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

To study the role of free radical-induced myocardial injury during heart transplantation, five groups of dog hearts were orthotopically transplanted. Control group I and experimental groups II, III, and IV (each n = 8) were reperfused for 1 hr after 49 min of operational ischemia. Control group V (n = 4) remained ischemic for 90 min. In the three experimental groups, the free radical scavengers superoxide dismutase (10 mg/kg; group II), catalase (10 mg/kg; group III), or both (10 mg/kg each; group IV) were administered just before reperfusion and during reperfusion for 1 hr. The generation of free radicals, remained at low levels in all groups during ischemia, but significantly increased when groups I-IV were reperfused. This increase was also associated with an increase in creatinine kinase MB isoenzyme. In the experimental groups, free radical scavengers significantly inhibited the appearance of thiobarbituric acid reactive substances and the release of creatinine kinase MB isoenzyme during reperfusion (P less than 0.05). Regarding cardiac functions, 60 min after the termination of the cardiopulmonary bypass, a significant improvement was demonstrated in the treated groups (P less than 0.05). These results indicate that (1) the generation of oxygen free radicals occurs primarily during reperfusion, (2) both superoxide dismutase and catalase reduce production of free radicals during this time, and (3) combined administration did not provide a greater improvement in cardiac metabolic recovery. This study confirms the efficacy of free radical scavengers during heart transplantation.
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PMID:Oxygen-derived free radical damage in canine heart transplantation. 264 62

A previous article (Part I) described the patient population and operative management of 666 patients who had surgery for nonruptured abdominal aortic aneurysms. This article details the perioperative complications and, by chi-square and logistic regression analysis, identifies the variables that are associated with each complication. In summarizing the results (below) the incidence of each complication is listed, along with the predictive risk factors in parentheses that have significance levels less than 0.05. Vascular morbidity data are as follows: intraoperative bleeding, 4.8%; postoperative bleeding requiring transfusion, 2.3% or repeat operation, 1.4% (large volume of blood transfusion and/or use of an autotransfusion device); intraoperative limb ischemia, 3.5%; graft thrombosis, 0.9% (femoropopliteal disease and/or distal anastomosis at the femoral level); distal thromboembolism, 3.3% (male sex, femoral popliteal disease, and/or intraoperative graft thrombosis); amputation, 1.2%; graft infection, 1 case. General morbidity data are as follows: cerebrovascular event, 0.6%; paraplegia, 1 case; cardiac event, 15.1% (age, previous episode of congestive heart failure, and/or electrocardiogram [ECG] evidence of a previous myocardial infarction); myocardial infarction, 5.2% (advancing age, angina, and/or prolonged aortic cross-clamp time); congestive heart failure, 8.9% (previous history of congestive heart failure, ECG evidence of ischemia, and/or chronic obstructive lung disease); arrhythmia requiring treatment, 10.5% (preoperative ventricular premature beats and/or respiratory failure requiring ventilation for more than 48 hours); new arrhythmia, 8.4% (angina and/or chronic obstructive lung disease); respiratory failure, 8.4% (chronic obstructive lung disease, large volume of blood transfused, and/or occurrence of postoperative bleeding, cerebrovascular accident, congestive heart failure, or myocardial infarction); renal damage with rise in creatinine or blood urea nitrogen, 5.4% and/or renal failure requiring dialysis, 0.6% (elevated preoperative creatinine, suprarenal aortic cross-clamping, and/or renal vein ligation); diarrhea without evidence of ischemia colitis, 7.1% and ischemic colitis, 0.6% (pelvic flow interrupted); prolonged ileus, 11.0% (aortoiliac occlusive disease, deterioration of renal function, prolonged ventilation, and/or preoperative history of angina); superficial wound infection, 1.5% and deep infection, 0.5% (femoral anastomosis and/or female sex); coagulopathy, 1.1% (large volume of blood transfused).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Multicenter prospective study of nonruptured abdominal aortic aneurysm. Part II. Variables predicting morbidity and mortality. 264 60

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

To determine the frequency of renal dysfunction associated with the use of aminoglycosides with cyclosporine A (CyA) in children, the records of 26 consecutive children receiving CyA after liver transplantation were reviewed. Fourteen patients with normal baseline serum creatinine concentrations received an aminoglycoside postoperatively. These children received CyA and an aminoglycoside for 249 days (average, 17.8 days/patient). Forty of the 249 days included treatment with vancomycin or amphotericin B. Twelve children (86%) showed no evidence of renal dysfunction after aminoglycoside therapy. Two children developed renal dysfunction and eventually succumbed. In neither case could aminoglycoside nephrotoxicity be identified as the main cause of renal dysfunction. Multiple other factors, including ischemia and high CyA concentrations, probably contributed to renal deterioration. We conclude that aminoglycosides can be used safely in children receiving CyA following liver transplantation, provided serum CyA concentrations are followed closely and other risk factors for renal dysfunction are minimized.
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PMID:Use of aminoglycosides during cyclosporine A immunosuppression after liver transplantation in children. 266 91

