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1 Anesthesiology Research Laboratories, Departments of Anesthesiology and Physiology, and Cardiovascular Research Center, The Medical College of Wisconsin, Milwaukee 53226; and 2 Research Service, Veterans Affairs Medical Center, Milwaukee, Wisconsin 53295
Ca+ loading during reperfusion after
myocardial ischemia is linked to reduced cardiac function. Like
ischemic preconditioning (IPC), a volatile anesthetic given
briefly before ischemia can reduce reperfusion injury. We
determined whether IPC and sevoflurane preconditioning (SPC) before
ischemia equivalently improve mechanical and metabolic
function, reduce cytosolic Ca2+ loading, and improve
myocardial Ca2+ responsiveness. Four groups of guinea pig
isolated hearts were perfused: no ischemia, no treatment before
30-min global ischemia and 60-min reperfusion (control), IPC
(two 2-min occlusions) before ischemia, and SPC (3.5 vol%, two
2-min exposures) before ischemia. Intracellular
Ca2+ concentration ([Ca2+]i) was
measured at the left ventricular (LV) free wall with the fluorescent
probe indo 1. Ca2+ responsiveness was assessed by changing
extracellular [Ca2+]. In control hearts, initial
reperfusion increased diastolic [Ca2+] and diastolic LV
pressure (LVP), and the maximal and minimal derivatives of LVP
(dLVP/dtmax and
dLVP/dtmin, respectively), O2
consumption, and cardiac efficiency (CE). Throughout reperfusion, IPC
and SPC similarly reduced ischemic contracture, ventricular fibrillation, and enzyme release, attenuated rises in systolic and
diastolic [Ca2+], improved contractile and relaxation
indexes, O2 consumption, and CE, and reduced infarct size.
Diastolic [Ca2+] at 50%
dLVP/dtmin was right shifted by 32-53 ± 8 nM after 30-min reperfusion for all groups. Phasic
[Ca2+] at 50% dLVP/dtmax was not
altered in control but was left shifted by 
235 ± 40 nM
[Ca2+] after IPC and by 135 ± 20 nM
[Ca2+] after SPC. Both SPC and IPC similarly reduce
Ca2+ loading, while augmenting contractile responsiveness
to Ca2+, improving postischemia cardiac function
and attenuating permanent damage.
experimental; cellular; pathophysiology; acidosis; contractile function
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