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

Isolated working rat hearts were made ischemic by introducing a one-way aortic ball valve. After the ischemic period the hearts were perfused in a retrograde non-working way for 30 min. Flow rates, glycogen, ATP, and creatine-phosphate went down during the time of ischemia, whereas tissue lactate accumulated. For shorter periods of ischemia these values were normalized but after 30 min of ischemia the hearts seemed to be irreversibly damaged. There was a leakage of GOT, GPT, LDH, and CPK from all hearts when ischemic from 5 to 30 min. Different factors that might be of importance for the degree of ischemic injury were tested. The injury tended to be more severe at higher heart rates. Addition of adrenaline 10(-6)M resulted in excessive myocardial damage. A variation of pH from 7.1 to 7.7 did not alter the effects of the ischemic injury. One group of rats were injected with adrenaline for 8 weeks to simulate chronic stress. When hearts from these rats were made ischemic they were more prone to fail compared to controls. The failing hearts, on the other hand, had a lower leakage of enzymes, possibly due to a less severe myocardial damage. A high mechanical performance and a normal noradrenaline content of the hearts are key factors for the development of myocardial infarction, as indicated by this study.
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PMID:Factors of importance for the degree of ischemic injury in the isolated rat heart. 0 96

In order to determine the validity of clinical-chemical parameters for the prognosis of hepatic failure, 28 pigs were subjected to liver ischemia for 40--160 minutes duration. The following parameters were studied: GOT, GPT, gamma-GT, LAP, LDH, GlDH, AP and isoenzymes, total bilirubin, potassium, sodium and chloride. In a statistical comparison in the surviving animals, an unexplainable increase in GlDH activity was observed. In the other clinical-chemical parameters none was seen to be of use for the prognosis for either life or death in acute hepatic failure.
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PMID:[Acute hepatic coma. Experimental study on the predictive value of clinical-chemical findings for the prognosis of acute hepatic coma]. 96 33

Liver injury by 30-min ischemia following reperfusion was examined biochemically and histopathologically. A greater increase in the level of LDH was observed after 1-hr reperfusion. However, the level of LDH decreased in proportion to the period of reperfusion, while the levels of GOT and GPT were also increased rapidly and reached its peak at 12 hr following reperfusion and were almost restored to the control level by 48 hr. A similar increase was obtained in the lipid peroxides of the liver. In addition, cyt. P-450 content and NADPH cyt. c reductase activity decreased in proportion to the period of reperfusion up to 12 hr and then recovered by 96 hr. On the other hand, heme oxygenase activity was significantly increased by ischemia-reperfusion. The ischemia-reperfused liver resulted in various morphological changes with the period of reperfusion. The destruction of Disse's space, vacuolization of the cytoplasm and nonviable hepatocytes were observed after 12-hr reperfusion. These results indicate the greatest damages of the liver induced by 30-min ischemia following reperfusion is observed after 12-hr or 24-hr reperfusion. The liver injury by ischemia-reperfusion could be a useful experimental model to develop for future studies.
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PMID:[An injury of the liver caused by ischemia-reperfusion in rat liver. Report 2: Relationship between the damage of the liver and during the period of reperfusion]. 146 2

The present study evaluated the effect of glycyrrhizin (GR) on an injury of the liver caused by ischemia-reperfusion in rats. In the liver ischemia-reperfusion model, levels of serum GOT, GPT and LDH activities and lipid peroxides in the liver tissue were significantly increased. On the contrary, total glutathione content in the liver tissue and NADPH cytochrome P-450 reductase activity of liver microsomes were decreased. Pretreatment with GR 20 mg/kg, i.v. 10 min before induction of ischemia resulted in significant decreases in serum GOT, GPT, LDH activities and the lipid peroxide level and a higher tissue glutathione content during the period of reperfusion. Electron microscopic studies revealed various hepatocellular damages with an almost intact sinusoidal endothelium in ischemia-reperfused livers. However, the degree of damage was less severe in the livers from the rats pretreated with 20 mg/kg GR. The results indicate that GR is able to provide partial protection against ischemia-reperfused damage.
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PMID:Attenuation of dysfunction in the ischemia-reperfused liver by glycyrrhizin. 151 71

