Background: Hypothermia is cardioprotective, but it causes Ca(2+) loading and reduced function on rewarming. The aim was to associate changes in cytosolic Ca(2+) with function in intact hearts before, during, and after cold storage with or without cardioplegia (CP).
Methods and results: Guinea pig hearts were initially perfused at 37 degrees C with Krebs-Ringer's (KR) solution (in mmol/L: Ca(2+) 2.5, K(+) 5, Mg(2+) 2.4). One group was perfused with CP solution (Ca(2+) 2.5, K(+) 18, Mg(2+) 7.2) during cooling and storage at 3 degrees C for 4 hours; another was perfused with KR. LV pressure (LVP), dP/dt, O(2) consumption, and cardiac efficiency were monitored. Cytosolic phasic [Ca(2+)] was calculated from indo 1 fluorescence signals obtained at the LV free wall. Cooling with KR increased diastolic and phasic [Ca(2+)], whereas cooling with CP suppressed phasic [Ca(2+)] and reduced the rise in diastolic [Ca(2+)]. Reperfusion with warm KR increased phasic [Ca(2+)] 86% more after CP at 20 minutes and did not increase diastolic [Ca(2+)] at 60 minutes, compared with a 20% increase in phasic [Ca(2+)] after KR. During early and later reperfusion after CP, there was a 126% and 50% better return of LVP than after KR; during later reperfusion, O(2) consumption was 23% higher and cardiac efficiency was 38% higher after CP than after KR.
Conclusions: CP decreases the rise in cardiac diastolic [Ca(2+)] observed during cold storage in KR. Decreased diastolic [Ca(2+)] and increased systolic [Ca(2+)] after CP improves function on reperfusion because of reduced Ca(2+) loading during and immediately after cold CP storage.