Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Jaundice is a disorder of bilirubin metabolism and has many causes. History and physical examination help establish the diagnosis in 70 to 80 percent of patients. Elevation of alkaline phosphatase and gamma-glutamyl transpeptidase suggests cholestasis, either intrahepatic (e.g., medication reactions) or extrahepatic (e.g., choledocholithiasis), whereas markedly elevated serum aminotransferases are indicative of hepatocellular damage from infection, toxins or ischemia. Ultrasound examination is a useful initial procedure when extrahepatic obstruction is suspected. Endoscopic retrograde cholangiopancreatography and computed tomography may be better used to diagnose obstruction at the level of the pancreas or distal common bile duct. The treatment is based on the etiology of jaundice and includes removal of offending medications or toxins, therapy for underlying liver disease or surgery for extrahepatic obstruction.
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PMID:Jaundice. 154 99

Three cases of bile duct necrosis owing to hepatic arterial infusion chemotherapy (HAI) were reported. Regarding HAI, transcatheter hepatic arterial embolization (TAE) was applied in two cases (hepatocellular carcinoma: 1; metastasis: 1) and 5-fluorouracil (continuous) combined with leucovorin (one shot) therapy (LV + 5-FU) was given to one metastatic case. In the data of blood biochemistry, serum alkaline phosphatase, gamma-glutamyl transpeptidase, and leucine aminopeptidase values characteristically elevated without the elevation of total bilirubin value. Hepatic tumors degenerated with necrosis in all cases and no viable cells were histologically recognized. Although the destruction of bile ducts was locally detected adjacent to these tumors in TAE cases and was more widespread in the LV + 5-FU case, these lesions were very similar in each case. Therefore, we concluded that both ischemia and drug toxicity induced bile duct necrosis and the necrosis around the bile duct was the secondary change due to the leaked bile juice.
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PMID:[Bile duct necrosis and hepatic necrosis following hepatic arterial infusion chemotherapy]. 165 26

The urinary activities of N-acetyl-beta-D-glucosaminidase (NAG), gamma-glutamyl transpeptidase (gamma-GTP) and alanine aminopeptidase (AAP) are known to elevate markedly in initial phase of clinical acute renal failure (ARF). This study was performed to clarify the pathophysiological mechanism of the activation of these enzymes using experimental postischemic reperfusion ARF in rats. The relation between the levels of the lysosomal enzymes and lipid peroxidation induced by oxidant stress in these animal models was the main focus of this study. Renal ischemia was made by clamping renal artery for 30 minutes to create a complete ischemia and reflow. Catheterized urine was collected to measure changes of the activities of NAG. gamma-GTP and AAP from 60 to 480 minutes after reperfusion of the kidney. The activities of renal tissue glutathione peroxidase (GSH-Px), NAG and gamma-GTP, and the values of renal contents of glutathione (GSH) and malondialdehyde (MDA) were measured in each sample. It is already known that GSH redox cycle plays an important role in removing various hydroperoxides induced by oxidant stress, generating oxidated GSH from GSH in scavenging process. In order to confirm if GSH plays an important role in intrinsic anti-oxidant system in this model, buthionine sulfoximine (BSO) which is gamma-glutamylcysteine synthetase inhibitor, was administered intraperitoneally to decrease renal GSH contents before the procedure renal ischemia. The following results were obtained; 1) urinary activities of NAG, gamma-GTP and AAP were elevated markedly in GSH depleted rats compared with controls, 2) renal tissue activities of NAG were higher in BSO administered rats than controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Experimental studies on the elevation of urinary enzyme activities and its pathogenesis in acute renal failure]. 167 93

To investigate the properties of the vessels newly formed in cerebral infarcts, we performed enzyme histochemical study for alkaline phosphatase and gamma-glutamyl transpeptidase that are membrane enzyme of capillary endothelial cells in the brain as well as immunohistochemical study for factor VIII related antigen and laminin. Adult mongolian gerbils were used in the experiment to produce cerebral infarcts. The animals showing clear neurological signs of ischemia after occlusion of the left common carotid artery were selected. Following one hour ischemia blood flow was reperfused and the animals were allowed to grow and sacrificed at predetermined intervals ranging from two days to two years. The stainings for alkaline phosphatase and gamma-glutamyl transpeptidase were performed by Brustone method and Rutenburg method respectively, and those for factor VIII related antigen and laminin by PAP method, in frozen sections. Four days after ischemia, vessels of a slightly large size that were running irregularly with reactivity of factor VIII related antigen and circumscribed by laminin were observed in the marginal zone of the infarcts. These newly formed vessels increased in number during the second and the third week also in the center of the infarcts, and one month after ischemia began to decrease. However, a number of vessels were seen in the infarcts, whose features were comparatively similar to those of normal vessels. These vessels remained as long as for two years. The number of the vessels with alkaline phosphatase and gamma-glutamyl transpeptidase activity did not increase during the first week. They increased later during the second and third week.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Histochemical study on enzymatic barrier of the newly formed vessels in infarcts]. 246 63

