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

The ability of the calcium entry blocker verapamil to ameliorate the effects of renal ischemia was studied in ten sheep. Postanesthesia, bilateral cutaneous ureterostomies were placed in each sheep to facilitate urine collection and analysis. Both kidneys were made ischemic for one hour by occluding each renal artery. However, immediately before occlusion of the right renal artery, 0.05 mg/kg of verapamil was injected into the artery. Comparison of urinary creatinine excretion and urine volume for 72 h after reversal of ischemia demonstrated that those kidneys pretreated with verapamil had greater functional preservation (p less than .05). In this study, verapamil appeared to provide protection against renal damage after an ischemic insult.
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PMID:Effect of the calcium entry blocker verapamil on renal ischemia. 333 79

We report herein the results of a randomized prospective trial comparing maintenance cyclosporine (CsA)-prednisone immunosuppression to a regimen of azathioprine-prednisone-antilymphocyte globulin (ALG) in cadaver renal transplant recipients. Fifty-six patients were entered into this study with 31 assigned to the ALG group and 25 to the CsA group. These two groups were well matched for most major determinants of graft outcome and the mean renal preservation time was 37 hr in each group. The incidence of acute tubular necrosis (ATN) was high in both groups (58% ALG, 72% CsA, NS). There were five cases of primary nonfunction in the CsA group and only one in the ALG group (P = .05). Of the kidneys that functioned, the mean serum creatinine nadir (1.5 vs. 2.2 mg/dl, P = .06) and the mean number of days to reach the serum creatinine nadir (24.2 vs. 43.3 days, P = .03) were both less in the ALG group. The actuarial one-year graft survival rate in the ALG and CsA groups is 78% and 48%, respectively (P less than .05). This difference is mainly due to the large number of primary nonfunctioning grafts in the latter group, which we attribute to the effect of CsA's nephrotoxicity superimposed on renal ischemia incurred prior to transplantation. These data emphasize that, in order to realize the full benefit of CsA in cadaver transplantation, renewed emphasis must be placed on minimizing ischemic renal damage.
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PMID:Detrimental effect of cyclosporine on initial function of cadaver renal allografts following extended preservation. Results of a randomized prospective study. 352 55

To evaluate the mechanisms for a low fractional excretion of Na (FENa less than or equal to 1.0) in acute renal failure (ARF) of a sustained nature, causes were determined independent of FENa in 41 patients without volume depletion, obstruction, vasculitis or glomerulonephritis. The 16 patients (39%) with low FENa had lower incidence of preexisting azotemia, lower peak serum creatinine, but higher incidence of renal ischemia and earlier testing (by 1.7 days). Seven of ten such patients converted to high FENa on repeat, whereas FENa remained high in 15 of 17 patients with initially high values. The initial FENa was a direct function of time from the onset of ARF. Low FENa in acute but sustained renal failure is therefore best explained by milder insults; earlier determinations, and/or super-imposed renal ischemia.
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PMID:Low fractional excretion of sodium in acute renal failure: role of timing of the test and ischemia. 356 2

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

To determine if moderate hyperglycemia produced by dextrose administration was detrimental in normothermic renal ischemia, 15 halothane-anesthetized mongrel dogs underwent right nephrectomy and 60 minutes of left renal artery and vein occlusion. Six dogs received 1 L of lactated Ringer's solution (LR) and six others received 1 L of 5% dextrose in lactated Ringer's solution (D5LR). Three sham-operated dogs received 1 L of D5LR and underwent right nephrectomy but no occlusions. All dogs received 500 mL of fluid before occlusion and 500 mL after occlusion. The blood glucose concentration for the LR group was 7.6 mmol/L (137 mg/dL) after 500 mL and 7.2 mmol/L (130 mg/dL) after 1000 mL. In the D5LR group, the blood glucose concentration was 21.5 mmol/L (387 mg/dL) after 500 mL and 20.2 mmol/L (363 mg/dL) after 1000 mL. In the sham-operated group, the blood glucose concentration was 22.8 mmol/L (410 mg/dL) after 500 mL and 20.7 mmol/L (373 mg/dL) after 1000 mL. At 30 hours, the plasma creatinine concentration rose from 70 to 300 mumol/L (0.8 to 3.4 mg/dL) in the LR group and from 90 to 500 mumol/L (1.0 to 5.8 mg/dL) in the D5LR group; the increase for the D5LR group was significantly greater than that for the LR group. In the sham-operated group, the plasma creatinine concentration was stable throughout the 30-hour period. This study demonstrates a significant detrimental effect of dextrose administration on renal function during normothermic ischemia.
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PMID:Dextrose administration exacerbates acute renal ischemic damage in anesthetized dogs. 359 69

Renal ischemia was produced in anesthetized rats by a bilateral ligation of the renal artery, vein, and ureter. Pretreatment with hydralazine (0.3-10.0 mg/kg i.v.) resulted in a dose dependent reduction in elevated plasma creatinine levels 24 hr after a 60 min ischemic episode, indicating a protective effect on post-ischemic renal function. Hydralazine (3.0 mg/kg, i.v.) produced a fall in arterial blood pressure and exaggerated and/or extended post-ischemic depressions in renal blood flow, renal transport activity (in vitro para-aminohippurate uptake) and renal ATP levels. These results indicate that the hypotensive activity of hydralazine may have indirectly benefited the post-ischemic kidney by prolonging a relative anoxic condition which possibly allowed renal cells to recover under conditions where minimal tubular activity was present.
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PMID:Protective effects of hydralazine in a renal ischemia model in the rat. 360 Jan 94

