Effect of thromboxane synthetase inhibition on vulnerability to ventricular arrhythmia following coronary occlusion.

Abstract:

:Release of thromboxane (TXA2) during acute myocardial infarction may be an important contributing factor in the genesis of ventricular fibrillation (VF). We assessed the effect of selective TXA2 inhibition on vulnerability to VF after total occlusion of the anterior descending coronary artery in chloralose-anesthetized cats. Animals were pretreated with vehicle or with CGS-13080, a TXA2 synthetase inhibitor, 3.0 or 9.0 mg/kg intravenously. There was an apparent dose-dependent protective effect following CGS-13080 administration, in which the decrease in VF threshold following coronary occlusion was attenuated. Also, the incidence of spontaneous ventricular arrhythmia in the first 30 minutes after occlusion was reduced by two thirds in the 9.0 mg/kg CGS-13080 group compared to the vehicle-treated animals. This protective effect does not appear to be due to a change in hemodynamics, effective refractory periods, or extent of ischemia. TXA2 released during coronary occlusion appears to be arrhythmogenic, and inhibiting its synthesis may be protective.

journal_name

Am Heart J

journal_title

American heart journal

authors

O'Connor KM,Friehling TD,Kelliher GJ,MacNab MW,Wetstein L,Kowey PR

doi

10.1016/0002-8703(86)90099-2

subject

Has Abstract

pub_date

1986-04-01 00:00:00

pages

683-8

issue

4

eissn

0002-8703

issn

1097-6744

pii

0002-8703(86)90099-2

journal_volume

111

pub_type

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