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

Acute renal failure is most commonly associated with renal ischemia, although nephrotoxins such as antibiotics, radiographic contrast media and anesthetic agents have become important causes. Although the pathophysiology has not been completely explained, renal vasoconstriction appears to be an important factor. Oliguria, isosthenuria and a urinary sodium concentration over 25 mEq per L are characteristic features. Control of volume and avoidance of metabolic disequilibrium can be accomplished by careful management and dialysis. The major causes of death are infection and the primary disease itself.
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PMID:Acute renal failure. 705 95

The high blood flow rate/gram of kidney tissue supplies mainly the renal cortex. The net effect of the interaction of the renin-angiotensin system, the kallikrein-kinin system and prostaglandins is to autoregulate renal blood flow within a narrow range. Drugs and neurogenic factors also influence renal hemodynamics. The renal circulation responds to changes in extracellular fluid volume, and in cardiac output. Renal ischemia occurs readily as these parameters decrease and prompt correction of circulatory dynamics can restore renal blood flow and prevent tubular necrosis. With hypovolemia or heart failure, angiotensin II is a mediator of efferent arteriolar constriction promoting a proportionately greater fall in renal plasma flow than in glomerular filtration rate, thereby augmenting sodium reabsorption. With renal failure, glomerulotubular balance is affected conversely promoting sodium loss. Appreciating these distinctions allows recognition of inappropriate sodium retention or loss. With such data, prognosis can be estimated more accurately and attempts to restore circulatory dynamics can be guided.
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PMID:Pathophysiology of renal hemodynamics. 726 10

To study the role of renal prostaglandins (PGs) in renovascular hypertension, PGE2 and PGF2 alpha concentrations in both inner and outer medullae of the kidney were measured by radioimmunoassay in rabbits with hypertension produced by left renal artery constriction. In the acute phase, a week after surgery, PGE2 in the inner and outer medullae and PGF2 alpha in the inner medulla were significantly increased in both the constricted and opposite kidneys (p less than 0.01). In chronic phase, 5 weeks after surgery, PGs returned to normal concentrations with the exceptions of PGE2 in the outer medulla and PGF2 alpha in the inner medulla of the constricted kidney. These results suggest that increased renal PGs may not be the cause of hypertension but a defensive reaction to renal ischemia, hypertension and sodium load.
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PMID:Intrarenal prostaglandins E2 and F2 alpha in experimental renovascular hypertension. 728 73

Although acute renal failure, caused either by renal ischemia or nephrotoxic agents, is usually characterized by oliguria, a severe fall in glomerular filtration rate, and a fall in renal blood flow, some patients and experimental models display a non-oliguric pattern of renal injury. The present study was designed to evaluate the mechanism of preservation of high urinary flow rate under this condition. Following the administration of the aminoglycoside gentamicin to rats for five days, a decrease in concentrating ability was demonstrated, caused by impaired vasopressin-mediated water transport. Further treatment resulted in a fall in Cin to 15 percent of control, although RBF was reduced to only 67 percent of control, and urine flow rate rose above control levels. Induction of acute and renal failure with dichromate was associated with variable high or low urinary flow rates according to pre-injury intake of sodium. Urine volume correlated directly with cortical blood flow. These data suggest that the non-oliguric pattern of acute renal injury is caused by preservation of cortical perfusion in the setting of severe tubular injury.
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PMID:Studies on the mechanism of non-oliguric experimental acute renal failure. 732 6

