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

Models of post-ischemic acute renal failure were prepared in rats. The effects of adenosine triphosphate-magnesium chloride (ATP-MgCl2) administration following renal ischemia on possible changes in renal function and renal cellular metabolism following ischemia were studied using the model. The results obtained revealed the following: 1) Over 40 minute-renal ischemia led to significant lowerings of renal cellular ATP level and energy charge (EC) by as much as 45 to 57% and 4.1 to 7.4% of the control, respectively, at 90 min following re-establishment of renal blood flow. Significant increases in Na+ in renal tissues were observed, but no changes in K+. Further, lactate level in renal tissues tended to increase with prolonged ischemic time by as much as 27 to 31% of the control, with a renal cellular anaerobic metabolism observed. On the other hand, at 24 hr following recirculation of the kidney, plasma creatinine (P-Cr), blood urea nitrogen (BUN) and fraction excretion of sodium (FENa) increased significantly, and creatinine clearance (C-Cr) and urine osmotic pressure decreased significantly, as compared with the control, indicating ischemic acute renal failure. 2) Intravenous injection of ATP-MgCl2 at a dose of 25 mumole/kg and a rate of 1.0 mumol/min after 40 min of renal ischemia led to significant lowerings of P-Cr, BUN and FENa to 36, 35 and 35% of the control (injected with physiological saline solution), respectively, and to significant elevation of C-Cr and urine osmotic pressure by as much as 41 to 31% of the control respectively, at 24 hr after reperfusion. The above results suggested that the ischemic acute renal failure was caused by the decreases in renal cellular ATP and EC with ischemia, resulting in renal cellular metabolic disturbances. It was further suggested that ATP-MgCl2 administered for such a pathological condition could make significant improvements in renal function.
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PMID:[Effect of adenosine triphosphate-magnesium chloride administration for post-ischemic acute renal failure (I)]. 660 69

To investigate the possible protective effect of Ca2+ blockers in ischemic acute renal failure (ARF), verapamil, in a dose of 10 micrograms/kg body wt/min was administered for 100 min, starting 15 min before the total occlusion of the left renal artery after right nephrectomy in rats. Mean 24-hr creatinine clearance, blood urea, and serum creatinine levels, 24 hr after declamping, were used as a measure of kidney function. These values which were 135 +/- 1.9 microliter/min, 231 +/- 22 mg%, and 2.25 +/- 0.22 mg%, respectively, in the untreated rats, were found to be significantly different, i.e., 326.3 +/- 33.2 microliter/min, P less than 0.001, 112 +/- 25 mg%, P less than 0.001, and 1.26 +/- 0.28 mg%, P less than 0.01, respectively, in the verapamil-treated animals. Increased 24-hr total urine creatinine, sodium, osmolality, and a lower fractional excretion of sodium were also observed in the verapamil-treated rats with ARF. The combination of propranolol 1 mg/kg body wt/min and verapamil 10 micrograms/kg body wt/min for 100 min had no additive effect on renal function. In another group of ARF rats in which verapamil was started after declamping, no alleviating effect was observed. It is concluded that verapamil, an inhibitor of cellular membrane transport, when given prior to the renal ischemia, offers a partial but significant protection in this model of ischemic ARF.
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PMID:Beneficial effect of verapamil in ischemic acute renal failure in the rat. 684 46

The urinary excretion of four enzymes (alkaline phosphatase: AP, leucine aminopeptidase: LAP, lactate dehydrogenase: LDH, muramidase: M) was measured in unanesthetized adult male Wistar rats within 48 h after either a single injection of mercuric chloride (HgCl2) (0.5-1.0 mg x kg-1), or of gentamicin (2.5-25 mg x kg-1), or of tobramoycin (2.5-25 mg x kg-1), or after 30 min of clamping of both renal arteries. Glomerular filtration rate (GFR), TmPAH, plasma urea, urinary protein and sodium excretion were measured simultaneously. The excretion of AP, LAP and LDH, but not that of M, increased significantly above control levels after renal ischemia or the nephrotoxic agents; the increase was dose-related after HgCl2. GFR was not depressed, but TmPAH decreased after the higher doses of the toxic agents. Though more sensitive for detecting minor grades of acute renal damage than function tests, measurements of urinary enzyme excretion were fraught with large inter-individual variation, and variable time-course of changes in different types of renal damage. Short-term exposure (3 months) to phenylmercuric acetate was associated with a significant decrease of the urinary excretion of AP, and of LAP, and of AP activity measured histochemically in proximal tubular cells.
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PMID:Urinary enzyme excretion and changes in renal functions induced by toxic substances or by renal ischemia in rats. 693 3

