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

The results of our experiments demonstrated that one hour of ischemia followed by one hour of reflow in the kidney caused a reduction in (Na+K+)ATPase activity and microsomal sulfhydryl content as well as an increase in microsomal lipid peroxidation. Renal venous malondialdehyde concentration was increased soon after reperfusion of the ischemic kidney. All these changes were rectified by an infusion of 0.123 mmol N-(2-mercaptopropionyl)glycine/kg over a 70 min period. On the other hand, an in vitro addition of 0.01-0.5 mM N-(2-mercaptopropionyl)glycine to a membrane preparation in the presence of H2O2 and Fe3+ did not prevent but rather potentiated the free radical effect on the enzyme activity. However, addition of superoxide dismutase alone or with catalase together with 2-MPG were effective in preventing the enzyme depression induced by H2O2. The results therefore indicate that free radical generation participates in the evolution of ischemia/reperfusion cell injury and thiol-reducing agents may be beneficial in alleviating the cell damage in vivo.
 ...
PMID:Effects of N-(2-mercaptopropionyl)glycine on ischemic-reperfused dog kidney in vivo and membrane preparation in vitro. 283 50

Global ischemia in guinea-pig hearts for 60 to 90 min depressed microsomal and mitochondrial Ca2+ uptake activities. Reperfusion of the 60 min ischemic hearts resulted in incomplete recovery of contractile function and calcium uptake activities of both mitochondrial and microsomal fractions. On the other hand, reperfusion of the 90 min ischemic hearts further depressed the microsomal Ca2+ uptake activity. Coronary occlusion for 90 min in dog hearts was found to decrease microsomal Ca2+-pump and sarcolemmal Na+-K+ ATPase activities. Reperfusion of these regional ischemic hearts further depressed the microsomal Ca2+ uptake and Ca2+-stimulated ATPase as well as sarcolemmal Na+-K+ ATPase activities whereas mitochondrial Ca2+ uptake was increased. Perfusion of rat hearts for 60 min with hypoxic medium resulted in depression of the sarcolemmal Na+-dependent Ca2+ uptake and ATP-dependent Ca2+ uptake activities. Reperfusion of these hypoxic hearts failed to recover the sarcolemmal Na+-Ca2+ exchange and Ca2+-pump activities. These results demonstrate that membrane defects with respect to Ca2+ transport processes in ischemic/hypoxic hearts may be associated with irreversible injury.
 ...
PMID:Alterations in heart membrane calcium transport during the development of ischemia-reperfusion injury. 284 10

Marker enzyme activities of different subcellular fractions were analyzed in cortex homogenates from rat kidney after different periods (15, 30, 60, and 90 min) of warm ischemia. Lactate dehydrogenase, alanine aminopeptidase, N-acetyl-beta-D-glucosaminidase, and succinate-cytochrome c reductase were not altered by ischemia in these periods. ATPase (2,4-dinitrophenol-stimulated and azide-sensitive), 5'-nucleotidase, K-Mg-nitrophenylphosphatase decline within 30 min of ischemia, whereas the microsomal enzymes glucose-6-phosphatase and NADPH-cytochrome c reductase decreased not before 60 min of ischemia. The early decrease of ATPase and of plasma membrane enzymes can be regarded as a consequence of membrane alterations. This enzymatic approach may be helpful to evaluate pharmacological agents for preventing and reserving ischemic effects in kidneys in a rational manner.
 ...
PMID:Changed enzyme activities in rat kidney during ischemia. 286 6

We investigated the response of mitochondrial function and microsomal adenosine triphosphatase (ATPase) activity in rat liver tissue subjected to in vitro ischemia at either 0 degree C to 4 degrees C or 37 degrees C for 30 to 60 minutes. Mitochondrial coupling, expressed as respiratory control index, was preserved at up to 60 minutes' cold ischemia. However, respiratory control index was decreased significantly from control by 30 minutes of warm ischemia. Both microsomal magnesium-activated ATPase and sodium-potassium ATPase activity were significantly increased by 60 minutes of warm ischemia yet were unaltered by 60 minutes of ischemia at 0 degree C to 4 degrees C. Warm ischemia produces deleterious effects on energy-generating (mitochondria) and energy-utilizing (ATPase) activity. Hypothermia provides a significant prolongation of cellular viability in ischemic tissue in terms of bioenergetic status. In addition to organ procurement and transplantation, hypothermic cytoprotection may prove valuable in areas such as shock, ischemia, and other clinical conditions of compromised visceral perfusion.
 ...
PMID:Hepatic microsomal adenosine triphosphatase and mitochondrial function. Response to cold and warm ischemia. 295 19

This work deals with changes in sedimentation of proteins in subcellular fractions isolated from the ischemic brain of Mongolian gerbils. We analysed protein content and the activity of marker enzymes in P2, S2, M and S3 subfractions isolated after 10 min ischemia, ischemia combined with apnea or 1 h later, after recirculation. On the basis of protein balance, the distribution of marker enzymes and electrophoretic analysis of proteins in brain subfractions it was shown that in ischemia some fraction of proteins which are normally cytosolic and microsomal, cosediment with the crude mitochondrial pellet. This effect, aggravated in ischemia complicated by apnea, is reversible and after 1 h recirculation the protein distribution in the brain normalizes completely.
 ...
PMID:Ischemia modifies protein distribution in gerbil brain subcellular fractions. 302 Jun 64