An early change following mild renal ischemia is the loss of the renal microvilli, which then regenerate morphologically within 6 h. We studied microvillar regeneration in rats with 25 min of renal artery occlusion and subsequent reflow. At subsequent intervals the rats were injected intraperitoneally with [14C]choline and [3H]leucine; 25 min later they were killed and their renal brush border membranes isolated. At 30 min of reflow of blood there was a 77% reduction in the incorporation of [3H]leucine into microvillar protein compared with that of the opposite control kidney (P less than 0.02). The incorporation rose to normal within 60 min. At 30 min of reflow, the incorporation of [14C]choline into phospholipids increased twofold (P less than 0.005), then returned toward normal values after 2 h. The altered incorporation of tracers was not due to change in membrane turnover or substrate pools. The activities of alkaline phosphatase, gamma-glutamyl transpeptidase, and alpha-glucosidase decreased 50% following ischemia (P less than 0.02) and returned to control values within 2 h. Thus, renal damage severe enough to partly efface microvilli is repaired metabolically within several hours.
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PMID:Regeneration of the renal brush border after renal ischemia in rats. 611 66

Alterations in the levels of glutathione, glutathione disulfide, malondialdehyde, and the activity of gamma-glutamyl transpeptidase in nonischemic and ischemic parts of the left ventricle and in the right ventricle were studied in canine hearts after occlusion of the left anterior descending coronary artery for 60 minutes and subsequent reperfusion for 20 minutes. Ischemia caused no significant change in malondialdehyde concentration and gamma-glutamyl transpeptidase activity in ischemic or nonischemic parts of the left ventricle, but it increased the activity of gamma-glutamyl transpeptidase in the continuously perfused right ventricle. Reperfusion of the ischemic areas of the left ventricle was accompanied by accumulation of malondialdehyde and an increase in gamma-glutamyl transpeptidase activity, not only in the reperfused and adjacent areas of the left ventricle, but also in the continuously perfused right ventricle. An increase in the level of glutathione disulfide and decrease in glutathione occurred in all parts of the myocardium during coronary occlusion; these changes were maintained in reperfusion. The findings indicate that the effects of acute occlusion and reperfusion of the left anterior descending coronary artery on myocardial concentrations of glutathione, glutathione disulfide and malondialdehyde or gamma-glutamyl transpeptidase activity are not confined to the local area.
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PMID:Evaluation of ischemia-reperfusion injury by malondialdehyde, glutathione and gamma-glutamyl transpeptidase: lack of specific local effects in diverse parts of the dog heart following acute coronary occlusion. 790 90

Leukotriene C4 (LTC4) increases vascular permeability in systemic, brain tumor, and ischemic brain capillaries, but not in normal brain capillaries. This study examines whether the abundance of gamma-glutamyl transpeptidase (gamma-GTP) in normal brain capillaries might act as an enzymatic barrier to vasoactive leukotrienes in the brain. Blood-brain barrier (BBB) permeability was determined by quantitative autoradiography using 14C-aminoisobutyric acid. Ischemia was produced by occluding the middle cerebral artery. Seventy-two hours after occlusion, gamma-GTP activity in ischemic brain disappeared, and LTC4 (4-micrograms total dose), which was infused into the carotid artery ipsilateral to the occlusion, selectively increased permeability, Ki, approximately twofold within core ischemic tissue and adjacent tissue, compared to vehicle alone in seven brains (15.53 +/- 6.03 vs. 7.29 +/- 3.36, p < 0.05, and 8.76 +/- 4.02 vs. 4.32 +/- 2.65, p < 0.05, respectively). No effect on BBB was seen in nonischemic brain tissue. Twenty-four hours postocclusion, gamma-GTP activity was still present, and LTC4 infusion did not increase permeability within ischemic tissue. However, inhibition of gamma-GTP with acivicin allowed LTC4 to increase permeability even 24 hours after occlusion in ischemic core and adjacent tissue compared to vehicle alone in seven brains (17.21 +/- 16.32 vs. 8.23 +/- 6.58, p < 0.05, and 11.78 +/- 7.96 vs. 4.56 +/- 1.93, p < 0.01, respectively). Acivicin almost completely blocked both the histochemical activity of gamma-GTP in brain capillaries and the metabolism of LTC4 in isolated bovine capillaries. These findings suggest that gamma-GTP may help normal brain capillaries resist the vasoactive effects of LTC4. In contrast, gamma-GTP is lost in injured brain capillaries, which allows LTC4 (in combination with other factors) to increase vascular permeability in ischemic brain and brain tumors.
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PMID:Enzymatic barrier protects brain capillaries from leukotriene C4. 793 22

