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Decreased coronary blood flow is not responsible for myocardial dysfunction during bupivacaine-induced cardiotoxicity
1Department of Anesthesiology, Kawasaki Medical School, Kurashiki-City, Japan.
Insights
Bupivacaine causes cardiotoxicity by decreasing coronary blood flow and myocardial oxygen demand, not by impairing regional myocardial function. This study investigated bupivacaine
Area of Science:
- Cardiovascular Pharmacology
- Anesthesiology
- Cardiac Physiology
Background:
- Bupivacaine is known to cause dose-dependent vasoconstriction.
- The impact of reduced coronary blood flow on myocardial dysfunction during bupivacaine-induced cardiotoxicity remains unclear.
Purpose of the Study:
- To investigate the role of decreased coronary blood flow in bupivacaine-induced cardiotoxicity.
- To determine if reduced coronary blood flow contributes to regional myocardial dysfunction.
Main Methods:
- Utilized in situ beating beagle hearts with an autoperfusion circuit to the left anterior descending coronary artery (LAD).
- Measured LAD blood flow (QLAD) and calculated myocardial oxygen consumption using Fick's principle.
- Assessed regional myocardial function (% systolic shortening, % post-systolic shortening) via sonomicrometry during bupivacaine infusion.
Main Results:
- Bupivacaine infusion decreased QLAD and induced regional myocardial dysfunction (reduced %SS, increased %PSS).
- Acetylcholine and adenosine increased QLAD but did not reverse myocardial dysfunction.
- A positive correlation was observed between regional myocardial oxygen consumption and %SS.
Conclusions:
- Decreased coronary blood flow (QLAD) during bupivacaine cardiotoxicity does not cause regional myocardial dysfunction.
- The observed decrease in QLAD parallels a reduction in myocardial oxygen demand.
- Bupivacaine-induced cardiotoxicity's mechanism is not solely explained by reduced coronary blood flow.
Background:
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.
Methods:
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.
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 myocardial dysfunction was not reversed. There was a positive correlation between regional myocardial oxygen consumption and %SS in the whole study.
Conclusions:
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.