Drugs online research references
Gastroenterology. 1986 Feb;90(2):362-7.
Role of oxygen radicals in ischemia-induced lesions in the cat stomach.
Perry MA, Wadhwa S, Parks DA, Pickard W, Granger DN.
Ischemia in a stomach that contains acid may produce severe gastric mucosal injury. The extent to which oxygen-derived free radicals are involved in the pathogenesis of this injury was investigated in the present study. Local gastric ischemia was achieved by reducing celiac artery pressure to 30 mmHg for 1 h. Ischemic injury was assessed by recording the loss of 125I-albumin and 51Cr-red cells across the gastric mucosa. Cats were treated with a xanthine oxidase inhibitor (allopurinol), a superoxide radical scavenging enzyme (superoxide dismutase), and a scavenger of hydroxyl radicals (dimethyl sulfoxide). The damage associated with ischemia only occurred during reperfusion of the stomach and was worst in the antrum. The level of xanthine oxidase in the antrum was twice that of the corpus. Treatment with allopurinol, superoxide dismutase, and dimethyl sulfoxide reduced 51Cr-red cell loss to 15%, 25%, and 21% of control (untreated) animals, respectively. The data indicate that oxygen-derived free radicals play a role in ischemic injury to the stomach and that the hydroxyl radical, a secondary radical produced from the superoxide anion, appears to be the major oxygen radical contributing to ischemic damage.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3753593&dopt=Abstract
J Lipid Mediat Cell Signal. 1994 Mar;9(2):135-43.
Arachidonate metabolism in ischemia-reperfusion associated with pancreas transplantation.
Hotter G, Closa D, Pi F, Rosello-Catafau J, Bulbena O, Badosa F, Fernandez-Cruz L, Gelpi E.
Department of Neurochemistry, Centro de Investigacion y Desarrollo, CSIC, Barcelona, Spain.
The implication of eicosanoid metabolism and its relationship with oxygen free radical production in the process of ischemia-reperfusion associated with rat pancreas transplantation has been explored in this study. For this purpose male Sprague-Dawley rats were classified as follows: group I, control animals not surgically manipulated; group II, pancreas transplantation, after 30 min preservation in UW solution; group III, pancreas transplantation after 12 h preservation under the same conditions; group IV, same as group III but with administration of SOD 5 min prior to organ revascularization. The results show post-transplantation increases in 6-keto-PGF1 alpha, TXB2, LTB4 and 12-HETE in pancreatic tissue independent of preservation time. The fact that SOD administration could reverse these increases even though an efficient xanthine oxidase irreversible inhibitor such as allopurinol was present in the preservation solution suggests that eicosanoid generation in the recipient rat would be mediated by an oxygen free radical dependent mechanism not exclusively dependent on endothelial xanthine oxidase activity.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8012760&dopt=Abstract
Can J Cardiol. 1988 Oct;4(7):360-5.
Myocardial salvage with allopurinol during 24 h of permanent coronary occlusion: importance of pretreatment.
Kingma JG Jr, Miura T, Downey JM, Hearse DJ, Yellon DM.
Rayne Institute, St. Thomas' Hospital, London, UK.
Cardioprotection by allopurinol during ischemia is thought to be due to inhibition of xanthine oxidase-derived reactive oxygen intermediates. Previous studies have reported that long pretreatment with allopurinol limits tissue necrosis during acute myocardial ischemia. This study investigated whether a prolonged pretreatment with allopurinol was necessary for cardioprotection. Tissue necrosis was measured in a closed chest canine model of permanent coronary occlusion when the drug was administered post coronary occlusion. In 20 dogs the coronary artery was occluded by an embolus injected into the left coronary artery. Three groups were studied: untreated controls (saline given intravenously post occlusion); allopurinol 1 min post occlusion (25 mg/kg given intravenously, 1 min post occlusion); and allopurinol 30 mins post occlusion (25 mg/kg given intravenously 30 mins post occlusion). Dogs in both drug treatment groups also received allopurinol (25 mg/kg intravenously) every 8 h post coronary occlusion. After 24 h of permanent coronary occlusion tissue necrosis was evaluated using triphenyl tetrazolium chloride staining and was related to major baseline predictors of infarct size, including anatomic risk zone and coronary collateral flow. In control dogs, infarct to risk zone ratio was inversely related to subepicardial collateral flow; analysis of covariance indicated that allopurinol administered post coronary occlusion did not shift this relationship. Treatment with allopurinol within the first minutes after coronary occlusion was ineffective in limiting tissue necrosis in this model of permanent coronary occlusion, therefore, long pretreatment with allopurinol is necessary for cardioprotection.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3228762&dopt=Abstract
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