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

Forty adult rats were subjected to stepwise two- and four-brain vessel occlusion and propentofylline 25 mg/day per kilogram body weight was intraperitoneally administered for 1 week or 3 weeks. Adenosine 5'-triphosphate, creatine phosphate, adenosine 5'-diphosphate and adenosine were determined in rat parietotemporal cortex by high-pressure liquid chromatography; lactate and pyruvate were measured spectrophotometrically. Stepwise and permanent long-term brain vessel occlusion gradually reduced the concentration of energy-rich phosphates and induced a marked increase in the concentration of adenosine, a parameter of ischemia. Three weeks of propentofylline treatment resulted in a significant increase in cerebral adenosine 5'-triphosphate concentration from 2.16 +/- 0.15 [(-)-propentofylline] to 2.70 +/- 0.24 nmol/mg wet weight during four-vessel occlusion (+25%). This was associated with an enhancement of the adenosine 5'-triphosphate/adenosine 5'-diphosphate ratio (+33%), mainly because of the significant reduction in adenosine 5'-diphosphate concentration. Propentofylline did not prevent the increase in lactate concentration during permanent brain vessel occlusion, but significantly reduced the tissue concentration of adenosine. In summary, the results demonstrate that continuous propentofylline administration over 3 weeks induced a striking increase in rat cortical adenosine 5'-triphosphate concentration during long-term brain vessel occlusion. Thus, propentofylline may have possible neuroprotective effects and could be used in the treatment of patients with chronic cerebrovascular disorders.
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PMID:Increased ATP production during long-term brain ischemia in rats in the presence of propentofylline. 966 93

This study aims to determine if the protective role of adenosine in liver ischemic preconditioning is mediated by the activation of adenosine receptors and to ascertain which of these receptors is implicated in the process. Administration of adenosine A1 and A2 receptor antagonists to preconditioned animals indicates that hepatic preconditioning is mediated by the activation of adenosine A2 receptors. Propentofylline (an inhibitor of adenosine transport into cells) in the preconditioned group, subjected to previous administration of an adenosine A2 receptor antagonist, prevented the negative effect of the latter on the protection offered by preconditioning. An increase of NO production was detected just immediately after hepatic preconditioning, and the administration of an adenosine A2 receptor antagonist to the preconditioning group prevented this increase, thus abolishing the protective effect of preconditioning. However, the administration of a NO donor to the preconditioned group subjected to previous administration of the adenosine A2 receptor antagonist was able to maintain the preconditioning effects. In conclusion, these results indicate that, in preconditioning, the protective effect of adenosine could be a result of an increase in extracellular adenosine. This in turn would induce the activation of adenosine A2 receptors, which, by eliciting an increase in NO generation, would protect against the injury associated with hepatic ischemia-reperfusion.
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PMID:The protective role of adenosine in inducing nitric oxide synthesis in rat liver ischemia preconditioning is mediated by activation of adenosine A2 receptors. 986 58

The effect of propentofylline on mitochondrial respiratory activity was assessed in gerbils after 30 min of unilateral forebrain ischemia and 5 min of incomplete reperfusion. Cerebral blood flow (CBF) measured by hydrogen clearance was reduced to 12.6+/-2.1 ml/100 g per min in the ischemic hemisphere. Propentofylline at 10 mg/kg applied intraperitoneally raised CBF to 26.7+/-3.4 ml/100 g per min (P<0.05) in ischemic areas, however, CBF remained substantially reduced in comparison to the flow in the non-ischemic hemisphere (52.9+/-4.1 ml/100 g per min). Mitochondrial ADP-stimulated as well as uncoupled respiration was significantly reduced by approximately 60% after 30 min of ischemia. Since ADP-unstimulated respiration was not reduced, the respiratory control ratio declined markedly. Five minutes after application of propentofylline all indices of the mitochondrial respiratory capacity were normalized despite persisting reduction in CBF.
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PMID:Propentofylline rapidly normalizes mitochondrial respiration in a gerbil low flow unilateral forebrain ischemia. 1294 59


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