DECREASED CORONARY BLOOD-FLOW IS NOT RESPONSIBLE FOR MYOCARDIAL DYSFUNCTION DURING BUPIVACAINE-INDUCED CARDIOTOXICITY

Background. Although previous studies have shown that bupivacaine prod uces a dose-dependent vasoconstriction, the possible effects of decrea sed coronary blood now on myocardial dysfunction during bupivacaine-in duced cardiotoxicity have not been investigated. Methods. We carried o ut 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 oxyg en consumption was calculated using Fick's principle. Regional myocard ial function (systolic shortening: %SS, post-systolic shortening: %PSS ) of the LAD-supplied region was evaluated by the sonomicrometric tech nique. While saline or bupivacaine (10 mu g/ml) was continuously infus ed into the LAD in a crossover design, the effects of a vehicle (basel ine), acetylcholine (1 and 3 mu g/min), nitroglycerin (10 mu g/min) an d adenosine (10 mu g/ min) on coronary haemodynamics and regional myoc ardial function were evaluated. Results. 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 myoca rdial dysfunction was not reversed. There was a positive correlation b etween regional myocardial oxygen consumption and %SS in the whole stu dy. Conclusions. The results of this study indicate that the decrease in QLAD during bupivacaine-induced myocardial toxicity is not responsi ble for regional myocardial dysfunction, and, moreover, that it parall els a decrease in myocardial oxygen demand.