The ability of the mixed endothelin (ETA/ETB) receptor antagonist (+/-)-SB 209670 to prevent and reverse ischemia-induced acute renal failure (ARF) was studied in rats with moderate and severe ARF. Uninephrectomized, chronically instrumented Sprague-Dawley rats were used. Moderate and severe ARF was induced by occlusion of the renal artery for 30 and 45 min, respectively. During the 24 hr after 30-min ischemia (moderate ARF), glomerular filtration rate (GFR) decreased by 95%, and fractional excretion of sodium increased from 0.6% to 10%. Infusion of (+/-)-SB 209670 at 10, 30 and 100 micrograms/kg.min for 30 min before, during and 60 min after renal ischemia had a moderate effect on renal function. Thus, with the highest dose, the ischemia-induced reduction in GFR was 70%. This dose, however, had no effect in rats when given before, during and after 45 min of renal ischemia (severe ARF). In contrast, when infused at 30 micrograms/kg.min for 3 hr on the day after ischemia, (+/-)-SB 209670 markedly increased survival rate (75%) in rats with severe ARF by significantly increasing tubular reabsorption of Na+, followed by a slow and gradual increase in GFR and reversal of the increase in plasma K+ concentration. Data from acute renal clearance studies in rats with moderate ARF showed that when infused 24 hr after ischemia, (+/-)-SB 209670 acutely reversed the impairment in sodium reabsorption without increasing GFR or renal blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nonpeptide endothelin receptor antagonists. V: Prevention and reversal of acute renal failure in the rat by SB 209670. 756 50

Endothelin is an important modulator of renal function via its binding to abundant receptors in renal tissue and by the ability of renal endothelial and epithelial cells to synthesize and release endothelin. In the kidney, endothelin may function as a paracrine-autocrine factor in the regulation of renal blood flow, glomerular hemodynamics, and sodium and water homeostasis. Recent evidence suggests that circulating endothelin may play an important role in renal regulation in cardiorenal states of endothelin activation. Endothelin is a potent renal vasconstrictor that has dual actions on glomerular filtration rate due to its ability to preferentially constrict efferent arterioles preserving glomerular filtration. Furthermore, endothelin modulates sodium excretion and water balance at the level of the proximal tubule and medullary collecting ducts, respectively, by mechanisms that are still unclear. In addition, endothelin stimulates the renin-angiotensin-aldosterone system and atrial natriuretic peptide release and inhibits arginine vasopressin-mediated water reabsorption in the inner medullary collecting duct. Recent studies using specific receptor antagonists have demonstrated a pathophysiologic role for endothelin during renal ischemia, cyclosporine-induced toxicity, and chronic renal failure. This review highlights recent research that supports an important role for endothelin as a locally produced vasoactive and natriuretic peptide in the regulation of renal hemodynamic and excretory functions.
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PMID:Physiologic and pathophysiologic roles of endothelin in the kidney. 785 Apr 14

Atrial natriuretic peptide (ANP) has been shown to reverse functional impairment in ischemic acute renal failure (ARF). To prolong and/or to enhance the effects of peptide, in this investigation dopamine (D) (3 micrograms/kg BW/min) was applied together with ANP (100 ng/kg BW/min) after 90 min unilateral renal artery occlusion in anesthetized dogs. ANP significantly increased creatine clearance, filtration fraction, diuresis, sodium excretion, sodium reabsorption, and free water clearance, as in postinfusion period only V remained elevated. D alone did not effect renal function beneficially. ANP+D improved kidney function impairment to a level comparable with that of ANP alone, but V and UNa.V remained increased in the postinfusion period. MAP was elevated during ANP+D infusion as compared to ANP alone and was sustained to the end of the experiment. We conclude that D does not potentiate the positive effects of ANP on postischemic kidney, but prolongs its action on UNa.V, possibly by maintenance of high MAP after renal ischemia.
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PMID:Atrial natriuretic peptide and dopamine in a dog model of acute renal ischemia. 797 98

