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)

Thromboxane B2 and 6-keto-PGF1 alpha (6KPGF1 alpha), the major stable metabolites of thromboxane and prostacyclin, are present in the CNS, where they appear to be mainly produced within and/or acting upon the vascular district. Their concentrations are of few pg/mg protein in rat brain cortex of animals sacrificed by microwave (MW) radiation, procedure which inactivates tissue enzymes and allows the determination of endogenous "basal" levels of eicosanoids. Levels of 6KPGF1 alpha and especially those of TxB2 increase several fold over the basal values in brain cortex of animals sacrificed by decapitation followed by a few minute interval before analysis (post-decapitation ischemia, PDI). Pretreatment of animals with the vasoactive drug papaverine, resulted in elevation of brain basal levels of 6KPGF1 alpha and with the carbochromene derivative AD6 in reduction of basal levels of TxB2, whereas the calcium antagonist nifedipine and dipyridamole did not modify basal levels of the two eicosanoids. Treatments with papaverine and AD6 reduced the accumulation of TxB2 and enhanced that of 6KPGF1 alpha occurring after PDI, to different extents, both resulting, however, in reduction of the TxB2/6KPGF1 alpha ratio. Nifedipine instead, decreased the release of both eicosanoids and resulted in elevation of the TxB2/6KPGF1 alpha ratio, whereas dipyridamole had no effect. In conclusion, the evaluation of the overall effects of drug treatments on the TxB2/6KPGF1 alpha ratio in cerebral tissue, provided useful informations on the pharmacological modulation of vascular eicosanoids in this district.
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PMID:Differential effects of various vasoactive drugs on basal and stimulated levels of TXB2 and 6-keto-PGF1 alpha in rat brain. 383 85

The role of mast cells in pulmonary artery occlusion/reperfusion injury was examined. Lung tissue was obtained from dogs after left pulmonary artery occlusion for 48 h (n = 5) or after similar occlusion followed by 4 h of reperfusion (n = 11). By light microscopy and morphometry, the percentage of mast cells increased 2.4-fold (p < 0.05) in nonoccluded right lungs and 2.9-fold (p < 0.05) in occluded left lungs without reperfusion compared with that in control lungs. After reperfusion, the occluded left lung contained 1.8-fold (p < 0.05) as many mast cells as the nonoccluded right lung and 4.2-fold (p < 0.05) more than that in control lungs. Hydroxyurea did not significantly affect the number of mast cells observed in the right and left lungs after ischemia/reperfusion; 39.8% and 54.4% of the mast cells were degranulated in nonoccluded right lung and occluded left lung preparations, respectively, after left pulmonary artery ischemia/reperfusion (each, p < 0.05 compared with control lungs). The release of eicosanoids into the airways during ischemia/reperfusion injury was also examined. Thromboxane B2 and leukotriene B4 were markedly increased (each, p < 0.05 compared with that in control lungs) in bronchial lavage fluids from both nonoccluded and occluded lungs compared with sham-occluded lungs. Thus, mast cell recruitment and degranulation may play a role in lung ischemia/reperfusion injury.
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PMID:Lung mast cells increase in number and degranulate during pulmonary artery occlusion/reperfusion injury in dogs. 838 32

Eicosanoids play an important role in mediating deleterious effects following skeletal muscle ischemia-reperfusion injury. It has previously been shown that oxygenated perfluorocarbon emulsion (O2 Fluosol-DA 20%) decreases the amount of muscle necrosis and neutrophil sequestration when given during the reperfusion phase following skeletal muscle ischemia. As thromboxane is known to alter the endothelial cytoskeleton, thereby favoring diapedesis of neutrophils, the effects of O2 Fluosol-DA 20% on thromboxane release in a canine gracilis muscle model were investigated. The gracilis muscle on one randomly selected side of 14 adult mongrel dogs (body-weight 22-26 kg) was subjected to 6 h of normothermic ischemia followed by 48 h of normothermic reperfusion. The control group (n = 7) underwent ischemia-reperfusion, but without any pharmacological intervention. The Fluosol group (n = 7) were infused with O2 Fluosol-DA 20% (4.3(0.2) ml O2/100 ml) at 12 ml/min for 40 min via the gracilis artery following the ischemic period. Thromboxane B2 levels were measured from blood samples obtained at pre-ischemia, and at 1 h and 48 h of reperfusion. The gracilis muscles were harvested at the end of the experiment and extent of muscle necrosis quantitated by serial transections, nitroblue tetrazolium staining and computed planimetry. The mean(s.e.m.) muscle necrosis in the control group (59(6)%) was significantly higher than in the Fluosol group (22(5)%, P < 0.05, t-test). Thromboxane levels (pg/ml) in the control group at 1 h of reperfusion were significantly higher than the pre-ischemic and 48-h reperfusion levels (7286(1383) versus 1336(592) and 2314(1297), P < 0.05 by ANOVA and Student-Newman-Keuls test). The thromboxane level in the Fluosol group at 1 h reperfusion was significantly lower than the control group (2700(556) and 7286(1383) pg/ml, respectively; P < 0.05, t-test). In contrast, there was no statistically significant difference between thromboxane levels in the Fluosol group at 1 h reperfusion compared with levels at pre-ischemia and 48 h reperfusion (2700(556) versus 1336(592) and 1400(474). Thus, perfluorocarbons are effective in decreasing skeletal muscle necrosis, probably by maintaining the endothelial integrity and preventing vasospasm, secondary to their inhibitory effect on thromboxane release. Perfluorocarbons may also minimize some of the deleterious pulmonary effects known to be caused by increased levels of eicosanoids during reperfusion.
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PMID:Perfluorocarbon emulsion prevents eicoasanoid release in skeletal muscle ischemia and reperfusion. 878 46


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