Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A sharp and unusually high increase in the serum of glutamic-oxalacetic and glutamic-pyruvic transaminase and of lactic-dehydrogenase accompanied the terminal events, acute pulmonary edema with cardiogenic shock, in 2 patients suffering from chronic congestive heart failure caused by dilatative myocardiopathy. Experimental and clinical data raises the possibility that the considerable enzymic increase may be due to the combined effect of chronic stasis and acute ischemia on the liver.
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PMID:[Acute hepatic ischemia and cardiogenic shock in patients with dilated cardiomyopathy]. 208 28

The transport time of enzyme from heart to plasma was studied in two experimental models. First, the enzyme alanine aminotransferase was slowly infused into the left ventricular wall in open-chest dogs. The half-life for the washout of alanine aminotransferase activity into plasma was 20 +/- 4 minutes (mean +/- SEM, n = 8) and was not different in ischemic and normally perfused tissue. From measurements of arteriovenous differences in alanine aminotransferase activity and left ventricular blood flow, it was concluded that 77 +/- 14% of total enzyme washout from ischemic tissue occurred by direct entry into the bloodstream. The corresponding value for the vascular permeability-surface area product was 264 +/- 55 ml.kg-1.hr-1. For a second model, we studied myocardial enzyme release into plasma after abrupt heart injury induced by 10 minutes of calcium-free coronary perfusion followed by reintroduction of calcium (calcium-paradox mechanism). The half-life for the release into plasma was 1.9 +/- 0.2 hours (mean +/- SEM, n = 6) and was again not influenced by sustained ischemia. Slower washout, as observed for this second model, is consistent with increased interstitial protein space and corresponds to a permeability--surface area product between 135 and 285 ml.kg-1.hr-1. These results were used to calculate the time course of cellular enzyme leakage from the rate of enzyme release into plasma in various forms of heart injury. Significant shifts between the time curves of evolving cellular injury and enzyme release into plasma are observed after 2 hours of ischemia followed by coronary reperfusion, but not after permanent ischemia.
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PMID:Time course of cellular enzyme release in dog heart injury. 222 57

This study tests the importance of amino acid transamination in determining the tolerance of immature hearts to ischemic damage. Amino acid transamination was inhibited metabolically by pretreatment with aminooxyacetic acid. The aminooxyacetic acid dose and duration were determined by incubating in vitro tissue homogenate and showing that an 8 mmol/L AOA dose for 5 minutes blocked 90% of alanine aminotransferase and aspartate aminotransferase activity. Control studies in nonischemic hearts showed that coronary perfusion with aminooxyacetic acid for 5 minutes did not impair myocardial performance. In contrast, pretreatment of immature puppies with aminooxyacetic acid severely impaired recovery after 45 minutes of normothermic global ischemia (30% versus 85% recovery in untreated hearts, p less than 0.05). Biochemical analyses of hearts undergoing ischemia showed aminooxyacetic acid to limit lactate production, impair glutamate utilization, prevent alanine production, and limit succinate accumulation (p less than 0.05). These data suggest that amino acid transamination is an important adaptive process in the immature heart that improves its resistance to ischemic damage.
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PMID:Studies of myocardial protection in the immature heart. II. Evidence for importance of amino acid metabolism in tolerance to ischemia. 224 11

Hepatic ischemia induced in vivo by ligation of the left hepatic lobe of rats for up to 2 hr had no effect on cytochrome P-450, cytochrome c reductase, or lobe histology; however, cytochrome b5 increased with ischemia duration. Ethylmorphine demethylation decreased 35% after 2 hr of ischemia. Reperfusion of tissue previously made ischemic for up to 2 hr was associated with appreciable necrosis as well as decreases in cytochrome P-450, cytochrome b5, cytochrome c reductase, and ethylmorphine demethylation. Serum alanine transaminase and aspartate transaminase concentrations were increased by reperfusion of previously ischemic tissue. Reperfusion of the previously ischemic lobe for 18 hr was associated with a greater loss of cytochromes P-450 and b5, cytochrome c reductase, and ethylmorphine demethylation than reperfusion for 1 hr. The total decrease in cytochrome P-450 and b5 content was equal to the decrease in total microsomal heme content, although cytochrome P-450 decreased more than cytochrome b5. Ethoxyresorufin deethylation by hepatic microsomes from 3-methylcholanthrene-treated rats was decreased by ischemia-reperfusion; however, pentoxyresorufin dealkylation by hepatic microsomes from phenobarbital-treated rats was not, suggesting specific cytochrome P-450 isozyme loss. In vitro NADPH-dependent lipid peroxidation in hepatic microsomes from control and phenobarbital- and 3-methylcholanthrene-treated rats resulted in a selective decrease of ethoxyresorufin but not pentoxyresorufin dealkylation, similar to that observed in livers subjected to ischemia-reperfusion in vivo. These data suggest that cytochrome P-450, ethylmorphine demethylation, and ethoxyresorufin deethylation are more susceptible to ischemia-reperfusion injury than cytochrome b5 or pentoxyresorufin dealkylation.
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PMID:Effects of hepatic ischemia-reperfusion injury on the hepatic mixed function oxidase system in rats. 225 Jun 63

