Optimal pressure for low pressure controlled reperfusion to efficiently protect ischemic heart: an experimental study in rats.

Recent work has demonstrated the benefit of low pressure (LP) reperfusion to protect the heart undergoing an ischemic insult. The goal of the present study was to determine the optimal pressure for the application of LP reperfusion. Isolated rats hearts (n = 30) were exposed to 40 minutes of global warm ischemia followed by 70 minutes of reperfusion with a pressure fixed at 100 cm H(2)O (normal pressure [NP] = control group), 85 cm (group LP [low pressure]-85), 70 cm (group LP-70), or 55 cm (group LP-55). Cardiac function was assessed during reperfusion using the Langendorff model. Myocardial necrosis was assessed by measuring lactate dehydrogenase (LDH) and creatine kinase (CK) leakage in the coronary effluents. Functional recovery was progressively and significantly improved with decreased perfusion pressure. Rate-pressure product (RPP) averaged 3765 +/- 408, 6824 +/- 439, and 12,036 +/- 664 mm Hg/min, respectively, among the control, LP-85, and LP-70 groups (P < .001, LP-70 vs other groups). However, RPP collapsed in the LP-55 group. Similarly, necrosis as measured by LDH and CK leakage progressively reduced between LP-100 and LP-70 hearts (P < .01), with a drastic increase in enzyme in the LP-55 group. In conclusion, this study demonstrated that 70 cm H(2)O is an optimal LP to improve postischemic contractile dysfunction and attenuate necrosis during reperfusion.

Optimal time duration for low-pressure controlled reperfusion to efficiently protect ischemic rat heart.

Previous studies have shown the capacity of low-pressure (LP) reperfusion to protect the ischemic heart. The present study sought to determine the optimal time for the application of LP reperfusion. Isolated rat hearts (n = 30) were exposed to 40 minutes of global warm ischemia followed by 70 minutes of reperfusion. Reperfusion was performed under LP (LP = 70 cm H(2)O) for 0 (control group), 5 (group LP-5), 10 (group LP-10), 30 (group LP-30), or 60 (group LP-60) minutes. Following the LP period the hearts were reperfused with normal pressure (100 cm H(2)O) until the end of reperfusion. Cardiac function was assessed during reperfusion using the Langendorff model. Myocardial necrosis was assessed by measuring LDH leakage in the coronary effluents. Functional recovery was reduced among the control and LP-5 groups with rate-pressure products (RPP) averaging 3788 +/- 499 and 5333 +/- 892 mm Hg/min, respectively. RPP was significantly improved in other groups with RPP averaging 7363 +/- 1159, 7441 +/- 863, and 7269 +/- 692 mm Hg/min in LP-10, LP-30, and LP-60 (P < .01). Similarly, necrosis measured by LDH leakage was significantly reduced in LP-10, LP-30, and LP-60 hearts (P < .01). This study demonstrated that LP reperfusion improves postischemic contractile dysfunction and attenuates necrosis when applied for at least 10 minutes.