Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0920646 (renal ischemia)
 2,515 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experiments were undertaken to investigate further the effect of furosemide on renin secretion in the anesthetized dog. To separate the effects of the macula densa and the baroreceptor mechanisms, experiments were conducted in kidneys made nonfiltering by combining 2.5 hours of renal ischemia with ureteral ligation. Furosemide, in a dose of 5 mg/kg, increased renin secretion and decreased renal resistance in dogs with a nonfiltering kidney. Prior dilation of the nonfiltering kidney with either acetylcholine or papaverine prevented changes in both resistance and renin secretion. However, following dilation of the intact filtering kidney with acetylcholine, furosemide caused an increase in renin secretion. Infusion of d,l-propranolol decreased renin secretion in both the filtering and the nonfiltering kidneys. Following propranolol treatment, furosemide increased renin secretion in the filtering kidney but had no effect on renal resistance. These experiments indicate that furosemide stimulates renin secretion by both the macula densa and the baroreceptor mechanisms. The data suggest that stimulation of the sympathetic nervous system may alter renin secretion by modulating the renal baroreceptor, but sympathetic innervation does not appear to be involved in the macula densa mechanism.
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PMID:Control of renin secretion in the dog. Effects of furosemide on the vascular and macula densa receptors. 118 38

In the present study 1 h of total occlusion of the left renal artery in conscious rats was chosen as experimental model of ischemic acute renal failure (ARF), while the contralateral kidney was left intact. Chronic high dietary sodium intake, acute isotonic saline infusion, or administration of saralasin did not protect from ARF. Furosemide, mannitol, and verapamil converted oliguric into non-oliguric ARF in 100%, 75%, and 60% of the animals, resp. Protection from oliguria and preservation of GFR inversely correlated with the depression of cortical ATP-concentration (control: 1.32 +/- 0.07 mumoles/g wet weight) 6 h after ischemia by 16%, 41%, and 58% in mannitol- and verapamil- treated rats and in untreated rats, resp. At this time, Na-K-ATPase enzyme activities in renal cortex and papilla were unaffected, while enzyme activity in outer medulla was suppressed from 15.4 +/- 1.4 to 9.4 +/- 1.0 mumoles Pi/mg protein h in all groups of animals. The results suggest that in this model of ARF renal ischemia not only affects cellular energy supply in renal cortex but also causes severe structural and functional impairment in the outer medulla, probably leading to tubular obstruction and depression of glomerular function. Pharmacological protection from ischemic oliguric ARF cannot be achieved by prior induction of high urine flow rates alone but depends on the degree of metabolic and functional reserve of the injured tubular epithelium.
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PMID:Renal functional and metabolic studies on the role of preventive measures in experimental acute ischemic renal failure. 641

The influence of dihydralazine, propranolol, clonidine, furosemide and reserpine on the clearance of I125 hippurate in rats in alcohol intoxication was investigated. It was found that both in acute and subacute ethanol intoxication the renal blood flow was impeded. Reserpine and propranolol did not significantly change the half time of I125 hippurate in blood both in animals treated and not treated with alcohol. Furosemide prolonged the clearance of hippurate and increased kidney ischemia in alcohol intoxication. Dihydralazine and clonidine increased the effective renal blood flow in normal animals but not in acute and subacute ethanol intoxication.
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PMID:Effects of some hypotensive drugs on the clearance of I125 hippurate in rats after acute and subacute ethanol intoxication. 668 71

