Characterisation of the excitation-contraction coupling system of the hypothermic myocardium following ischaemia and reperfusion.

The excitation-contraction coupling system of the globally ischaemic, hypothermic myocardium (60 min at 10 to 16 degrees C; I, n = 7) was studied by evaluating the functional integrity of the sarcoplasmic reticulum (SR) and the myofibrils (M). Comparison was made to the identical model followed by reperfusion (R, n = 7) and to sham-operated, time-matched controls (C, n = 7). Calcium uptake velocity from both the 60 min ischaemic group (I) and the reperfusion group (R) was significantly depressed (c = 0.960 +/- 0.05, I = 0.535 +/- 0.033, R = 0.662 +/- 0.035 micromolCa2+ . mg-1 . min-1, P less than 0.01). In contrast, SR . CA2+-ATPase activity was not affected by the hypothermic, ischaemic process (C = 1.150 +/- 0.08, I = 1.338 +/- 0.199 mumol Pi . mg-1 . min-1) but exhibited a small, significant depression after reperfusion (R = 0.940 +/- 0.04 mumol Pi . mg-1 . min-1, P less than 0.05). Myofibrillar pCa-ATPase curves in both experimental groups were significantly depressed (maximal ATPase activity: C = 0.18 +/- 0.01, I = 0.125 +/- 0.005, R = 0.115 +/- 0.01 mumol Pi . mg-1 . min-1; P less than 0.01). Kinetic analysis of the myofibrillar pCa-ATPase data, utilising double reciprocal plots, demonstrated an increase in injury in the hypothermic myocardium results from a breakdown of those subcellular structures responsible for the maintenance of the excitation-contraction coupling system. The ischaemic period, rather than reperfusion seems to be the major contributing factor in this sequence of pathological events.