Decreased coronary blood flow is not responsible for myocardial dysfunction during bupivacaine-induced cardiotoxicity.

Abstract

Although previous studies have shown that bupivacaine produces a dose-dependent vasoconstriction, the possible effects of decreased coronary blood flow on myocardial dysfunction during bupivacaine-induced cardiotoxicity have not been investigated. We carried out the present study using the in situ beating hearts of six beagles. An autoperfusion circuit was established from the left carotid artery to the anterior descending coronary artery (LAD). Its blood flow (QLAD) was measured with an electromagnetic flow meter, and myocardial oxygen consumption was calculated using Fick's principle. Regional myocardial function (systolic shortening: %SS, post-systolic shortening: %PSS) of the LAD-supplied region was evaluated by the sonomicrometric technique. While saline or bupivacaine (10 micrograms/ml) was continuously infused into the LAD in a crossover design, the effects of a vehicle (baseline), acetylcholine (1 and 3 micrograms/min), nitroglycerin (10 micrograms/min) and adenosine (10 micrograms/min), on coronary haemodynamics and regional myocardial function were evaluated. Bupivacaine caused a decrease in QLAD and regional myocardial dysfunction (a decrease in %SS and an increase in %PSS) at the baseline. While acetylcholine and adenosine increased QLAD with intracoronary bupivacaine-infusion, regional myocardial dysfunction was not reversed. There was a positive correlation between regional myocardial oxygen consumption and %SS in the whole study. The results of this study indicate that the decrease in QLAD during bupivacaine-induced myocardial toxicity is not responsible for regional myocardial dysfunction, and, moreover, that it parallels a decrease in myocardial oxygen demand.