Renal atherosclerosis and fibromuscular dysplasia are the most common causes of curable human renovascular hypertension and renal failure. Vascular reconstruction often preserves renal function, but renal failure is rarely reversed, especially after days of anuria. We report a case of a 23-year-old woman who as a child underwent a nephrectomy for congenital hydroureter and renal hypoplasia. She later experienced fibromuscular dysplasia of the remaining renal artery, which ultimately progressed to a complete occlusion and 31 days of total anuria. The patient was revascularized, and within 2 months renal function returned with a blood urea nitrogen and creatinine of 9.0 and 1.0 mg/dl, respectively. After a follow-up of 6 months the patient's blood pressure remained 120/80 to 130/80 mm Hg without administration of hypertension medication. In this report we emphasize that under selected circumstances a kidney can survive prolonged ischemia and that delayed revascularization may reestablish renal function.
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PMID:Successful revascularization of an occluded renal artery after prolonged anuria. 272 67

Ischemic insult has been considered a cause of cellular injuries under certain circumstance, such as the disturbance of energy metabolism, the alternation of calcium homeostasis, the production of oxygen radical and the release of lysosomal protease. The present study was designed to clarify the pathophysiological effects of coenzyme Q10 (CoQ10), diltiazem, superoxide dismutase (SOD) and urinastatin on the development and progression of ischemic acute renal failure (IARF) of the rat. At 24 hours after reflow following 45 minutes ischemia, serum urea nitrogen, creatinine and fractional excretion of sodium were 99.3 mg/dl, 3.14 mg/dl, 5.95% respectively, in non-treated IARF rats. Renal ATP content was reduced to 0.91 micrograms/mg. prot. from 10.59 micrograms/mg. prot. at 10 minutes after ischemic insult, and remained at almost the same level throughout the entire 45 minutes ischemia. Although the subsequent blood reflow resulted in the recovery of ATP content, it was up to 50% of normal level at 24 hours after reflow following 45 minutes ischemia. During the ischemic period, the pathological changes were mild, whereas, after reflow, tissue involvement was mainly localized in the S3 segment of the proximal tubule. Major alteration were the loss of brush border, high amplitude swelling of mitochondria with matrical densities and fragmentation of the epithelial cell. At 24 hours after reflow, it was observed that renal function was superior in IARF rats treated with CoQ10, diltiazem, SOD and urinastatin. The treated rats also had higher ATP contents and showed less pathological changes than non-treated rats. Among these inhibitory agents, diltiazem exerted the most reliable effect. From these results, it was concluded that IARF was obviously caused by such pathophysiological mechanisms as mentioned above. Especially, Ca influx into the cells is one of the most important factors on pathogenesis of IARF.
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PMID:[Pathophysiological mechanism of ischemic acute renal failure: protective effect of coenzyme Q10, Ca channel blocker, superoxide dismutase and protease inhibitor against ischemic acute renal failure]. 274 96

To investigate the potential myocardial ischemic effects of ritodrine, we studied 36 singleton and four twin preterm pregnancies during ritodrine therapy. We serially determined serum creatinine phosphokinase (CPK-MB fraction) and lactic dehydrogenase isoenzymes and performed electrocardiography before and during ritodrine infusion and again within the first 24 hours of oral drug therapy. We observed that serum CPK-MB and lactic dehydrogenase isoenzymes remained within the normal range during therapy periods. The incidence of sinus tachycardia and non-specific T wave changes were 100% and 25%, respectively. In three of four twin pregnancies, ST-T segment depression in leads I, V4, V5, and V6 of the electrocardiogram was noted. Our study suggests that (1) the recommended ritodrine regimen does not produce direct myocardial damage, and (2) ritodrine may cause cardiac ischemia as determined by electrocardiography, which theoretically would progress to myocardial damage if not treated properly.
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PMID:Cardiac isoenzymes and electrocardiographic changes during ritodrine tocolysis. 224 70