Tubular transport abnormalities have recently been characterized in a rabbit model of ischemic acute renal failure (ARF). These studies demonstrated severe observable morphologic and functional changes in the proximal nephron together with functional changes in the distal nephron. Tubular debris was often produced by perfusion of proximal nephron segments. In the present study, agents used to prevent ARF were tested in this rabbit model of ARF. Rabbits were infused with either 5% body wt 5% manitol or 20 micrograms . kg-1 . min-1 furosemide in 5% body wt normal saline for the 60 min preceding 60 min of total renal ischemia. Mannitol 1) prevented the development of ARF, 2) maintained fluid reabsorption in the proximal convoluted tubule (PCT) (0.59 +/- 0.03 vs. 0.52 +/- 0.1 nl . mm-1 . min-1) and proximal straight tubule (PST) (0.34 +/- 0.05 vs. 0.39 +/- 0.07 nl . mm-1 . min-1), 3) depressed NaCl reabsorption in the cortical thick ascending limb of Henle's loop (TALH), and 4) did not prevent a decrease in ADH-mediated osmotic water flow in the cortical collecting tubule (CCT). Furosemide 1) partially preserved renal function, 2) partially protected the PCT (0.63 +/- 0.05 vs. 0.38 +/- 0.04 nl . mm-1 . min-1) and PST (0.32 +/- 0.04 vs. 0.22 +/- 0.02 nl . mm-1 . min-1), and 3) did not change the transport capacity of the TALH or the ADH response of the CCT. Preservation of proximal nephron integrity was also reflected by the absence of debris formation. There is a direct relation between an agent's ability to protect the functional integrity of the cells of the proximal nephron and its ability to preserve renal function.
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PMID:Prior mannitol and furosemide infusion in a model of ischemic acute renal failure. 679 34

In the present review, the possibilities of ergometric and pharmacological "intervention" with a view to improving the validity of scintirenography are reported. Exercise renography at present does not have a defined role in clinical routine. This procedure, however, gives additional information in hypertensive patients with respect to renal ischemia. Captopril scintirenography can be recommended as a screening test for renovascular hypertension. Furosemide-"intervention" differentiates between obstructive uropathy and dilatation of renal collecting system without obstruction. This is true especially in newborns with congenital abnormalities of the upper urinary tract, in order to stratify these young patients for surgical or conservative treatment.
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PMID:[Intervention in nuclear medicine kidney diagnosis]. 784 1

A protective action of lasix, dichlothiazide, and triampur (dichlothiazide + triamterene) was studied in experiments on rats. Ischemia was simulated by obstruction of kidney vessels and ureter for 90 min. Lasix and dichlothiazide produced a protective effect in renal ischemia and at the same time resulted decrease of lifetime of experimental rats. Triampur increased the lifetime and decreased the losses of potassium in kidney tissue.
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PMID:[The action of diuretics in renal ischemia]. 870 84

The intensity of lipid peroxidation increases in ischemic damage to the kidneys. That furosemide possesses antioxidant properties was established on a model of in vitro total kidney ischemia. It is supposed that the protective effect of furosemide in ischemic damage is due to inhibition of lipid peroxidation. However, such an effect is not encountered in kidney ischemia in an intact organism. Furosemide does not prevent the fall of selenium concentration in the kidney after ischemia.
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PMID:[The antioxidative properties of furosemide in renal ischemia]. 902 84

A reduction in glomerular filtration rate (GFR) is a primary characteristic of ischemic acute renal failure. The present study was undertaken to examine the roles of angiotensin II, tubuloglomerular-feedback (TGF) mechanism, and tubular obstruction for the GFR reduction in the post-ischemic kidney. Renal ischemia was induced by occlusion of the bilateral renal arteries for 60 min, and renal function was examined at 2 and 24 h after the onset of reflow. After the end of 2-h reflow, the GFR was not significantly changed, but the urine flow increased significantly. On the other hand, at the end of 24-h reflow, the GFR and urine flow decreased markedly along with increased filtration fraction. The renal blood flow significantly decreased at 24 h, but not 2 h, after reflow, which was accompanied by increased total renal vascular resistance. Furosemide infusion (1 mg/min/kg) after 24 h of reflow prevented the reduction in GFR and filtration fraction without no changes in renal blood flow and total renal vascular resistance. Pretreatment of enalapril and losartan did not prevent the reduction in GFR, indicating that angiotensin II was not involved. In morphological examinations, tubular obstruction was seen in the proximal and distal tubules of kidneys both at 2 and 24 h after the onset of reflow. In two rabbits subjected to 48 h of reflow, the tubular obstruction was not observed, despite GFR remained depressed. These results suggest that the late reduction in GFR in postischemic kidneys is not mediated by angiotensin II, but is mediated, at least in part, by the TGF mechanism. The tubular obstruction may be not prerequisite for the GFR reduction in rabbits.
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PMID:Mechanism of reduced GFR in rabbits with ischemic acute renal failure. 1080 59

