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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ischemia results in the marked reduction of renal proximal tubule function which is manifested by decreased Na+ and H2O reabsorption. In the present studies the possibility that altered Na+ and H2O reabsorption were due to ischemia-induced loss of surface membrane polarity was investigated. Following 15 min of renal ischemia and 2 hr of reperfusion, proximal tubule cellular ultrastructure was normal. However, abnormal redistribution of NaK-ATPase to the apical membrane domain was observed and large alterations in apical membrane lipid composition consistent with loss of surface membrane polarity were noted. These changes were associated with large decreases in Na+ (37.4 vs. 23.0%, P less than 0.01) and H2O (48.6 vs. 36.9%, P less than 0.01) reabsorption at a time when cellular morphology, apical Na+ permeability, Na+-coupled cotransport, intracellular pH and single nephron filtration rates were normal. We propose that the abnormal redistribution of NaK-ATPase to the apical membrane domain is in part responsible for reduced Na+ and H2O reabsorption following ischemic injury.
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PMID:Loss of epithelial polarity: a novel hypothesis for reduced proximal tubule Na+ transport following ischemic injury. 254 Dec 48

The main purpose of our study is to investigate the possible protective effects of Fructose 1-6 diphosphate (FDP) and Danshen (Salvia Miltiozzhiza Bunze) on renal cortical Na-K-ATPase activity after renal ischemia and gentamicin nephrotoxicity. An 18.6% reduction in renal cortical Na-K-ATPase activity was shown after 30 min of renal pedicle clamping and 60 min of reflow, and a 32.5% reduction after 90 min of single injection of 100 mg/kg gentamicin. Light and electronic microscopy revealed no significant morphologic changes in both groups in the experiment. 4g/kg FDP and 18g/kg Danshen were infused 60 min after reflow in the ischemic group, 90 min after injection of gentamicin in the gentamicin-treated group and 90 min in the sham-operated group separately. The enzyme activity in the FDP-treated groups was found to be higher than that in the control kidneys while in the Danshen-treated groups no significant difference could be found. Our study showed that FDP and Danshen could prevent the decline of renal cortical Na-K-ATPase activity induced by ischemia and gentamicin. FDP could increase this enzyme activity while Danshen showed no such direct effect.
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PMID:Effects of FDP and Danshen on renal cortical Na-K-ATPase activity in rats after treatment with renal ischemia and gentamicin. 256 Sep 55

In order to clarify the cause of the decrease in the urinary excretion of NAG (U-NAG) in severe ischemic renal injury in rabbits, we studied intrarenal energy metabolism in ischemic renal injury. After 5 min of ischemia, energy charge and ATP significantly decreased by 50% and 29% respectively. These parameters, however, did not significantly show the change in more than 5 min of renal ischemia. Energy charge and ATP did not reflect the degree of renal injury produced by ischemia, while it was indicated that the longer the period of ischemia until 120 min of ischemia, the less the rate of intrarenal ATP resynthesis at 30 min after reflow. Intrarenal lactate content increased significantly from the 5 min ischemia group to the 180 min. These results suggest that no improvement in intrarenal energy metabolism with increasing duration of renal ischemia is showed and ischemic renal injury develops progressively. It is probable that the decrease in U-NAG in severe ischemic renal injury is due to the inability of the kidney to wash out NAG into the urine, although NAG may be released from the injured tubular cells in proportion to ischemic renal injury. Therefore, in spite of severe ischemic renal injury, U-NAG may show low values, and may lead to misjudgement that the proximal tubular cells are intact. U-NAG should be measured repeatedly and estimated in association with the other renal function tests, especially creatinine clearance, for the correct evaluation of ischemic renal injury.
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PMID:[Intrarenal energy metabolism in ischemic renal injury in rabbits]. 258 23

To determine the timing and location of renal cell regeneration after ischemic injury to the kidney and to assess whether exogenous epidermal growth factor (EGF) enhances this regenerative repair process to accelerate recovery of renal function, experiments were undertaken in rats undergoing 30 min of bilateral renal artery clamp ischemia followed by reperfusion for varying time intervals. Renal cell regeneration, as reflected by incorporation of radiolabeled thymidine within the kidney, began between 24 to 48 h and reached a peak at 72 h after renal ischemia. As demonstrated by histoautoradiography, renal thymidine incorporation was essentially confined to tubule cells. Morphometric analysis of histoautoradiograph sections of renal tissue demonstrated that the majority of labeled cells were found in renal cortex, but some labeled cells were also located in the inner stripe of the outer medulla, suggesting that injury to medullary thick ascending limbs also occurs in this ischemic model. Exogenous EGF administration produced increases in renal thymidine incorporation compared with non-treated animals at 24, 48, and 72 h after ischemic injury. This accelerated DNA replicative process was associated with significantly lower peak blood urea nitrogen (BUN) and serum creatinine levels, averaging 63 +/- 20 and 3.1 +/- 0.4 mg/dl in EGF-treated ischemic rats compared with 149 +/- 20 and 5.1 +/- 0.1 mg/dl, respectively, in nontreated ischemic rats, and was also associated with a return to near normal BUN and serum creatinine levels in EGF-treated animals approximately 4 d earlier than that observed in nontreated animals. This report is the first demonstration that EGF accelerates the repair process of a visceral organ after an injurious insult.
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PMID:Epidermal growth factor enhances renal tubule cell regeneration and repair and accelerates the recovery of renal function in postischemic acute renal failure. 259 59