A study of the renal receptors and types of stimuli which give origin to supraspinal and spinal-mediated autonomic reflexes is presented. Multiunit and single unit recordings from the afferent renal nerves of male Sprague-Dawley rats have revealed two groups of renal chemosensitive receptors (chemoreceptors). These we have called renal R1 and R2 "chemoceptive" receptors. R1 receptors do not have a resting discharge but are activated after 38.7 +/- 3.3 (S.E) sec (n = 40) of complete renal ischemia (occlusion of the renal artery). Other activating stimuli are associated with a marked impairment in renal blood flow (prolonged occlusion of the renal vein and the hypotension of systemic asphyxia or hemorrhage). Their discharge is characterized by trains of impulses which cease abruptly upon re-entry of blood into the kidney. They are not responsive to increases or decreases in renal perfusion pressure or to increases in renal venous or ureteral pressure. In contrast, R2 receptors have a resting discharge and respond vigorously to backflow of normal urine (nondiuretic) into the renal pelvis. The results of the backflow into the pelvis of different test solutions (diuretic and nondiuretic urine, 1 M urea, 1 M mannitol and solutions of NaCl and KCl) indicate that this response is dependent upon the composition of the fluid bathing the renal pelvis rather than the increase in pelvic pressure or pelvic distension. The resting discharge rate is highest in nondiuretic conditions and declines substantially after diuresis is induced by extracellular volume expansion. R2 receptors are also activated by renal ischemia produced by clamping the renal artery. It is concluded that these two groups of afferent sensory units are renal chemosensitive receptors, (chemoreceptors) which respond to the chemical environment of renal interstitium.
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PMID:Renal chemoreceptors. 727 33

The role of volume depletion and renal ischemia in the development of renal functional impairment in glycerol-induced ARF is not clear. This study was designed to evaluate the role of volume depletion in this model by determining the hemodynamic and functional alterations which occur between 3 and 18 hr after glycerol administration and the reversibility of these changes in response to Ringer loading. Three hours after glycerol, Cln and RBF, measured by flowmeter, were reduced 70% and 52%, respectively, in comparison with control values. FeNa was 0.04%. Ringer loading increased Clkn to 103% and RBF to 93% of control values. Qualitatively similar results were found 6 hr after glycerol. At 18 hr, Cln and RBF were 47% of control values. After Ringer loading, RBF rose to 100% of control. The response of Cln, however, was a function of the baseline FeNa. Cln incrased substantijally in rats with low FeNa but changed only slightly in animals in which this parameter was increased. These studies indicate that the early reduction in the Cln is dependent upon the fall in RBF. At 12 and 18 hr, however, the fall in Cln is not blood flow-dependent, and a second mechanism must be operative. FeNa seems to be a reliable index of the functional status of a given animal.
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PMID:Sequential studies on the pathophysiology of glycerol-induced acute renal failure. 740 Jun 68

This study investigates the role of verapamil, a calcium channel blocker, combined with allopurinol, a xanthine-oxidase inhibitor, when given at reperfusion after severe renal ischemia injury in the rat. Male Sprague-Dawley rats were subjected to 60 minutes of warm ischemia by cross clamping the whole left renal pedicle (artery and vein). At the end of ischemia, the clamps were removed and a contralateral nephrectomy was performed. The animals (n = 40 per group) were divided into five groups; Group 1, ischemic control (IC) receiving lactated Ringer's; Group 2, allopurinol (A) 100 mg/kg; Group 3, verapamil (V) 1.25 mg/kg; Group 4, receiving a combination of A + V at the same concentrations; and Group 5, sham group. Each drug was given intravenously at the end of the ischemic period at reperfusion. Survival was evaluated at 7 days. Renal damage was assessed by kidney function tests (serum creatinine and blood urea nitrogen, or BUN), light histology. Lipid peroxidation was measured in renal tissue using the TBA (thiobarbituric acid) assay. The best survival rate was seen in the combination group of A + V (70% at 7 days; p < .01 vs. control). Single drugs were not as effective as the combination when compared to the IC. Serum creatinine at 24 and 48 hours showed a significant difference between the IC and treatment groups. At 72 hours there were no differences among the treated groups. Histological damage was more pronounced in the IC (Grade 4.0) than in the allopurinol (3.4 +/- 0.8), verapamil (3.0), or A + V (2.2 +/- 0.04).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Protective effect of combined allopurinol and verapamil given at reperfusion in severe renal ischemia. 773 32

