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

Free radicals have long been well known by physicists but have only interested biologists since 1969 when Fridovich showed that O2 was produced during an enzymatic oxidation. O2 and related radicals are highly toxic. This implies that, in all aerobic cells, mechanisms exist which inactivate free radicals as soon as they are produced by oxidative metabolism. O2 radicals are eliminated by a family of enzymes called superoxide dismutases (SOD). These SOD are present in the cytosol (CuSOD) and in the mitochondria (MnSOD). Overproduction of free radicals, originating in molecular oxygen, may explain the lesions which result from inflammation, ischemia, and radiation exposure. Free radicals can cause damage to membranes, macromolecules, and DNA. Whether free radical production is mainly intracellular or extracellular may determine to a degree which kind of damage will occur.
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PMID:[Free radicals in medicine and biology]. 629 65

The development of myocardial ischemia is known to elicit the formation and enlargement of collateral vessels. The stimulus for these events is unknown. We have investigated the possibility that cardiac tissue releases a factor that can stimulate endothelial cell proliferation. Hearts from New Zealand rabbits were made progressively ischemic by differential hypothermia. Extracts from these hearts were tested for their growth-stimulating ability and were found to increase the proliferation of fetal bovine aortic endothelial cells as well as DNA synthesis by 3T3 cells. The level of activity in the extracts appears to be related to the degree of ischemia as measured by creatine phosphokinase levels. The liberation of an endothelial cell growth factor by ischemic cardiac tissue may function in the initiation and/or potentiation of coronary collateral formation.
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PMID:Do ischemic hearts stimulate endothelial cell growth? 646 72

Warm ischemia produces DNA damage which is characterized by both single- and double-strand breaks with 5'-PO4 and 3'-OH ends. In contrast, cold ischemia produces mostly single-strand breaks for the first 60 hr and then, abruptly, double-strand damage is produced. Cold ischemia produces both 5'-OH and 5'-PO4 termini, but 5'-OH ends do not appear until after 24 hr of storage. Cold ischemia, also produces 3'-PO4 ends but we have not found any 3'-OH termini. Mechanisms for DNA degradation during warm and cold ischemia are presented to account for these results. It is suggested that damage to the genetic code may be prevented if degradation of the DNA can be confined to the production of the easily repairable 5'-PO4/3'-OH opposed ends.
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PMID:A description of the damaged DNA produced during tissue injury. 651 May 13

The creatinuria after musculoskeletal injuries was studied in 31 patients. In addition to creatine the urinary outputs of creatinine, total nitrogen, and 3-methylhistidine were studied. Plasma creatine, creatinine, and guanidinoacetate concentrations were measured in some patients. In rats the effect of bilateral hind-limb ischemia was observed on the urine outputs of creatine and creatinine, and on the creatine, protein, and DNA contents of the hind limbs and carcass. In man the creatinuria was positively related to the severity of the injury and this relationship was stronger than with the urinary output of either creatinine or total nitrogen. In the rat creatinuria was related to the duration of the limb ischemia. The mechanism of the creatinuria is not known but the experiments on rats showed part of the excess creatine to be derived from the damaged muscle and excreted shortly after the injury, and part from the undamaged muscle of the carcass which provided the delayed excretion. It is suggested that creatinuria could be used as an indicator of the post-traumatic 'flow' phase.
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PMID:Post-traumatic creatinuria. 673 28

Rats were fed a protein-free diet until 20-30% of body weight was lost and then hemorrhagic shock or liver ischemia was induced. Alkaline sucrose gradients were used to analyze for breaks in DNA. Whereas reversible shock caused no DNA damage in five rats on the standard diet, DNA damage was found in ten animals subjected to severe shock. In contrast, ten rats on the protein-free diet had no significant DNA breakage even after severe shock. Diet also influenced postoperative survival; ten of 15 rats on the standard diet compared to ten of 12 on the protein-free diet survived for the 1 h postshock liver sample. To examine the biologic effect animals were subjected to hemorrhagic shock without laparotomy and liver biopsy. Three of 18 rats on the standard diet and 12 of 20 animals on the protein-free diet lived longer than 2 h (P less than .001). One rat on the standard diet and three on the protein-free diet survived for longer than 72 h. After 30 and 60 min of liver ischemia, rats on both diets showed similar breakage of DNA with repair following reperfusion. After 120 min of liver ischemia, there was similar DNA breakage for both diets; however, for rats on the standard diet there was no repair while there was DNA repair for rats on the protein-free diet.
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PMID:Influence of a protein-free diet on survival and DNA following hemorrhagic shock and ischemia. 674 21

This study examines the effect of increasing duration of intestinal ischemia on the mucosal integrity and the release of the enzyme diamine oxidase from the small intestine. Acute ischemia was produced by the occlusion of the superior mesenteric artery, and the subsequent changes in DNA and 125I-albumin content in the lumen were taken as indices of intestinal lesions. Diamine oxidase activity was measured in the intestinal lumen, mucosa, lymph, and serum. Occlusions of the superior mesenteric artery for periods of more than 60 min resulted in significant leakage of 125I-albumin (i.v.) into the lumen. In contrast, luminal DNA content rose significantly after 15 min of ischemia and continued to increase proportionally with the increased duration of the occlusion up to 120 min. Similarly, diamine oxidase activity was augmented in the lumen after 15 min of occlusion and rose sharply as the ischemic period was lengthened up to 60 min, leveling off thereafter. Increases in the diamine oxidase activity were also observed in the intestinal lymph and serum, reaching levels that were 2.6 and 3.6 times that of the control respectively after 60 min of ischemia. These findings suggest that intestinal ischemia reduces the diamine oxidase content in the intestinal mucosa by desquamation of the surface epithelial cells and by releasing the enzyme into the intestinal interstitial fluid, from which at least a portion is transported to the blood via the lymphatics. The early release of diamine oxidase seems to occur before the mucosal barrier is broken.
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PMID:Effect of intestinal ischemia on diamine oxidase activity in rat intestinal tissue and blood. 677 62