Cellular damage of various organs by ischemia following reperfusion is assumed to be at least in part due to lipid peroxidation in biomembranes, and oxygen-derived free radicals play a major role. The level of lipid peroxides in liver tissue increased during 90-min ischemia. When reflow of hepatic blood was allowed, a greater increase in the lipid peroxides was observed. Similar increases were obtained in several serum markers (GOT, GPT and LDH) during the period of ischemia or ischemia-reperfusion. In addition, levels of cytochrome p-450 and NADPH cyt. c reductase activity decreased in proportion to the decrease in microsomal proteins during ischemia or ischemia-reperfusion. On the other hand, superoxide dismutase in blood was significantly increased by ischemia-reperfusion. Rats died within 2 days after liver ischemia of 90 min, while all animals subjected to 30-min ischemia survived. Histopathological examinations indicated that extensive coagulation with erythrocytes occurred and the extent was dependent on the time of ischemia. The liver injury by ischemia-reperfusion could be a useful experimental model for studying liver injury induced by free radicals, for developing hepatoprotective drugs, or for investigating liver transplantation.
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PMID:[An injury of the liver caused by ischemia-reperfusion in rat liver]. 190 28

Oxygen free radicals have been implicated as mediators of ischemia/reperfusion injury in a variety of organs. We investigated the role of oxidative injury and endogenous hepatic glutathione (GSH) in liver cell injury associated with complete hepatic ischemia and reperfusion. Forty-five minutes of complete hepatic ischemia followed by reperfusion caused an increase in serum GPT and a fall in hepatic GSH but no increase in hepatic lipid peroxidation products. Chemical depletion of hepatic GSH with diethyl maleate did not cause hepatocellular injury but augmented hepatic ischemia/reperfusion-induced SGPT release and promoted lipid peroxidation. Pretreatment with the selective, membrane-permeable oxygen radical scavenger dimethyl sulfoxide protected against the ischemia/reperfusion-induced drop in hepatic GSH but did not reduce SGPT release in normal rats. In rats sensitized to oxidative injury by depletion of endogenous GSH with diethyl maleate the oxygen radical scavenger protected against ischemia/reperfusion-induced lipid peroxidation and reduced the release of SGPT. These findings suggest that the rich hepatic supply with endogenous GSH has a crucial role in the protection against oxygen radical injury following short periods of total hepatic ischemia. Oxygen radical injury only occurs after depletion of these endogenous GSH stores.
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PMID:Oxygen free radicals and glutathione in hepatic ischemia/reperfusion injury. 202 Jan 91

In the majority of patients with intestinal infarction, it is generally agreed that the occlusion of mesenteric arteries or vein is the primary etiologic factor; however, some showed no evidence of thrombosis, embolization or vasculitis as the causative factor. In many patients, this particular type of infarction is the terminal event of the episode. From October 1977 to December 1986, 24 patients with mesenteric infarction were investigated following cardiovascular surgery in our institute. Among them, 15 were diagnosed with organic vascular occlusion; however, the other 9 showed no evidence of thromboembolism or any other organic vascular occlusive lesion of mesenteric vessels and were diagnosed as non-occlusive mesenteric infarctions. All of these patients were in severe cardiac failure (LOS) postoperatively. There was no typical symptom, although abdominal fullness and diarrhea were the major and consistent findings. In blood chemical analysis, the enzymatic levels such as serum GOT, LDH and CPK were significantly elevated and discrepancy between serum GOT and serum GPT was observed. In this clinical situation, it was difficult to establish a correct diagnosis mainly because of the few signs and symptoms present relating to the mesenteric infarction. On the other hand, when the correct diagnosis was made, these patients were too critically ill to be treated conservatively. The outcome of these patients was grave and all of them died which showed 100% of mortality rate. The conservative management did not produce favorable progress, which accelerated LOS and prevented patients from recovering from cardiac failure. The aggressive surgical approach to this particular type of acute mesenteric ischemia might have offered an improved prognosis from these catastrophic events.
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PMID:[Non-occlusive mesenteric infarction following cardiovascular surgery]. 202 11