Acute renal failure (ARF) is defined as a renal insufficiency of sudden onset (increase of creatinine and urea in the serum) combined with or without oliguria (less than 500 ml of urine per day). Nephrotoxins (drugs, contrast medium) or renal ischemia (hypovolemia, hypotension, shock, septicemia, treatment with CEI) may affect the renal tubulus through several pathways, all of which may result in ARF. Ultrasound allows to distinguish hydronephrosis from ARF which is characterized by increased width of the parenchyma and low echodensity of the medulla. ARF is usually reversible. If conservative therapy fails, dialysis treatment is necessary.
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PMID:[What should the general practitioner know about diagnosis and treatment of acute kidney failure?]. 778 97

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

Acute renal failure induced by the administration of gentamicin (GM) was studied enzymochemically in comparison with that in rats with tubular disorder resulting from postischemic reperfusion. Renal ischemia was caused by clamping the renal artery for 30 minutes to create complete ischemia and reflow. The activities of renal tissue glutathione peroxidase (GSH-Px) and the values to the renal contents of glutathione (GSH) and malondialdehyde (MDA) were measured in each sample. In order to confirm whether GSH plays an important role in the intrinsic anti-oxidant system in this model, buthionine sulfoximine (BSO), which is a gamma-glutamylcysteine synthetase inhibitor, was administered intraperitoneally to decrease the renal GSH content before the procedure in renal ischemia. On the other hand, the GM-induced ARF model was made by injection with GM 100 mg/kg during a period of 5 days. In the GM group, a significant increase in MDA and a reduction in the sphigomyelin (SPH)/phosphatidylcholine (PC) ratio and inactivation of PLA2 were observed. In the kidney tissue obtained 15 min. after reperfusion, the renal content of MDA was elevated markedly in the BSO-preadministered group. A reduction of SPH/PC ratio was also observed in the reperfusion model. PAL2 hydrolyzes the acyl group at the 2-position containing much of the highly unsaturated fatty acids that are easily oxidized. Further, PLA2 is considered to act directly on one of PC or phosphatidylinositol. Phospholipidosis thesauruses, noted in acute renal failure induced by GM, is considered to be caused by reduced liberation of lysosomal intramembranous phospholipid into the cytoplasm and accelerated peroxidation of intramembranous lipid.
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PMID:[Lipid peroxidation and tubular disorder in experimental acute renal failure-enzymochemical study in the rat kidney]. 807 17

After 45-min bilateral warm renal ischemia lethality amounted to 45% and 82% in 55- and 20-day-old rats, respectively (n = 176). Lethality rates were not significantly different after 20-min unilateral ischemia followed by contralateral nephrectomy after 24 hours (34 vs. 48% in young vs. adult rats; n = 168). The latter experimental approach was used to characterize age dependent differences in the susceptibility to ischemia. The degree of postischemic renal damage was the highest at the 1st and 2nd days after ischemia; at this time, lethality rates were similar in young and adult rats. However, urea concentration in serum was significantly more enhanced in young animals whereas that of creatinine was increased to the same extent in both age groups. The increase in protein excretion into urine was similar in young and adult rats, too. Furthermore, urine flow rates and GFR were significantly diminished after ischemia, independent of age. However, excretion of Na+ and K+ was distinctly more depressed in immature individuals. Finally, the glutathione content in kidney tissue of both age groups was reduced and lipid peroxidation was significantly higher after ligation of the renal arteries. The relative changes were similar in both age groups although the glutathione content was significantly lower in 20-day-old control rats. 4-5 days after ischemia, most parameters returned to baseline values. In 55-day-old rats, 45-min ischemia has more severe consequences on renal function compared to 20-min ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of methods indicating higher susceptibility of immature rats to renal ischemia. 832 66


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