Hypoxic reperfusion limits functional impairment following cardioplegic arrest in isolated rat heart

Reperfusion injury decreases both systolic contractility and diastolic compliance. Several studies indicate that the sustained decrease in diastolic compliance is mainly due to reactive oxygen intermediates (ROI) generation and calcium overload.

Male Wistar isolated rat hearts were divided into 2 groups (n=10 each), perfused according to Langendorff technique and exposed to 45 min of ischemia. Hearts belonging to the first group were reperfused with Krebs-Henseleit solution at 600 mmHg pO2; a 150 mmHg pO2 perfusate was utilized in the second group during the first minute and switched to 600 mmHg pO2 thereafter. Modifications in diastolic compliance and systolic contractility were assessed by changes in left ventricular end-diastolic (LVEDP) and developed pressure (LVDP), and first derivative of the pressure curve (dP/dt).

Increase in LVEDP values, with respect to pre-ischemic data, were detected at 1, 5, 10, 20 min following reperfusion at 600 mmHg pO2, and were respectively: +40.17+/-18.61, +57.5+/-28.8, +59.8+/-30.5 and +63.2+/-34.1 mmHg. At 150 mmHg pO2 they were: +15.69+/-13.13, +22.4+/-14.1, +26.2+/-13.7 and +28.9+/-15.8, with a significant difference within the first 20 min (p<0.05). At high pO2 levels, LVDP decreased of 53.0+/-27.35, 60.5+/-22.6, 59.8+/-23.3 and 50.7+/-25.0 mmHg, versus 42.7+/-25.7, 38.0+/-29.5, 39.2+/-30.9 and 38.7+/-32.7 mmHg at lower pO2 (p=NS). The correspondent values of the dP/dt were 37.8+/-27.7, 30.1+/-17.2, 32.2+/-13.6 and 35.4+/-14.0% of pre-ischemic values at high pO2, versus 43.3+/-27.09, 51.9+/-25.1, 50.1+/-24.6 and 53.1+/-29.9% at lower pO2. Statistical significance was lower for LVDP and dP/dt than LVEDP.

Diastolic functional impairment was partially reduced within the first 20 min following low pO2 reperfusion, but without any significant improvement of contractility.