Fructose 1,6-diphosphate (FDP) has been shown to attenuate tissue injury associated with ischemia and shock by enhancing the anaerobic carbohydrate utilization and by inhibiting oxygen-free-radical generation by the neutrophils. Previously, we have reported that FDP prevents ischemic renal failure if administered prior to the ischemic insult. The present study was designed to determine whether this agent could prevent renal damage when administered during the postischemic reperfusion period. Rats were subjected to 30 min of bilateral renal artery occlusion and infused with FDP (350 mg/kg body wt) beginning 10 min after release of the renal artery clamps. Control rats received an equal volume of glucose/saline solution. A third group of rats were sham operated. Twenty-four hours after injury, BUN, creatinine, and fractional sodium excretion values were less in FDP-treated rats than in control rats (P less than 0.001, P less than 0.005, and P less than 0.001, respectively) and not different from values observed in sham-operated rats. Inulin clearance was greater (P less than 0.001) in FDP-treated rats than in control rats (665 +/- 38 microliters/min/g kidney wt). Renal histology was also better preserved in the FDP-treated group. These data suggest that FDP infused after the initiation of an acute ischemic insult provides significant, but not complete, functional and histologic protection from renal damage.
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PMID:Attenuation of ischemic renal injury with fructose 1,6-diphosphate. 277 Feb 78

In contrast to its importance in improving renal graft survival, nephrotoxicity is the most serious side effect of cyclosporine. Dosage reductions of CsA mitigate its nephrotoxic effect. However, CsA nephrotoxicity is still a problem in clinical transplantation. In this study the relationships among preexistent chronic histological lesions, donor age, and renal function after transplantation in 100 CsA treated renal allograft patients are described. Multivariate data analysis revealed a significant statistical effect of the presence of preexistent chronic histological lesions on nonimmediate function (-.42, less than 0.0001) that was relatively twice as large as the effects of cold ischemia time (-.21, less than 0.05). Also in predicting creatinine clearance at 1 and 3 months, preexisting chronic histological lesions had the most important effect (-.39, less than 0.0001; -.57, less than 0.0001, respectively), whereas the presence or absence of rejection episodes was less predictive (.24, less than 0.001; .20, less than 0.01, respectively). Preexistent chronic histological lesions had also significant effects in predicting conversion to azathioprine and prednisolone, because of CsA nephrotoxicity (-.42; less than 0.0001). The degree of CsA nephrotoxicity therefore varies according to the presence of preexistent chronic histological lesions. Because of the increase of these lesions with age, one has to be aware of an exaggerated CsA toxicity, especially in the older donor age group and in older patients treated with CsA for various reasons.
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PMID:Amplification of the nephrotoxic effect of cyclosporine by preexistent chronic histological lesions in the kidney. 279 11

The purpose of this study was to assess the degree, time sequence, and biochemical correlates of hypothermic protection against ischemic acute renal failure. Rats subjected to 40 minutes of bilateral renal artery occlusion (RAO) were made mildly hypothermic (32 degrees-33 degrees C, by cold saline peritoneal lavage) during the following time periods: 1) RAO only, 2) reperfusion only (beginning at 0, 15, 30, or 60 minutes after RAO and maintained for 45 minutes), or 3) during and after (0-45 minutes) RAO. Continuously normothermic (37 degrees C) RAO rats served as controls. The control rats developed severe acute renal failure (blood urea nitrogen [BUN], 95 +/- 4 mg/dl; creatinine, 2.2 +/- 0.1 mg/dl; and extensive tubular necrosis at 24 hours). Hypothermia confined to RAO was highly protective (BUN, 33 +/- 5 mg/dl; creatinine, 0.62 +/- 0.07 mg/dl; and minimal necrosis). Hypothermia partially preserved ischemic renal adenylate high-energy phosphate (ATP and ADP), increased AMP and inosine monophosphate concentrations, and lessened hypoxanthine/xanthine buildup (assessed at end of RAO). Hypothermia confined to the reflow period (beginning at 0, 15, and 30 minutes) was only mildly protective (e.g., BUN, 58-63 mg/dl); the degree of protection did not differ according to the time of hypothermic onset. Lowering reflow temperature to 26 degrees C had no added benefit. Hypothermia that started at 60 minutes after RAO conferred no protection. Combining ischemic and postischemic hypothermia abolished all renal failure (assessed at 24 hours). This study offers the following conclusions: Mild hypothermia can totally prevent experimental ischemic acute renal failure. Hypothermia is highly effective during ischemia, and it is mildly protective during early reflow; these benefits are additive. During early reflow, hypothermic protection is not critically time dependent. By 60 minutes of reflow, no effect is elicited; this absence of effect possibly signals completion of the reperfusion injury process. Hypothermia's protective effects may be mediated, in part, by improvements in renal adenine nucleotide content and, possibly, by decreasing postischemic oxidant stress.
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PMID:Degree and time sequence of hypothermic protection against experimental ischemic acute renal failure. 280 43


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