Magnetic resonance (MR) imaging and spectroscopy, chemical lactate measurements, and microscopic examinations were performed to investigate acute renal ischemia in rats. MR images (1H) and spectra (31P and 1H) were acquired on a 2.0-T superconducting small-bore magnet by using implanted coils. Occlusion of the renal artery induced a significant decrease in signal intensity of the renal parenchyma on T2-weighted images, which was most obvious in the outer medulla (-50 +/- 15%, n = 8, P less than 0.001) and was the result of venous congestion, as verified histologically, 31P spectroscopy demonstrated a drop in pH from 7.3 +/- 0.2 to 6.6 +/- 0.2 (n = 18, P less than 0.001), characterized by a time constant (Tc) in the same range as that of the depletion of ATP (2.3 +/- 1.3 min versus 1.9 +/- 1.2 min, n = 10, P = ns). By means of 1H spectroscopy, a lactate peak was detected within 1.5 to 4 min of ischemia, still increasing in intensity after 1 h of ischemia. The Tc of the lactate buildup (15.9 +/- 7.5 min, n = 8) was significantly longer than that of the drop in pH (P less than 0.005). The chemically measured intrarenal concentration of lactate was 1.3 +/- 0.5 mumol/g in control kidneys and 8.7 +/- 3.2 mumol/g (P less than 0.005) in kidneys made ischemic for 1 h. The present study demonstrated important features of acute renal ischemia: (a) acute ischemia induces venous congestion in the medulla; (b) accumulation of lactate is not the main cause of the intracellular acidification observed during ischemia.
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PMID:Study of acute renal ischemia in the rat using magnetic resonance imaging and spectroscopy. 260 55

Two cases of renal segmental infarction and 1 case of renal patchy ischemia demonstrated by magnetic resonance imaging (MRI) are reported. MRI of renal infarction in two renal grafts following surgical ligation revealed an area of noncorticomedullary differentiation and an area with a low signal intensity. Renal ischemia in 1 patient with acute renal dysfunction with severe loin pain and patchy renal vasoconstriction was visualized as an ill-defined focus of low signal intensity in the renal cortex, indicating a long T1 relaxation time. Delayed wedge-shaped contrast enhancement was demonstrated on CT scan in the same area. The common finding in renal infarction and ischemia in our cases was the area of low signal intensity on MRI.
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PMID:Magnetic resonance imaging in renal infarction and ischemia. 264 69

Hyperglycemia worsens ischemic injury in several ischemic models. To determine whether renal lactate accumulation was associated with hyperglycemia-exacerbated postischemic renal dysfunction and mortality, halothane-anesthetized rats underwent right nephrectomy and 45 min of left renal artery and vein occlusion. Prior to ischemia, rats received saline (n = 22), glucose (2 g/kg, n = 22), or insulin (4 U/kg, n = 18). Sham-operated glucose-treated rats (2 g/kg, n = 4) underwent right nephrectomy and no vascular occlusion. As anticipated, glucose pretreatment elevated plasma glucose, while insulin pretreatment lowered plasma glucose; both were significantly different from values in saline controls. Creatinine was unchanged in sham-operated rats but was significantly higher in glucose-treated rats at 24 and 48 hr postischemia compared to saline controls. No statistical differences in creatinine were found when comparing saline controls to insulin-treated rats. Eighteen percent of glucose-treated rats survived to 72 hr postocclusion, while 45% of insulin-treated rats, 73% of saline control rats, and 100% of sham-operated rats survived this period. In a separate but identical treatment protocol, renal tissue was serially sampled and lactate content was determined in rats pretreated with saline (n = 7), glucose (n = 6) or insulin (n = 6) or sham-operated (n = 2) and receiving identical operation. Tissue lactate concentration did not change during serial sampling in the sham group. During ischemia, lactate was significantly higher in glucose-treated rats and significantly lower in insulin-treated rats as compared to saline controls. The adverse effects of exogenous glucose and attendant hyperglycemia on renal function during normothermic renal ischemia are demonstrated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hyperglycemia exacerbates and insulin fails to protect in acute renal ischemia in the rat. 265 96