Non-protein thiols (NP-SH) and the activities of the glutathione status-regulating enzymes gamma-glutamylcysteine synthetase (G-GCS), gamma-glutamyl transpeptidase (G-GT) and glutathione reductase (GR) were assessed in perfused rabbit hearts subjected to severe (60 min) or mild (7 min) total ischemia and 30 min reperfusion. Severe ischemia significantly decreased NP-SH, which were further depressed on reperfusion together with a significant decline in G-GCS activity; G-GT and GR activities were unchanged. Specific analytes were unaffected by mild ischemia-reperfusion. Thus, impaired enzymatic biosynthesis of GSH is operative in the reperfused rabbit myocardium after 60 min ischemia. This phenomenon may favour myocardial GSH depression and oxidative reperfusion injury after severe ischemia.
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PMID:Impaired glutathione biosynthesis in the ischemic-reperfused rabbit myocardium. 870 34

Advances in liver surgery and transplantation have lead to a steady increase in the number of these interventions. Prompt quantitative assessment of hepatic of hepatic function and a patient's subsequent morbidity and mortality following surgery remain difficult despite the currently utilized historic markers of hepatic parenchymal injury (e.g., aspartate transaminase [AST], lactate dehydrogenase [LDH] gamma-glutamyl transpeptidase [GGT]). Increases in serum glycohydrolase activities appear to provide sensitive and quantitative markers of hepatic ischemia/reperfusion injury. In 10 male swine (25 to 35 kg body weight) following 30, 45, and 90 minutes of acute hepatic ischemia, the systemic release of eight different glycohydrolases and lipid peroxides into serum were determined and compared with pre- and postischemic serum levels of LDH, GGT, and AST. The rapid release of glycohydrolases into serum was directly proportional to the length of the ischemic period from 30 to 90 minutes; e.g., beta-glucosidase, mean 1.9-fold increase at 30 minutes; 8.3-fold at 45 minutes; and 22.8-fold at 90 minutes; P < .002) and the activities peaked within the first 3 hours postischemia. In constrast, AST, LDH, and GGT were released slowly and peaked 20 to 30 hours after hepatic blood flow was restored. In swine with fatal outcomes (90 minutes of ischemia), all enzyme levels increased continuously during the final hours of life. However, in swine that survived hepatic ischemia/reperfusion injury (45 minutes of ischemia) the glycohydrolases, but not AST, LDH, and GGT, declined after 2 to 3 hours' postischemia and the serum lipid peroxide levels followed the same pattern. Serum beta-galactosidase and beta-glucosidase levels are sensitive markers that rise as quickly as traditional enzyme markers (AST, LDH, GGT) following hepatic ischemic injury; moreover, the glycohydrolases have the added value of serving as predictors of survival.
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PMID:Glycohydrolases as markers of hepatic ischemia-reperfusion injury and recovery. 870 56

Extracellular metabolism of the protective substance glutathione (gamma-glutamyl-cysteinyl-glycine) may generate cysteine, glycine, several gamma-glutamyl-containing dipeptides and possibly free glutamate, all of which could participate in neurotoxicity. In the present study, we have examined how blockage of gamma-glutamyl transpeptidase, the key enzyme in glutathione degradation, influences the extracellular concentrations of glutathione, cysteine and related metabolites during anoxia/aglycemia of rat hippocampal slices. The net efflux, i.e., the increase in extracellular concentration due to changes in release and/or uptake, of cysteine, cysteine sulfinate, gamma-glutamyl-glutamate, gamma-glutamyl-glutamine, glutathione, gamma-glutamyl-cysteine and glutamate increased as a result of anoxia/aglycemia. These increases in net efflux of cysteine, cysteine sulfinate, gamma-glutamyl-glutamate and gamma-glutamyl-glutamine were reduced or blocked by acivicin, an inhibitor of gamma-glutamyl transpeptidase. In contrast, acivicin caused an increase in both basal and anoxia/aglycemia-induced net efflux of glutathione whereas the basal and anoxia/aglycemia-induced efflux of glutamate was unchanged by acivicin treatment. The effect of acivicin on the efflux of gamma-glutamyl-cysteine was similar to that of glutathione although less pronounced. Addition of beta-mercaptoethanol to the incubation medium during and after 30 min of anoxia/aglycemia decreased the net efflux of cysteine sulfinate specifically, indicating that the increase in cysteine sulfinate during anoxia/aglycemia may be partly derived from the spontaneous oxidation of cysteine. The results suggest that gamma-glutamyl transpeptidase may be involved in the regulation of the extracellular concentrations of cysteine, several gamma-glutamyl-containing dipeptides and glutathione but not glutamate during ischemia.
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PMID:Net efflux of cysteine, glutathione and related metabolites from rat hippocampal slices during oxygen/glucose deprivation: dependence on gamma-glutamyl transpeptidase. 997 25


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