Hypothermic cardioplegia reduces the occurrence of spontaneous diastolic myofilament motion of the ischemic-reperfused rat heart

Spontaneous diastolic myofilament motion of the isolated ischemic-reperfused rat heart was studied by the technique of laser spectroscopy. Scattered light intensity fluctuations (SLIF) from the exposed surface of the left ventricle of the quiescent perfused (Langendorff) rat heart were quantified by the autocorrelation function (R1F: frequency weighted by power), and by determining the average power of the SLIF signal (PS). The stabilized mean control (±SE) R1F (mV2/s2) and PS (mV2/s) values were: 0.87±0.07 and 21.3±1.5 respectively. SLIF were characterized to index the extent of cell Ca2+-loading and the integrity of the sarcoplasmic reticulum (SR) functions by low Na+ and ryanodine perfusions. Low Na+ perfusion significantly increased the R1F values and produced pronounced spectral peaks between 0.5 and 2.5 Hz frequency bands; whereas ryanodine (1 μM) perfusion completely abolished the SLIF signals. Ischemia (34°C, 60 min.) produced nearly a 12-fold increase in the R1F and PS values accompanied by a four-fold increase in the left ventricular end-diastolic pressure (LVEDP) during the reperfusion period (34°C, 30 min.) Pronounced reperfusion SLIF peaks were evident at the frequency bands between 0.25–5.0 Hz. Hypothermic (10°C) preservation during ischemia reduced the frequency and the amplitude of the SLIF signals at various frequencies and prevented the rise in LVEDR. As compared to hypothermia alone, hypothermic cardioplegia offered a slightly better preservation. But hypothermia alone or in combination with cardioplegia failed to completely normalize the post-ischemic R1F and PS values. The results of this study indicate that hypothermic cardioplegia reduced the occurrence of spontaneous diastolic intracellular Ca2+ oscillations of the reperfused rat heart, but failed to completely normalize them.