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)

N-dimethyl propranolol (UM-272) has been shown to protect the heart from injury produced by ischemia. In the present study we examined the effects of UM-272 on the function of isolated rabbit cardiac mitochondria and microsomes. Concentrations of 13 micrometers or below were without effect on these organelles. UM-272 (130 micrometers) significantly decreased respiratory control of mitochondria utilizing glutamate plus malate, or succinate, as substrates. At 1.3 mM, UM-272 increased the initial rate of basal oxygen consumption, and decreased the rate of ADP-stimulated respiration. UM-272 was slightly more potent than d,1-propranolol. At a concentration of 1.3 mM, UM-272 significantly decreased the rate and maximum amount of 45CaCl2 accumulated by microsomes in the presence of ATP and oxalate. Concentrations of drug that suppress cellular metabolism are close to those required to prevent ischemic injury. We suggest that sarcolemmal and intracellular actions of the drug which help to depress oxygen demand and ATP utilization may account for part of the drug's protective effects.
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PMID:Effects of N-dimethyl propranolol (UM-272) on isolated cardiac mitochondria and microsomes. 49 13

To determine the protective effects of different methods of cardioplegia, studies on ATP/lactate levels and ultrastructure were performed in human papillary muscles obtained during mitral valve replacement. In group I (n = 5), plain ischemic arrest in hypothermia (systemic venous temperature = 24 degrees C) was accomplished. In group II (n =12), the heart was arrested by injection cardioplegia using magnesium-aspartate-procaine at systemic venous and myocardial temperatures of 24 degrees C. In group III (n = 12) Bretschneider infusion cardioplegia at systemic venous and myocardial temperatures of 26 degrees C and 19 degrees C respectively was applied. With regard to ultrastructural changes there were no clearcut differences in the three methods of hypothermic cardiac arrest after 60 minutes of ischemia. Ischemic changes tended to be slightest in group III (infusion cardioplegia). ATP decay and lactate increase were significant in group I and moderate to minimal in groups II and III after the same period of time. It is concluded that for aortic cross-clamp times up to 60 minutes, body hypothermia and injection cardioplegia using magnesium-aspartate-procaine at a myocardial temperature of 24 degrees C provide adequate protection of the myocardium. For ischemia times beyond 70 minutes, profound myocardial hypothermia below 20 degrees C is preferred.
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PMID:Ultrastructural and biochemical changes of human papillary heart muscle during different methods of induced cardiac arrest. 49 22

In an isolated rat liver perfusion system the effects of normothermal ischemia on hepatic functions were investigated. After 30 minutes of anoxy bile production and BSP elimination capacity of the liver are significantly reduced. The quantity of secreted "ascites" from the surface of the liver several times high after anoxic damage, while oxygen consumption, portal venous pressure and ammonia elimination do not differ significantly from the controls. Pretreatment with insulin plus glucose, isoproterenol, hypoxanthine, chlorpromazine and glucagon (5 micrograms/100 g i.v., or 0.2 mg/100 g s.c.) does not reduce noticeably the normothermal anoxic lesion of the liver Glucagon (50 micrograms/100 g i.v.), allopurinol, dibenzyline, ATP-MgCl2 and aspartic acid enhance significantly the ischemia-tolerance of liver in vitro.
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PMID:Ischemic damage of the liver. Part I: In vitro investigation of the prevention of the ischemic lesion of the liver. 49 24

A new model for the study of ischemic liver lesion on rats has been worked out. Pretreatment with allopurinol, dibenzyline, methylprednisolone, glucagon, ATP-MgCl2 and aspartic acid reduced the overall mortality of ischemic liver injury. Administered after the anoxic hepatic lesion only glucagon and aspartic acid had beneficial effect on the survival rate. Under the influence of 30 minutes of normothermal ischemia the DNA synthetizing ability of the liver decreased. Aspartic acid, glucagon and ATP-MgCl2 significantly enhanced the regeneration of the ischemically damaged liver. These procedures might be suitable for donor pretreatment in liver transplantation, as well as for the treatment of other pathological states, causing a normothermal ischemia of the liver.
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PMID:Ischemic damage of the liver. Part II: In vivo investigation of the prevention of the ischemic lesion of the liver. 49 25

