dogs were identified varying in the time of ischemia and revascularization: (early--3 and 6 h and late--9 and 12 h), characterized by temporary oligoanuria and acute renal failure. Morphological appearance of the kidneys was described with due consideration of the pathology and compensatory rearrangement of glomerular epytheliocytes metabolism.
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PMID:[Pathomorphology of acute renal failure in ischemia of the extremities and their revascularization]. 340 69

The purpose of this study is to confirm previous evidence for reactive oxygen species (ROS) as critical mediators of postischemic renal injury by documenting lipid peroxidation after ischemic-hypoxic insults and by demonstrating that antioxidants confer protection. Renal malondialdehyde (MDA) concentrations, an index of lipid peroxidation, were measured using uncorrected and tissue-chromagen-corrected methods in 1) cortical (C), outer medullary stripe (OMS), inner medullary (IM) whole renal tissues, and C and OMS mitochondria obtained 15 min after in vivo renal artery occlusion (RAO; x 45 min); 2) C, OMS, and IM whole tissues obtained 15 min after completing 45 min of ischemia in an isolated perfused kidney; and 3) isolated proximal tubular cell (PTC) suspensions after 45 min of hypoxia with 15 min of reoxygenation. Despite significant oxygen deprivation-induced injury in each of these systems, no significant rise in MDA concentrations could be documented, with the sole exception of the in vivo IM region (by uncorrected MDA assay only). The latter rise could be attributed to medullary vascular congestion causing a hemoglobin-induced artifact in the MDA assay. Sixty-minute in vivo RAO plus reflow also did not raise MDA. To validate the MDA assay 4.2 mM H2O2 was added to PTC. An abrupt fourfold rise in MDA resulted. Pretreatment of 30- and 45-min RAO rats with two antioxidants (allopurinol or superoxide dismutase) failed to confer functional or morphological protection. We conclude that ROS may not be critical consistent mediators of in vivo postischemic acute renal failure.
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PMID:Evidence against oxidant injury as a critical mediator of postischemic acute renal failure. 341 3

In ischemic acute renal failure oxygen free radicals may mediate injury. In addition, iron appears to play a critical role in hydroxyl radical formation and lipid peroxidation during reperfusion of ischemic kidneys. To determine whether iron may play a similar role in pigment (heme protein)-induced acute renal failure, we studied the effects of the iron chelator deferoxamine in two experimental models of pigment-induced acute renal failure, intramuscular glycerol injection and intravenous hemoglobin infusion without and with concurrent ischemia in the rat. Intramuscular injection of 50% glycerol (5 ml/kg) caused inulin clearance to fall to 0.13 +/- 0.03 (SE) ml/min (normal value, 1.0-1.2 ml/min). Continuous infusion of deferoxamine beginning at the time of glycerol injection significantly attenuated this renal dysfunction. Deferoxamine-treated animals had an inulin clearance of 0.37 +/- 0.06 ml/min (P less than 0.01). Glycerol injection was also associated with significant lipid peroxidation, measured as renal malondialdehyde content. Deferoxamine-treated glycerol-injected rats had renal malondialdehyde content not significantly different from control animals. In another model of heme pigment-induced renal injury, hemoglobin was infused to produce hemoglobinuria. Inulin clearance 1 h after hemoglobin infusion was significantly reduced to 0.84 +/- 0.5 ml/min (P less than 0.025). Infusion of deferoxamine after hemoglobin prevented the hemoglobin-induced decrease in inulin clearance. Thirty minutes of renal ischemia followed by infusion of hemoglobin resulted in more severe renal dysfunction with inulin clearance of 0.54 +/- 0.08 ml/min. Deferoxamine infused at the time of reperfusion attenuated the fall in glomerular filtration rate after ischemia and hemoglobin infusion:inulin clearance 1.04 +/- 0.07 (P less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemoglobin- and myoglobin-induced acute renal failure in rats: role of iron in nephrotoxicity. 341 10

A marked defect in renal concentration ability associated with hypoxic lesions in the medullary thick ascending limb (mTAL) characterizes the isolated rat kidney perfused with cell-free solutions. Addition of erythrocytes to the perfusion medium, a maneuver known to eliminate signs of hypoxic cellular injury to mTALs, greatly improved renal concentrating ability. When indomethacin was given to kidneys perfused with erythrocyte-enriched medium, concentrating ability was further improved by the drug to an average U/Posm of 2.45 +/- 0.81, and medullary cellular structure remained normal in appearance. Since renal hypoperfusion predisposes to acute renal failure from non-steroidal antiinflammatory drugs (NSAIDs) and medullary ischemia might play a role in chronic analgesic nephropathy, a synergism between NSAIDs and medullary hypoxia was evaluated in the isolated perfused rat kidney. Indomethacin and naproxen added to the perfusion medium (at 10(-4) and 5 X 10(-4) M, respectively) effectively depressed prostaglandin E2 (PGE2) production by the isolated kidney but did not improve its concentrating ability when perfused with cell-free medium. Quantitation of hypoxic injury to mTALs, regularly observed in this model, indicated that both indomethacin and naproxen increased the extent and severity of damage in the deeper, most hypoxic portions of the inner stripe. Addition of PGE2 to cell-free perfusate reduced the extent of hypoxic damage to the mTAL. These results suggest that in medullary hypoxia, prostaglandins protect mTAL cells by either vasodilatation or reduction in active transtubular transport. NASAIDs, by suppressing prostaglandin production, could predispose the renal medulla to hypoxic injury.
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PMID:Inhibition of prostaglandin synthesis in rat kidney perfused with and without erythrocytes: implication for analgesic nephropathy. 346 23

