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)

A study was designed to examine ventricular arrhythmias in the acute phase of experimental myocardial infarction in the pig and to evaluate possible antiarrhythmogenic influence of the beta-adrenergic blocking drug pindolol (Visken) and the calcium antagonist Ro 11-1781. Ventricular fibrillation (VF) occurred in 17 of 18 animals, in 4 almost immediately after coronary occlusion and in 12 with a delay of about 17 min. VF was almost always induced by episodes of ventricular tachycardia (VT) which were started by single ventricular premature beats (VPBs). VPBs occurred in 3 phases, whereas VT and VF coincided only with phase 1 and phase 3. The prematurity index QR/QT of single VPBs decreased significantly with time after coronary occlusion. The beta-adrenergic blocking drug pindolol and the calcium antagonist Ro 11-1781 did not prevent VT or VF.
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PMID:[Ventricular arrhythmias in the acute stage of experimental swine myocardial infarct; effect of the beta blocker pindolol and the calcium antagonist Ro 11-1781]. 71 14

Myocardial function is impaired by ischaemia, and it remains depressed during reperfusion following short periods of ischaemia (stunned myocardium). We tested whether ischaemic and reperfusion dysfunction, in particular the time course of its recovery, can be distinguished by postextrasystolic potentiation (PESP). In eight open-chest dogs, posterior systolic wall thickening (sonomicrometry) was reduced by graded occlusion of the left circumflex coronary artery (LCX) from 17.4 +/- 6.8% (SD) during control conditions to 10.7 +/- 1.3% (mild ischaemic dysfunction), 7.2 +/- 2.3% (moderate ischaemic dysfunction), 3.6 +/- 1.4% (severe ischaemic dysfunction), and -4.4 +/- 3.6% (complete coronary occlusion). Extrasystoles with constant prematurity and a fully compensated postextrasystolic interval were induced after at least 4 min steady-state ischaemia. After each ischaemic period full recovery of posterior systolic wall thickening was assured. During 8 h of reperfusion following a 15-min LCX occlusion, extrasystoles were induced when posterior systolic wall thickening was comparable to one degree of the preceding ischaemic dysfunction. The increases in posterior systolic wall thickening induced by PESP were 10.5 +/- 5.8% during control conditions, during ischaemia they were 11.5 +/- 3.5% (mild dysfunction), 12.3 +/- 4.6% (moderate dysfunction), 12.6 +/- 4.1% (severe dysfunction) and 10.4 +/- 4.4% (complete coronary occlusion), and during reperfusion they were 12.8 +/- 8.2% (severe dysfunction), 13.0 +/- 9.7% (moderate dysfunction) and 10.7 +/- 2.2% (mild dysfunction).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Postextrasystolic potentiation does not distinguish ischaemic from stunned myocardium. 189 37

Impaired excitation-contraction coupling has been suggested as the underlying mechanism of postischemic contractile dysfunction of reperfused myocardium in in-vitro studies. To test this hypothesis in situ, postextrasystolic potentiation (PESP) following an extrasystole with constant prematurity and three different postextrasystolic time intervals (compensated, regular, abbreviated) was analyzed in 12 anesthetized dogs. Changes in regional inotropic state were assessed by comparison of end-systolic wall thickness (sonomicrometry) during PESP to the respective pressure-matched values of an end-systolic pressure/wall-thickness relationship established during brief manual clamping of the aorta. Before ischemia, posterior end-systolic wall-thickness was increased by 0.19 +/- 0.35 (SD) mm during PESP with an abbreviated, by 0.36 +/- 0.42 mm with a regular, and by 0.60 +/- 0.42 mm with a compensated postextrasystolic interval. Baseline systolic wall thickening was decreased from 16.2 +/- 5.4% (before ischemia) to -3.0 +/- 3.4% at the end of 15 min left circumflex coronary occlusion, and to 2.8 +/- 7.5% at 10 min, 7.2 +/- 3.9% at 4 h, and 7.9 +/- 4.1% at 8 h reperfusion. Stepwise increases in regional inotropic state during PESP with increasing postextrasystolic intervals were not different in normal and reperfused myocardium. Thus, excitation-contraction coupling appears not to be impaired during inotropic stimulation of reperfused myocardium in situ.
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PMID:Recruitment of a time-dependent inotropic reserve by postextrasystolic potentiation in normal and reperfused myocardium. 238 19