Although the search for effective methods of renal prophylaxis during aortic surgery spans many decades, definitive answers are scarce. The literature is voluminous, yet the amount of work clearly relevant to the specific clinical situation of perioperative prophylaxis is small. Given the significant morbidity and subsequent mortality involved with perioperative ARF, it is difficult to sit back and do nothing when pharmacologic agents empirically are believed to possibly benefit the patient. Care must be taken to apply data from different clinical scenarios in the literature to the situation at hand. Drugs felt to be innocuous, even in low doses, may be insidiously counterproductive or damaging if they are not managed properly. Maintaining an adequate preload and stable hemodynamics seems to be the most logical universal approach at this time. Furosemide treatment without maintaining an adequate volume status once diuresis commences may be detrimental, which is true with the diuretic effects induced by mannitol or dopamine. The tachycardia resulting from a relative hypovolemia and from the beta effects of dopamine can cause myocardial ischemia from increased oxygen demand. Low urine output does not portend a negative outcome in the face of an adequate intravascular volume any more than an induced diuresis prevents renal injury. Currently, minimization of renal ischemia and maintenance of an adequate intravascular volume and renal hemodynamics are the keys to optimizing renal outcome during aortic surgery. Other maneuvers are not definitive and should be cautiously undertaken.
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PMID:Intraoperative management of renal function in the surgical patient at risk. Focus on aortic surgery. 1109 87

Loop diuretics are known to affect renal hemodynamics and possibly gene transcription, but the specific effect of furosemide on renal angiogenesis gene expression after acute ischemia is not known. We utilized an acute renal failure model in rats to test the hypothesis that furosemide improves renal hemodynamics and alters the transcriptional signature of acute ischemic nephropathy. Twenty-four male Sprague-Dawley rats were anesthetized by the intraperitoneal administration of 50 mg/kg urethane. Animals were divided into four groups (n = 6 each): (1) sham-operated group infused with saline; (2) sham-operated group infused with 30 microg/kg/hr furosemide (equivalent to a human dosage of 2 mg/hr); (3) unilateral renal ischemia (1 hr, left renal artery cross-clamping) followed by 6 hr of reperfusion; and (4) renal ischemia/ reperfusion (I/R) with furosemide. Renal artery blood flow (RBF), renal cortical perfusion (RCP), and renal corticomedullary tissue oxygen tension (PO2) were recorded throughout. Following 6 hr of reperfusion, left kidney RNA was used to probe microarrays. Gene expression was measured as percent positive control and confirmed using reverse transcriptase polymerase chain reaction. Physiologic data were analyzed by calculating area under the curve, and gene expression data were compared by using multiple analysis of variance with Tukey's post-hoc tests. Furosemide significantly increased RBF (P < 0.05) and PO2 (P < 0.05) in postischemic kidneys. Furosemide attenuated nine of the 13 ischemia-induced and 41 of 78 ischemia-suppressed angiogenesis-related genes. This attenuation was statistically significant (P < 0.05) for 17 I/R injury-suppressed genes. Data from this rat model of ischemic nephropathy suggest that furosemide improves renal hemodynamics and attenuates ischemia-related changes in gene expression.
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PMID:Effect of furosemide infusion on renal hemodynamics and angiogenesis gene expression in acute renal ischemia/reperfusion. 1652 16


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