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

We examined the effects of two degrees of hypothermia on hepatic oxygen delivery and uptake, hepatic lactate uptake as a marker of hepatic function, and the effect of hypothermia on ischemia-reperfusion injury in the liver in miniature pigs (n = 18, 21-30 kg body wt). Hepatic arterial and portal venous blood flows were measured while hepatic oxygen delivery was progressively decreased without venous congestion in the preportal area. With decreases in hepatic blood and oxygen supply, oxygen extraction gradually increased from 50 to 90% in the normothermic group and from 25 to 70 and 84% in the hypothermic (30. and 34 degrees C, respectively) groups. The values of critical hepatic oxygen delivery were between 7.3 and 11.9 ml O2.min-1.100 g-1 without significant differences among the groups. During reperfusion after ischemic insult, hepatic oxygen uptake returned to base-line values in both hypothermic groups but remained substantially below base-line values in normothermic groups of animals. Hepatic enzyme concentrations (lactate dehydrogenase, alanine aminotransferase, aspartate aminotransferase, and alcohol dehydrogenase) were substantially increased (up to 30-fold) in normothermic animals, but the concentrations did not increase in either of the hypothermic groups. These results demonstrated that hypothermia per se does not affect hepatic oxygen delivery but decreases hepatic oxygen demand and uptake, provides an effective protection from hepatic oxygen deprivation, and lessens reperfusion injury.
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PMID:Hypothermia, hepatic oxygen supply-demand, and ischemia-reperfusion injury in pigs. 236 Jun 37

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

The viability of the graft after liver transplantation is considered to be expressed as the sum of the hepatocellular activity by re-flowing of the hepatic blood flow after transplantation and the hepatocellular injury derived from the cold ischemia of the liver which is indispensable for transplantation. In order to elucidate the hepatocellular injury in ischemic liver graft cold ischemic liver model without hepatectomy was prepared and liver functions, serum insulin, glucagon and cyclic AMP after glucagon loading were measured. The following results were obtained. 1) Influence of anoxia due to ischemia of the liver expressed by s-GOT, disappeared 2 days after operation but it lasted for long time by s-GPT. Re-elevation of s-GOT, s-GPT observed after 2 days or more was considered to be derived from the hepatocellular necrosis due to rejection. Incidentally, Al-phosphatase was useful for judging the rejection, but s-total bilirubin, s-total cholesterol and albumin were considered to be not useful as parameters for evaluating the viability of the graft. 2) The rejection and the hepatocellular necrosis had not influence on serum insulin, but serum glucagon corresponded to the hepatocellular necrosis and was useful index for the judgment of the hepatocellular damage in the graft. 3) The level of c-AMP after glucagon loading and the c-AMP response corresponded very well to the hepatocellular activity of the graft, and they were considered to be useful indices for evaluating the viability of the graft.
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PMID:[Experimental study of orthotopic liver transplantation in dog--with reference to change of hepatic function, serum insulin, glucagon, c-AMP after liver transplantation and the viability of the graft]. 284 4

The changes in the contents of the main tricarboxylic acid cycle intermediates and related amino acids under total ischemia and subsequent reperfusion of isolated guinea pig heart were studied. The decrease in ATP and phosphocreatine during 30 min ischemia was accompanied by alanine formation and approximately stoichiometric glutamate loss. The increase in malate in ischemic myocardium corresponded to the anaplerotic flux aspartate----oxaloacetate----malate. The succinate production was commensurable to alpha-ketoglutarate formation in the alanine aminotransferase reaction. The release of bulk amount of lactate, alanine and succinate into the myocardial effluent was observed during an early phase of the reperfusion using 1H NMR. In contrast to these metabolites, malate release was not observed in the reperfusion. By the 30th min of the reperfusion the decrease in lactate, alanine, malate and succinate tissue contents to the preischemic values was accompanied by the recovery of ATP and phosphocreatine. The results suggest that the formation and the release of succinate and alanine from the heart, complementary to that of lactate, reflect profound disturbances in energy metabolism.
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PMID:Metabolism of the tricarboxylic acid cycle intermediates and related amino acids in ischemic guinea pig heart. 289 8


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