After a 5-hour period of donor pretreatment with cyclophosphamide (CY) and methylprednisolone (P) (100 mg/kg each), cold storage of pretreated canine renal allografts may cause early and severe postoperative renal insufficiency. This renal insufficiency is mediated by CY metabolites and depends on the number of hours of cold storage, for severe renal insufficiency is not observed after 6 hours of cold storage but is invariably present after cold storage beyond 18 hours. The renal insufficiency is associated with coagulation necrosis of the proximal tubules, particularly the pars recta. Since the repair of ischemia-medicated proximal tubular lesions requires mitotic activity, results suggest that the proximal tubules of donor pretreated kidneys are subjected to a concentration of CY metabolites sufficient to cause an extent of DNA damage that, in the absence of a sufficient time for nuclear repair, inevitably leads to cell death and renal insufficiency when the tubular cells are driven to mitosis by cold storage-mediated ischemia.
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PMID:Donor pretreatment-mediated and cold storage-dependent proximal tubular necrosis--a unique form of acute renal insufficiency. 704 21

Ischemia, anoxia, and hypoxia of the brain have been shown to inhibit protein synthesis in the central nervous system. To obtain data on the changes in DNA-dependent RNA and DNA polymerase as they pertain specifically to neurons and glia, nuclear enriched neuronal and glial fractions were prepared, by sucrose-gradient centrifugation, from spinal cords of adult dogs that had been subjected to prolonged ischemia. The isolated fractions were assayed for enzyme activity by a radiochemical technique. RNA polymerase was affected more than DNA polymerase, activity being reduced considerably in both neurons and glia. Possible causes of the difference in sensitivity to ischemia are discussed.
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PMID:Effect of ischemia on the activity of DNA-dependent RNA polymerase and DNA polymerase. 725 10

The patterns of expression of the bcl-2, bax, and bci-X genes were examined immunohistochemically in neurons of the adult rat brain before and after 10 min of global ischemia induced by transient cardiac arrest. High levels of the cell death promoting protein Bax and concomitant low levels of the apoptosis-blocking protein Bcl-2 were found in some populations of neurons that are particularly sensitive to cell death induced by transient global ischemia, such as the CA1 sector of the hippocampus and the Purkinje cells of the cerebellum. Moreover, within 0.5 to 3 hr after an ischemic episode, immunostaining for Bax was markedly increased within neurons with morphological features of degeneration in many regions of the brain. Use of a two-color staining method for simultaneous analysis of Bax protein and in situ detection of DNA-strand breaks revealed high levels of Bax immunoreactivity in many neurons undergoing apoptosis. Postischemic elevations in Bax protein levels in the hippocampus, cortex, and cerebellum were also demonstrated by immunoblotting. At early times after transient ischemia, regulation of Bcl-2 and Bcl-x protein levels varied among neuronal subpopulations, but from 3 hr on, those neurons with morphological evidence of degeneration uniformly contained reduced levels of Bci-2 and particularly Bci-X immunoreactivity. The findings suggest that differential expression of some members of the bcl-2 gene family may play an important role in determining the relative sensitivity of neuronal subpopulations to ischemia and that postischemic alterations in the expression of bax, bcl-2, and bcl-x may contribute to the delayed neuronal cell death that occurs during the repurfusion phase after a transient ischemic episode.
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PMID:Upregulation of bax protein levels in neurons following cerebral ischemia. 747 1

We examined the polyamine metabolism in liver transplanted after cold ischemia and effects of putrescine administration on liver injury, liver regeneration, and survival rate after orthotopic liver transplantation in the rat. Male Wistar rats were used as donors and recipients. Grafts were stored in Euro-Collins solution for 6 h at 4 degrees C. Orthotopic liver transplantation was performed by the three cuff technique. The activities of aspartate aminotransferase, alanine aminotransferase and lactate dehydrogenase elevated and peaked 4 h after liver transplantation. Hepatic ornithine decarboxylase and spermidine/spermine N1-acetyltransferase activities were also elevated and peaked 8 h after the operation. In agreement with the increases in ornithine decarboxylase and spermidine/spermine N1-acetyltransferase activities, the putrescine content increased and spermidine content decreased in the transplanted liver. Putrescine administrated intraperitoneally improved the survival rate, decreased serum transaminase level and increased the [3H]thymidine incorporation into the liver DNA. These findings suggest that both biosynthetic and biodegradative pathways are stimulated in liver transplantation, resulting in the increase in the formation of putrescine from ornithine and from spermidine, and that putrescine administration improve the survival rate by protecting the damaged graft after cold ischemia and reperfusion and by stimulating liver regeneration.
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PMID:Polyamine metabolism in the rat liver after orthotopic liver transplantation. 749 79


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