Abstract
We tested the hypothesis that low pressure reperfusion following global ischemia compromises functional recovery in hearts compared with longer durations of ischemia and normal pressure reperfusion. Male Sprague-Dawley rats underwent heart excision, isolation and perfusion with bovine blood solution or Krebs-Henseleit buffer. Hearts were subjected to either twenty minutes of global ischemia with normal pressure (85 mm Hg) reperfusion (control) or 3 minutes of global ischemia followed by 17 minutes of low pressure (20 mm Hg) reperfusion before normal pressure reperfusion to model cardiopulmonary resuscitation (CPR). At the end of the reperfusion period, rate pressure product (RPP in mmHg/min) in both buffer- and blood-perfused hearts was noticeably compromised in CPR-modeled hearts as compared to control (buffer-perfused: RPP = 17,000 ± 1,873 (control) versus RPP = 6,733 ± 3,720 (CPR); blood-perfused: RPP = 8,037 ± 2,290 (control) versus RPP = 2,672 ± 900 (CPR)). Oxygen delivery was significantly depressed at the end of full reperfusion in CPR-modeled blood-perfused hearts as compared to control blood-perfused hearts. This data suggests greater damage in low pressure CPR-modeled hearts in comparison with hearts subjected to full reperfusion. This data also infers that CPR yielding very low perfusion pressure can inhibit functional recovery of the heart.
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