These data provide evidence that despite equal magnitudes of jeopardized myocardial mass, acute ischemia induced by thrombotic coronary occlusion results in a greater incidence of MVA than does nonthrombotic balloon occlusion. These findings suggest that the process of intracoronary thrombosis itself exerts arrhythmogenic effects above and beyond the impact of ischemia on myocardium induced by coronary occlusion.
1 Idioventricular rate responses and adrenoceptor number have been examined in normal Langendorff hearts perfused at 70cmH2O and in 'ischaemic' hearts perfused at lOcmH2O. 2 In hearts perfused at normal pressure, ventricular rate responses to phenylephrine in the presence of propranolol were biphasic with low concentrations of phenylephrine reducing, and high concentrations increasing, ventricular rate. Both responses were abolished in the presence of prazosin (100nM). In hearts perfused at low pressure, the negative chronotropic responses to phenylephrine were no longer present and positive chronotropic responses were enhanced compared with those of control tissues. The number of ventricular [3H]-prazosin binding sites was also significantly increased during ischaemia. 3 Idioventricular rate responses to isoprenaline were depressed in ischaemic tissues compared with controls, but [3H]-dihydroalprenolol binding was not altered in these hearts. 4 The incidence and duration of arrhythmias which occurred during 30min of global ischaemia and reperfusion were not significantly altered in the presence of 100 nm prazosin. 5 These results demonstrate that reducing the perfusion pressure of rat isolated hearts enhances aadrenoceptor-mediated responses and increases a-adrenoceptor density. Whether the increase in aadrenoceptor responsiveness during ischaemia investigation.is involved in arrhythmogenesis requires further
Our observations indicate that the responses of ischemic myocardium to reperfusion are influenced by factors beyond those effects attributable to ischemia and reperfusion per se. Pharmacological lysis of coronary thrombi results in alterations characteristic of reperfusion injury and associated with impaired functional recovery. Such changes are also evident, although to a lesser extent, when reperfusion of northrombotic occlusions is induced by mechanical recanalization in the presence of a systemic lytic state but not in its absence. However, such effects were not seen with direct mechanical recanalization of thrombotically occluded vessels. In aggregate, these findings indicate that induction of a systemic lytic state, together with products released by lysis of intracoronary thrombi, generates an inurious milieu that exerts adverse effects on reperfused myocardium.
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