In the paper are presented the results of total enzyme activity investigation: GOT, GPT, LDH and CPK, and of the CPK isoenzymes in the cerebrospinal fluid of 148 examinees and in the serum of 67 examinees with an acute stroke, who were treated at the Intensive Care Unit of the Department of Neurology and Institute of Neuropathology, Clinical Medical center "Rebro". The aim was to determine the reliability of the applied methods in the diagnosis of cerebrovascular diseases, particularly in the differential diagnosis of cerebral hemorrhage, ischemia and subarachnoidal hemorrhage. The highest frequency of pathologic findings of the tested enzymes in the whole group of patients with CVA was obtained in the determination of the CPK total activity assessment, then followed the assessments of LDH activity, isoenzyme CPK profile, GOT and finally GPT activity. A larger number of pathologic findings of all mentioned enzymes and CPK isoenzymes was found in the group of patients with ICH. In the patients with ICH and ISI, who survived stroke a higher incidence of normal findings of the total enzymic activities was found, while in those who died from ICH a higher incidence of pathologic findings could not be established. The correlations between the total CPK activity in the serum and in the cerebrospinal fluid does not exist, as well as the correlation between the CPK isoenzyme profile in the serum and CSF.
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PMID:Study of serum and cerebrospinal fluid enzymes in diagnosis and differential diagnosis of cerebrovascular diseases. 229 Apr 71

The role of superoxide and lipid peroxidation in liver injury induced by ischemia-reperfusion was investigated in rats. Ischemic condition of the liver was created by applying small clamps to the right branch of portal vein and the right hepatic artery for 15 min. Clamping of hepatic artery and portal vein could decrease the hepatic blood flow to about 30% of that measured before the clamping. Levels of serum GPT and thiobarbituric acid (TBA) reactive substances in the liver tissue were significantly increased 30 min after the reperfusion following 15 min of ischemia. The increase in serum GPT and TBA reactants in the liver tissue was significantly inhibited by the treatment with superoxide dismutase combined with catalase. The treatment with allopurinol significantly inhibited the elevation of serum GPT levels and showed a tendency to inhibit the increase in TBA reactants in liver tissue. These results suggest that active oxygen species and lipid peroxidation may play an important role in the pathogenesis of ischemia-reperfusion injury in the liver, and hypoxanthine-xanthine oxidase system may be one of the main sources of active oxygen species.
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PMID:[Role of active oxygen species and lipid peroxidation in liver injury induced by ischemia-reperfusion]. 232 99

In hepatic preservation by simple perfusion and hypothermic storage, a portal and hepatic washout before revascularization would avoid receptor hyperkaliema. In this report we study the effectiveness of this washout with Haemaccel at room temperature. Large-White pigs were used and eight livers were perfused "in situ" via the portal wein with Hartmann's solution containing 10,000 IU of heparin at 4 degrees C, and afterwards, via portal and arterial routes with C2 solution at 4 degrees C. After a cold ischemia time of less than 31/2 hours a liver washout via the portal vein and hepatic artery with Haemaccel before portal revascularization was done. The high concentrations of glucose, K+, GOT, GPT and LDH in the effluents obtained during the washout are attributed to Haemaccel hyperosmolarity. A portal and arterial hepatic washout associated with free drainage of the first 50-100 ml of portal venous blood after hepatic portal revascularization through the infrahepatic inferior vena cava (IH-IVC), prevents hyperkaliemia from occurring after a portal and arterial revascularization in the orthotopic liver transplant (OLT) in pigs.
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PMID:Washout of the pig liver with Haemaccel after hypothermic preservation. 237 95


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