Male Sprague-Dawley rats were maintained on high protein (60%), normal protein (20%), low protein (5%), or no protein (0%) diets for two or four weeks prior to 45 minutes of renal ischemia induced by renal pedicle clamping. Most (93%) of the rats on the high protein diet died within three days following renal ischemia. In addition, 69% of the rats on normal protein diets also died, most before the fourth day following ischemic insult. In contrast, 88% of the rats on the low protein diet lived, although some exhibited elevated serum creatinine levels for up to one to two weeks following ischemia. Finally, all of the rats on no protein diets lived, and most (75%) exhibited normal serum creatinine levels by the fourth day following ischemia. Shifting the diets of high protein and normal protein adapted rats to no protein diets immediately following ischemia did not improve postischemic survival. Also, changing the diets of no protein adapted rats to high protein diets immediately following ischemia did not significantly affect postischemic recovery. When rats were maintained on no protein diets for shorter periods of time prior to ischemia, it was found that approximately a week on this diet is necessary to provide maximum protection from postischemic acute renal failure. These findings demonstrate a dramatic effect of dietary protein prior to ischemic induced acute renal failure, and suggests that preoperative dietary protein intake should be an important consideration in those situations which are predisposed to postoperative acute renal failure.
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PMID:Dietary protein prior to renal ischemia dramatically affects postischemic kidney function. 378 77

Sprague-Dawley rats were injected with known nephrotoxic doses of tobramycin and then subjected to varying amounts of warm renal ischemia. Analysis of serum creatinine at the time of sacrifice revealed no statistically significant difference among controls and the two doses of tobramycin at any given duration of ischemia. Light microscopy revealed no worsening of tubular necrosis with increasing doses of tobramycin.
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PMID:Tobramycin and renal ischemia. 378 4

Thromboxane (Tx) synthase but not cyclo-oxygenase inhibitors prevent acute tubular necrosis (ATN) after renal ischemia, a phenomenon believed to be due to stimulation of the endogenous production of vasodilating prostaglandins (PG). This study directly tests that vasodilating PG protect against the consequences of renal ischemia. Anesthetized, 500-g rats had right nephrectomy and 45 minutes of left renal pedicle clamping or sham clamping. The rats were treated with intravenous (I.V.) saline 1.9 mL/h starting 40 minutes after clamping or sham clamping. All rats except the sham group (N = 8) were pretreated 1 hour before ischemia with ibuprofen (12 mg/kg) to prevent prostanoid synthesis. Beginning 5 minutes before clamp release, the rats were treated intravenously for 2 hours with: saline vehicle (N = 9), PGE1 400 ng/kg/min (N = 6), nitroprusside 4 micrograms/kg/min (N = 8), or dopamine 3 micrograms/kg/min (N = 11). After 24 hours, sham rat creatinine level was 0.5 mg/dL and weight of the left kidney was 86.5% of the previously removed right kidney. Compared with sham rats, ischemia and saline treatment resulted in a rise in creatinine level to 2.7 mg/dL (p less than 0.05) and a rise in kidney weight to 101.9% (p less than 0.05); PGE1 led to a creatinine level of 1.1 mg/dL, a value lower than that of the rats treated with saline (p less than 0.05), and a kidney weight of 92.0%, a value similar to that of sham rats; nitroprusside and dopamine led to a rise in creatinine levels to 3.2 mg/dL (p less than 0.05) and 2.3 mg/dL (p less than 0.05), respectively, as well as a rise in kidney weight to 108.0% (p less than 0.05) and 105.4% (p less than 0.05), respectively. Histologic examination showed ATN in rats treated with saline, nitroprusside, and dopamine, but not in rats treated with PGE1. These results indicate that PGE1 protects the cyclo-oxygenase-treated kidney against ischemia-induced ATN.
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PMID:Vasodilator prostaglandins (PG) prevent renal damage after ischemia. 381 90

These experiments were designed to determine the influence of age on the response of the kidney to ischemia. Renal ischemia was induced in female Fischer-344 rats, 3-4 or 37-38 months old, by renal arterial and venous occlusion followed by 0, 1, 24, or 96 hr of reflow. Age-matched controls were sham operated but were not subjected to ischemia. A transient postischemic increase in blood urea nitrogen (BUN) and serum creatinine was observed in young rats. In old rats, BUN and serum creatinine remained markedly elevated through 96 hr postischemia. In vitro renal cortical slice accumulation of organic ions was inhibited to a greater extent in old rats than in young rats 96 hr postischemia. Histologically, renal tubular damage was more severe in old than in young rats 24 and 96 hr postischemia. Tubular regenerative activity was similar in old and young rats at 96 hr, but restoration of tubular architecture was more complete in young rats. Organic ion accumulation by renal cortical slices from naive old rats was inhibited by in vitro anoxia (treatment with 100% N2) to a greater extent than tissue from young rats. These data suggest that old rats are more susceptible to renal ischemia than are young rats and these differences in susceptibility may reflect intrinsic age-related differences in basal renal metabolism.
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PMID:Age-related differences in susceptibility to renal ischemia in rats. 382 87


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