Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151814 (coronary occlusion)
3,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intravenous infusion of acetylstrophanthidin to 6 dogs, after a 60 min left anterior descending coronary artery occlusion, was associated with a 43.0 +/- 10.5% decrease in the dose of digitalis needed to produce ventricular arrhythmias as compared to the pre-ischemic dose (97.5 +/- 8.0 microgram/kg). Reperfusion of the ischemic region for 2 h after a 90 min occlusion resulted in a 54.4 +/- 6.7% decrease in the arrhythmogenic dose. Direct intracoronary infusions of digitalis into the ischemic region, after a 90 min coronary occlusion followed by 2 h of reperfusion, was associated with a 47.7 +/- 6.4% decrease in the dose of digitalis needed to produce arrhythmias. The pre-ischemic (control) arrhythmogenic dose of digitalis via the intracoronary infusion method was 1.5 +/- 0.3 microgram/kg (mean +/- S.E.M. of 7 dogs). Sodium pump activity, estimated from the ouabain-sensitive 86Rb uptake in sodium-loaded ventricular slices, was significantly higher in slices obtained from the ischemic regions (6.84 +/- 0.30 nmoles 86Rb/mg dry wt. (mean +/- S.E.M.), than from the non-ischemic regions (3.43 +/- 0.64 nmoles 86Rb/mg dry wt.). Sensitivity of the sodium pump activity to the inhibitory effect of ouabain also was increased in the ischemic regions as indicated by a shift in the log dose--response curve to the left. Thus, it appears that there is an increase in myocardial sensitivity to the toxic effect of digitalis after temporary ischemia and it appears to be related to an increase in the sensitivity of the Na+,K+-ATPase or sodium pump to the inhibitory effect of digitalis.
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PMID:Ischemic-induced alterations in cardiac sensitivity to digitalis. 48 58

Reperfusion arrhythmias (RA) especially ventricular tachycardia (VT) and ventricular fibrillation (VF) remain the most important causes of sudden death following reperfusion. In isolated rat hearts grape seed proanthocyanidin extract (GSPE) had been proved to reduce the incidence of reperfusion-induced VF and VT. However the mechanism of this protection remained unclear. The aim of this study was to elucidate the potential mechanism of this protection of GSPE. The myocardial ischemia reperfusion (IR) model was induced by 30 min coronary occlusion and 120 min reperfusion in open chest anesthetized rats. The ultrastructure of ischemic cardiomyocytes was observed. An isobaric tag labeling for relative and absolute quantification (iTRAQ) proteomics was used to identify differentially expressed membrane proteins. Western blot was performed to verify the results of iTRAQ. The results demonstrated GSPE can significantly reduce the incidence of VT and VF induced by reperfusion in vivo. We identified 92 differentially expressed proteins. Western blot analysis confirmed GSPE increased the expression of Na(+)/K(+)-ATPase alpha1 subunit (p<0.01). We found the subunit distribution of Na(+)/K(+)-ATPase was changed after reperfusion. Na(+)/K(+)-ATPase alpha1 subunit was decreased in IR group (without GSPE-treated) compared to sham group while it was significantly increased in GSPE group. The decrease of free radical generation induced by GSPE may lead to the up-regulation of Na(+)/K(+)-ATPase alpha1 subunit. This change of subunit distribution may lead to the increase of activity of Na(+)/K(+)-ATPase which may result in the protection of GSPE against reperfusion arrhythmias. Our experiments provided new avenues for the treatment of reperfusion arrhythmias.
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PMID:The molecular mechanism of protective effects of grape seed proanthocyanidin extract on reperfusion arrhythmias in rats in vivo. 2046 Jul 51