Platelets have been implicated in the pathophysiology of ischemia-reperfusion injury. In this study, antiplatelet effects of cyclic GMP (cGMP)- and cyclic AMP (cAMP)-mediated agents were evaluated in renal ischemia in pentobarbital-anesthetized rats. Renal ischemia was induced by unilateral occlusion of the left renal artery (40 min) followed by reperfusion (30 min) with the contralateral kidney serving as control. 111Indium-labeled platelets, drugs or vehicle were administered 30 min before induction of renal ischemia. Occlusion of the left renal artery for 20, 40 or 60 min resulted in a 100, 300 and 600% increase (over contralateral right kidney) in the platelet-associated 111indium activity in the ischemic kidney. In all subsequent studies the kidney was occluded for 40 min to test the antiplatelet activity of individual agents. 8-Br-cGMP (0.1 and 0.3 mg/kg/min i.v.), zaprinast (0.1 mg/kg/min i.v.) and sodium nitroprusside (0.003 and 0.01 mg/kg/min i.v.) significantly attenuated platelet accumulation in renal ischemia, whereas 8-Br-cAMP (0.3 mg/kg/min i.v.) or milrinone (0.1 mg/kg i.v. bolus, plus 0.01 mg/kg/min) did not. Minoxidil (0.01 and 0.03 mg/kg/min i.v.), a vasodilator which produced equihypotensive effects as the cGMP-mediated agents, and milrinone failed to prevent platelet accumulation. These results demonstrate that modulation of the platelet function by cGMP agents can be dissociated from their blood pressure lowering effects. cGMP is known to inhibit both platelet adhesion and aggregation, whereas cAMP is only active against aggregation. The present findings provide further evidence that cGMP-mediated drugs may afford effective antiplatelet action in an in vivo model of ischemia-reperfusion injury.
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PMID:Cyclic GMP but not cyclic AMP prevents renal platelet accumulation after ischemia-reperfusion in anesthetized rats. 799 27

The after effects of renal ischemia were studied in hypoxia-adapted rats. It was felt that chronic hypoxia animals which had already adapted to a low oxygen level might be more tolerant of renal ischemic insult; however, chronic hypoxia is always accompanied by polycythemia, which may cause severe RBC trapping and consequently might enhance renal damage after renal ischemia. Chronic hypoxic rats were prepared by exposure in an altitude chamber 15 h per day for 4 weeks. The plasma sodium, potassium, urea, and creatinine levels were determined to compare the changes in these parameters between the baseline and 3 h after a 45-min occlusion of both renal arteries in 12 sea-level (SLB) controls and in 12 chronic hypoxic (CHB) and 11 chronic hypoxic plus RBC pheresis (to reduce hematocrit: CH + P) rats. From the parameters measured, the CHB rats were found to be more tolerant of renal ischemia. However, this was not the case in the rats with pheresis. It is concluded that after chronic hypoxia, some humoral factors in the plasma may play an important role in reducing the renal damage after ischemic insult.
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PMID:Ischemic renal failure in chronic hypoxic rats. 804 64

We investigated the effects of a non-protein diet on renal recovery in rats following 45-minute renal ischemia and mercuric chloride (3 mg/kg BW:S.C.) poisoning. The rats were fed a non-protein diet for one week before the renal insults. Renal functions were measured 24 hours after renal ischemia or 6 hours after mercuric chloride administration. In the ischemia investigation, the glomerular filtration rate (GFR), the renal plasma flow rate (RPFR) and the percent fractional sodium excretion (%FENa) of rats fed a regular diet (19.6% protein) were 25 +/- 7 microliters/min/g KW, 0.19 +/- 0.1 ml/min/g KW and 14.8 +/- 2.0, respectively. These values in the rats fed a non-protein diet showed better recovery, returning to a GFR of 114 +/- 32 microliters/min/g KW, an RPFR of 0.37 +/- 0.1 ml/min/g KW, and a %FENa of 2.43 +/- 0.6, respectively (p < 0.05). Furthermore, the seven-day survival rate was improved from 17% in the regular diet group to 100% in the non-protein diet group. In the mercuric chloride investigation, the renal functions in rats on a regular diet were shown by a GFR of 461 +/- 51 microliters/min/g KW, an RPFR of 1.91 +/- 0.2 ml/min/g KW, and a %FENa of 2.22 +/- 0.5. One-week feeding with a non-protein diet ameliorated the decrease in renal function, resulting in a GFR of 604 +/- 84 microliters/min/g KW, an RPFR of 2.15 +/- 0.5 ml/min/g KW, and a %FENa of 2.20 +/- 0.6. Consequently, there was a distinct beneficial effect on the survival of these rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Beneficial effects of a non-protein diet on renal function of rats exposed to ischemic and nephrotoxic insults. 825 2


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