The influence of long-term infusion of the calcium-entry blocker diltiazem on postischemic acute renal failure was investigated in conscious dogs monitored by implanted instruments. In 18 uninephrectomized beagle dogs on a salt-rich diet, an electromagnetic flow probe and an inflatable plastic cuff were placed around the renal artery. Acute renal failure was induced by inflating the cuff for 180 min in the conscious animal. Group A (n = 5, control) received an intraaortic injection of 0.9% NaCl (5 ml/day) from the 3rd day before until the 7th day after ischemia and group B (n = 6, posttreatment) an intra-aortic injection of diltiazem (5 micrograms X min-1 X kg-1) beginning at the end of ischemia until the 7th day. Group C (n = 7, pre- and posttreatment) received diltiazem from the 3rd day before until the 7th day after ischemia. In group A, renal blood flow dropped from 149 +/- 16 (preischemic) to 129 +/- 29 ml X min-1 on the 1st day after ischemia. In contrast, renal blood flow increased on the 1st postischemic day in both treatment groups by 29 +/- 15% (group B, P 0.05) and 14 +/- 13% (group C). In the following days, there was no significant difference in renal blood flow between groups A, B and C. In group B, the reduction of the glomerular filtration rate was similar to that in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The influence of long-term infusion of the calcium antagonist diltiazem on postischemic acute renal failure in conscious dogs. 351 3

Glomerular responses to angiotensin II (AII), arginine vasopressin (AVP), and norepinephrine (NE) were estimated in rabbits recovering from uranium-mediated nephropathy or ischemic acute renal failure (ARF) to examine roles of intraglomerular events in resistance to ARF. Uranyl acetate (UA, 0.8 mg/kg) produced ARF in some animals but did not in others. Rabbits recovering from UA-induced ARF were highly resistant to a rechallenge with a larger dose of the agent (2 mg/kg). Their glomeruli did not respond to AII, AVP and NE in vitro. In animals having not experienced ARF following the initial insult, however, resistance to the rechallenge was lower than in animals recovering from ARF, and the glomerular response to contractile stimuli was well sustained. A two hour clamping of the renal artery induced ARF in uninephrectomized rabbits. These animals were not resistant to an additional ischemia in the recovery phase, despite inhibited glomerular contractile responses to AII. These data indicate a nonspecific inhibition of glomerular responses to contractile stimuli in the recovery phase of ARF. It is unlikely, however, that resistance to ARF can be attributed to the loss of the glomerular contractile response.
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PMID:Loss of glomerular responses to vasoconstrictor agents in rabbits recovering from ARF. 354 13

Compromised kidney function in the perinatal period has been increasingly recognized during recent years, and acute renal failure is a frequent clinical situation in neonatal intensive care units. Renal underperfusion due to various prerenal conditions is assumed to be the most common cause of renal failure in neonates. With rapid restoration of renal blood flow, prerenal failure is completely reversible in the early course of the disease. If adequate treatment is delayed, however, structural damage to the kidneys by prolonged ischemia will ensue leading to a poor prognostic outcome. This review, therefore, mainly focuses on early diagnosis of disturbed neonatal kidney function and prophylactic therapeutical aspects which may be of particular benefit for critically ill newborns at high risk for developing acute renal failure.
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PMID:[Disorders of kidney function and acute kidney failure in newborn infants]. 356 18

Naloxone HCl (Nx) improves cardiopulmonary performance, reverses cellular hypoxia, and stabilizes lysosomal membranes in shock states. However, no detailed study has yet explored its potential role in renal ischemia, which is inevitable in transplantation and surgical and nonsurgical conditions associated with hypotension and shock. This functional and microanatomical study was carried out on dogs subjected to renal warm ischemia with contralateral nephrectomy. Group I (control; N = 4) had bilateral renal dissection and right nephrectomy. Groups II-IV had their kidney pedicles cross-clamped for 60 min and then reperfused. Group II (N = 9) ischemic kidneys received no treatment. Group III (N = 6) kidneys were flushed with pure Nx HCl (2 mg/kg) during ischemia. Group IV (N = 6) dogs received one iv Nx bolus (2 mg/kg) before clamping and another dose before declamping. Biopsies for adenine nucleotides, histology, and ultrastructure were obtained before ischemia, before reflow, and 15 min and 7 days after reflow. Serum creatinine and blood urea nitrogen were measured daily. Ischemia induced significant renal dysfunction, which was reversed by systemic Nx. Nx offered a remarkable protection against postischemic structural damage. Seventy percent of Group II cortical sections showed grade 4 acute tubular necrosis (ATN), and severe residual damage after a week. Eighty-three percent of Group IV sections showed grade 1 ATN and no residual damage after a week. One week survival was 33% in Group II and 100% in Group IV. Nx can be useful in prevention of acute renal failure in clinical situations with arterial hypotension and shock.
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PMID:Naloxone in renal ischemia: a functional and microanatomical study. 358 32


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