Halothane reduces dysrhythmias and improves contractile function after global hypoperfusion in isolated hearts.
We investigated the effects of halothane on changes in cardiac function during hypoperfusion and recovery of function after reperfusion in the isolated perfused guinea pig heart. Heart rate, atrioventricular (AV) conduction time, the incidence and severity of dysrhythmias, and isovolumetric left ventricular systolic pressure (LVSP) and its derivative were measured. Hearts (n = 85) were divided into three groups for 30 min of perfusion at 0% (no flow), 10%, and 25% of the control perfusion pressure (PP, 55 mm Hg). These groups were subdivided and exposed to 0%, 0.74% (0.23 +/- 0.01 mM), or 1.65% (0.51 +/- 0.01 mM) halothane 10 min before, during, and 10 min after hypoperfusion. Hypoperfusion was followed by 40 min of reperfusion at control PP. Exposure to 0.74% and 1.65% halothane before hypoperfusion produced a 9% and 13% decrease in heart rate, a 2% and 30% increase in AV conduction time, and a 25% and 51% decrease in LVSP and dLVP/dtmax, respectively. During the 30 min of hypoperfusion, heart rate decreased and AV conduction time increased; second- and third-degree AV block occurred in all hearts in the 0% and 10% PP groups, but only in some hearts in the 25% PP groups. Left ventricular systolic pressure rapidly decreased during hypoperfusion in all groups. During early reperfusion ventricular fibrillation and ventricular tachycardia occurred in the 0% and 10% PP groups but not in the 25% PP groups. During reperfusion 0.74% and 1.65% halothane greatly reduced the duration of ventricular fibrillation from 8.1 +/- 3.3 min to 1.5 +/- 0.8 and 1.9 +/- 1.2 min in the 0% and 10% PP groups, respectively. A concentration of 0.74% halothane increased the incidence of supraventricular tachycardia on reperfusion in the 10% group (from a control of 20% to 65%), and 1.65% halothane increased the duration (2.6 +/- 2.5 min) and incidence (38%) of supraventricular tachycardia on reperfusion in the 0% PP group. A concentration of 1.65% halothane facilitated recovery of LVSP after hypoperfusion in the 25% group but not in the 0% and 10% PP groups. These results indicate that halothane, in some instances, can have protective cardiac effects after graded hypoperfusion as assessed by improved contractility and by reduced severity of some dysrhythmias during reperfusion; however halothane may also increase the incidence of supraventricular tachycardia. The cardiac protection by halothane could be a result of reduced cardiac work before, during, and after hypoperfusion, or of some other direct protective cellular effects.
Buljubasic
N
N
Department of Anesthesiology, Medical College of Wisconsin, Milwaukee 53226.
Marijic
J
J
Stowe
D F
DF
Kampine
J P
JP
Bosnjak
Z J
ZJ
D000818:Animals; D001283:Atrioventricular Node / Q000187:drug effects / Q000502:physiology; D002316:Cardiotonic Agents / Q000494:pharmacology*; D003326:Coronary Circulation / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D006168:Guinea Pigs; D006221:Halothane / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects* / Q000502:physiology; D006339:Heart Rate / Q000187:drug effects*; D066298:In Vitro Techniques; D009200:Myocardial Contraction / Q000187:drug effects*; D015425:Myocardial Reperfusion / Q000379:methods*; D010477:Perfusion; D013610:Tachycardia / Q000188:drug therapy; D013617:Tachycardia, Supraventricular / Q000188:drug therapy; D013997:Time Factors; D014693:Ventricular Fibrillation / Q000188:drug therapy; D016277:Ventricular Function, Left / Q000187:drug effects
D002316:Cardiotonic Agents; D006221:Halothane