The rate of O2 radical generation in microsomal membranes (VO2), the activity of cytosol superoxide dismutase (Cu, ZnSOD) and mitochondrial superoxide dismutase (MnSOD), and the activity of xanthine oxidizing system (XO) after a two-hour ischemia following a 24-hour reoxygenation of the rat liver were investigated. The high value of VO2, as compared to Cu, ZnSOD activity, may result in regulation disorders in O2-SOD system during ischemia. During reoxygenation, xanthine oxidizing system in combination with lowered Cu, ZnSOD activity may substantially contribute to the disturbance.
 ...
PMID:[Disordered functioning of the superoxide radical-superoxide dismutase system in rat liver ischemia]. 302 43

To understand the subcellular basis of contractile failure due to ischemia-reperfusion injury, effects of 20, 60, and 90 min of global ischemia followed by 30 min of reperfusion were examined in isolated guinea pig hearts. Cardiac ultrastructure and function as well as Ca2+ transport abilities of both mitochondrial and microsomal fractions were determined in control, ischemic, and reperfused hearts. Hearts were unable to generate any contractile force after 20 min of ischemia and showed a 75% recovery upon reperfusion. However, there were no significant changes in the subcellular Ca2+ transport in the 20-min ischemic or reperfused hearts. When hearts were made ischemic for 60 and 90 min, the recovery of contractile force on reperfusion was 50 and 7%, respectively. There was a progressive decrease in mitochondrial and microsomal Ca2+ binding and uptake activities after 60 and 90 min of ischemia; these changes were evident at various times of incubation period and at different concentrations of Ca2+. Mitochondrial Ca2+ transport changes were only partially reversible upon reperfusion after 60 and 90 min of ischemia, whereas the microsomal Ca2+ binding, uptake and Ca2+ ATPase activities deteriorated further upon reperfusion of the 90-min ischemic hearts. Ultrastructural changes increased with the duration of the ischemic insult and reperfusion injury was extensive in the 90-min ischemic hearts. These data show that the lack of recovery of contractile function upon reperfusion after a prolonged ischemic insult was accompanied by defects in sarcoplasmic reticulum Ca2+ transporting properties and structural damage.
 ...
PMID:Reversibility of ultrastructural, contractile function and Ca2+ transport changes in guinea pig hearts after global ischemia. 302 83

Administration of alpha-tocopherol in combination with lidocaine prevented distinct alterations in lipid component of liver microsomal membranes of rats during the restoration period after 30 min total ischemia of liver tissue. These drugs reduced the ratio of saturated and unsaturated fatty acids down to the initial level within 3 days after ischemia, whereas the alterations in fatty acid composition were maintained within 21 days of the restoration period in control experiment. Considerable alterations in the patterns of fluorescent probe ANS binding with microsomal membranes during the postischemic period were not observed after administration of the drugs. Protective effect of the drugs involved transformation of lipid component in microsomal membranes.
 ...
PMID:[Changes in the lipid component of liver microsomal membranes during the postischemic period after administration of alpha-tocopherol and lidocaine]. 319 32

Total ischemia of rat liver tissue within 30 min caused distinct alterations in lipid component of endoplasmic reticulum membranes, which occurred within three weeks of the postischemic period. During this period the rate of microsomal lipids saturation was elevated due to an increase in the relative content of saturated fatty acids. Two-step alterations were observed in the patterns of fluorescent probe binding (I-amino naphthalene-8-sulfonate) as well as in sensitivity of cytochrome P-450 to the impairment in vitro after induction of lipid peroxidation in microsomal membranes. Within 1-3 days after the ischemia affinity of the fluorescent probe to microsomes was decreased, while stability of cytochrome P-450 to impairment during lipid peroxidation induction was increased. Within 7-14 days affinity of the fluorescent probe to membranes was markedly elevated and stability of cytochrome P-450 to the impairment in vitro was lowered in the reactions of lipid peroxidation.
 ...
PMID:[Structural changes in the lipid component of membranes of endoplasmatic reticulum in early and late periods after liver ischemia]. 336 23

The experiments on rats have shown that alpha-tocopherol and lidocaine pretreatment leads to a decrease in the level of ischemic cell necrosis in the liver. The volume of cell necrosis in the liver was significantly decreased (more than threefold) in the case of drug pretreatment. The combination of alpha-tocopherol with lidocaine fully prevented the decrease in N-dimethylation of amidopyrine and cytochrome P-450 and b5 concentration, and the development of destructive alterations of cytoplasmic reticulum in the unaffected rat hepatocytes. alpha-Tocopherol and lidocaine pretreatment was effective for the retention of the depression of microsomal monooxygenases by phenobarbital in remote periods after acute hepatic ischemia.
 ...
PMID:[Prevention, using alpha-tocopherol and lidocaine, of damage to the monooxygenase system activity and ultrastructure of hepatocytes following acute ischemia of the liver]. 368 56


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>