The effects of chronic ethanol ingestion on the rat kidney were studied. Rats were fed a liquid diet containing ethanol for 5 weeks to induce chronic alcoholism. Renal ischemia was introduced by clamping the renal artery and vein either for 10 or 20 min. The glomerular filtration rate (GFR) and the renal blood flow (RBF) were determined by using I125-iothalamate and I131-iodohippurate. In the absence of renal ischemia, there were no significant differences in the renal function between nonalcoholic rats (n = 5) and alcoholic rats (n = 5): 380 +/- 30 vs. 403 +/- 27 microliters/min/100 g body weight (BW) in GFR, and 3.1 +/- 0.1 vs. 3.1 +/- 0.2 ml/min/100 g BW in RBF. The recovery of GFR measured 2 h following 10-min renal ischemia in both groups was not significantly different; the values returned to 340 +/- 40 microliters/min/100 g BW (nonalcoholic rats) and 246 +/- 22 microliters/min/100 g BW (alcoholic rats), respectively. The changes of RBF following 10 min ischemia were also similar in both groups. However, the effects of alcoholism on the renal function became apparent when animals were subjected to more prolonged renal ischemia. In nonalcoholic rats (n = 5), GFR and RBF measured 2 h following 20 min renal ischemia were 245 +/- 51 microliters/min/100 g BW and 2.5 +/- 0.4 ml/min/100 g BW, whereas in alcoholic rats (n = 5) the GFR and RBF were significantly decreased to 93 +/- 15 microliters/min/100 g BW and 1.1 +/- 0.2 ml/min/100 g BW, respectively (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Kidneys of chronic alcoholic rats are more vulnerable to ischemic insult. 281 70

To evaluate the effect of thyroxin (T4) on recovery from ischemic acute renal failure, rats were treated with T4 (10 or 20 micrograms/100 g body wt.) or normal saline (NS) either immediately prior to, immediately after or 24 h after 45 min of renal ischemia. Animals given T4 prior to ischemia had no significant increase in Inulin clearance (Cin) (377 +/- 40 microliters/min per 100 g body wt.) as compared with saline-treated ischemic controls (306 +/- 54). In contrast, animals treated immediately after ischemia with either dose of T4 demonstrated significantly better kidney function (Cin 515 +/- 59 microliters/min per 100 g body wt., Uosm 842 +/- 88 mosmol/kg, FENa 0.52% +/- 0.12% and Cin 543 +/- 71, Uosm 939 +/- 103, FENa 0.48 +/- 0.12, for 10 and 20 micrograms/100 g body wt., respectively). Moreover, the improvement in renal function was sustained and Cin was significantly better at day 3 (748 +/- 70) and day 7 (990 +/- 75) compared with saline controls (560 +/- 30 and 732 +/- 45, respectively). Animals which received T4 24 h after ischemia showed significantly higher Cin when compared with ischemic controls. To assess the impact of T4 on recovery of renal ATP, 31P-NMR was used. T4-treated rats demonstrated 90% +/- 5% recovery of renal ATP by 120 min of reflow, whereas NS animals had only 64% +/- 1%. In addition, cellular morphology was better preserved in T4 animals. These data indicate that animals treated postischemically with T4 showed accelerated and sustained recovery from acute renal failure. This beneficial effect appears to be related to cellular mechanisms which are essential for the restoration of sublethally injured cells.
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PMID:Beneficial effect of thyroxin in the treatment of ischemic acute renal failure. 285 65

The effect of 30 min of renal artery occlusion on renal sodium reabsorption, oxygen consumption, and brush border integrity was studied in the immediate 1-h reflow period. Rats were studied using clearance and renal extraction measurements. Glomerular filtration rate and renal plasma flow were measured over four consecutive 15-min periods; renal venous samples were drawn via an indwelling catheter. Renal oxygen consumption (QO2) was calculated from renal blood flow, corrected for urine flow, and from blood oxygen content measured with a fuel cell analyzer. Brush border integrity was assessed by the excretion of the brush border marker enzyme gamma-glutamyltransferase as well as by morphologic observation. Ischemia induced a 10-fold rise in fractional sodium excretion in the initial 0- to 15-min period, rose to 20-fold during the subsequent two periods, 15-45 min, and then returned to the initial reflow period level. The progressive deterioration of renal function with reflow could not be attributed to an increase in the filtered Na+ load. Rather, Na+ reabsorption appeared to be related to the presence of intact brush borders at 0-15 min, their removal from the luminal surface between 15 and 45 min, and their return at 60 min of reflow. Renal QO2 was coupled to Na+ reabsorption in the initial 15-min and final 45- to 60-min reflow periods. However QO2 was significantly increased over the control level at 30-45 min of reflow. The results point to a significant role of brush border uptake in the development of functional impairment following renal ischemia and suggest that the associated rise in renal O2 consumption may be coupled to the reparation of this organelle.
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PMID:Renal sodium reabsorption, oxygen consumption, and gamma-glutamyltransferase excretion in the postischemic rat kidney. 286 Aug 9


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