The relationship of changes in regional coronary flow to the nature and degree of biochemical disturbances during occlusion of branches of the left anterior descending coronary artery and following reestablishment of flow was investigated in two groups of dogs: group I, moderate ischemia before reflow, and group II, severe ischemia prior to reflow. Regional coronary blood flow was determined before ligation, after 60 min of ischemia and after 15 min of reflow using labelled microspheres. Hearts made ischemic for 60 min but not reperfused served as controls. Groups I and II were distinguished by the following features. Group II showed a marked exacerbation of biochemical damage on reperfusion of the ischemic region (reduced levels of ATP, impairment of mitochondrial oxygen consumption and mitochondrial calcium binding). This was accompanied by significant subendocaridial hyperemia. Reperfusion in group I, on the otherhand, partially reversed these changes (increased level of ATP in the ischemic-reperfused region, improved mitochondrial oxygen consumption and calcium binding). Mitochondrial calcium uptake and oxidative phosphorylation (ADP/O ratio) were not affected in any group. These data illustrate that the degree of biochemical damage following reperfusion of the ischemic myocardium is determined by the degree of ischemia, and suggest that interference with ATP production by the mitochondria is not responsible for the damage.
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PMID:The relationship of regional coronary blood flow to mitochondrial function during reperfusion of the ischemic myocardium. 50 23

The effect of 1.5 to 2.5 h tourniquet ischemia on energy metabolism of the quadriceps muscle was studied using percutaneous needle biopsy technique in sixteen patients operated on for an inveterated knee injury. During occlusion there was a moderate decrease in ATP with an increase in ADP and AMP. This change resulted in a decreased energy charge potential. At the same time phosphorylcreatine (PC) decreased markedly while creatine (Cr) increased giving a constant total creatine (TCr). An accumulation of lactate during occlusion with values up to 80 mmol/kg d.m. (dry muscle) was seen. A 15% reduction in glycogen was calculated. After release of the tourniquet the active phosphate concentration and the energy charge potential returned to basal levels within 5 min and most of the metabolites in the glycolytic sequence were also normalized. Muscle lactate content was normal after 30 min of intact circulation. The results suggest that longterm tourniquet ischemia induces marked changes in energy metabolism in skeletal muscle, but that the changes are rapidly and completely reversible with restoration of blood flow.
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PMID:The effect of long-term arterial occlusion on energy metabolism of the human quadriceps muscle. 52 75

A reduction in myocardial oxygen supply during ischemia, not only leads to reduced aerobic ATP production but does not stimulate glycolytic ATP synthesis. The residual aerobically synthesized ATP comes primarily from continued inefficient (i.e., compared to glucose in terms of moles of ATP produced per mole of O2 consumed) oxidation of fatty acids. This leads to elevated tissue levels of long chain fatty acyl-CoA and fatty acyl-carnitine. Both are potentially cell damaging metabolic intermediates. Restriction of glycolysis is due to inhibition of glyceraldehyde-3-phosphate dehydrogenase by accumulated metabolites, such as H+, lactate and NADH. The reduced production of ATP leads to decreased levels of high energy phosphate stores which in turn may impair myocardial mechanical function.
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PMID:Energy metabolism in the ischemic heart. 55 21

A comparative investigation was made on muscle tissue of man, dog and rat during ischemia of five hours duration. The content of energy rich phosphates was measured. The ATP level decreased after two hours ischemia to 68% in man, to 45% in the dog, and to 23% in the rat. By five hours it had fallen further to 25% in man, 9% in the dog and only 1% in the rat. It is concluded that human muscle has a higher tolerance to ischemia.
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PMID:[Comparative study of energy metabolism of the skeletal muscles in man, dogs and rats during long-term ischemia]. 61 91

Both ischemia and ethionine decreased the membrane potential and ATP content in rat liver. In ethionine-treated rat liver, ischemia brought about a further decrease in membrane potential without significant decrease in ATP content.
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PMID:The relationship between membrane potential and ATP content in rat liver during ischemia. 62 Jul 36

The effects of pressure-induced ischemia on energy metabolism, measured as ATP and glucose content, is studied in hamster cheek pouch. Metabolic deterioration during ischaemia is studied and after 2 h the glucose content was significantly reduced but not the ATP content, which was significantly reduced after 4 h of ischemia. Restoration of glucose levels in the cheek pouch tissue was achieved within 30 min of recirculation after release of pressure. The cellular energy metabolism is unable after 4 h of ischemia to restore ATP levels in the tissue during the 120-min of postischemic observation time. There is a difference in ability to resume normal energy metabolism after 2 and 4 h of pressure-induced ischemia.
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PMID:Pressure-induced ischemia. II. A metabolic study in hamster cheek pouch. 63 Nov 45


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