Propofol attenuates ischemia-reperfusion injury in the isolated rat heart

The purpose of this study was to examine the direct effects of propofol on ischemia-reperfusion injury using an isolated Langendorff rat heart preparation. Hearts were perfused with Krebs-Henseleit (K-H) solution (control); intralipid; or 10, 30, and 100 microM propofol. Hearts were rendered globally ischemic for 25 min, then reperfusion was begun with K-H solution for 30 min. Treatment with 100 microM propofol delayed the onset of contracture during ischemia compared with control or intralipid treatments (6.4 +/- 2.1 vs 4.4 +/- 1.4 or 4.1 +/- 0.7 min, respectively; P < 0.05). During reperfusion, 100 microM propofol increased coronary flow and reduced lactate dehydrogenase release compared with control or intralipid treatments. After 30 min of reperfusion, left ventricular developed pressure (LVDP) returned to 55 and 76 mm Hg in the 30 and 100 microM propofol-treated groups, respectively, whereas LVDP was 39 mm Hg in the control group. The hearts treated with 100 microM propofol showed significantly lower left ventricular end-diastolic pressure compared with the control or intralipid groups 30 min after reperfusion (29 +/- 13 vs 48 +/- 5 or 48 +/- 11 mm Hg, respectively; P < 0.05). In histological evaluation, control and intralipid hearts had increased injury severity scores compared with hearts treated with 100 microM propofol (1.8 +/- 0.9 and 1.7 +/- 0.8 vs 1.0 +/- 0.7, respectively; P < 0.05). In conclusion, we suggest that propofol administered before and during global myocardial ischemia has cardioprotective effects on ischemia-reperfusion injury.

It is important to protect the heart from injury by ischemia and reperfusion. The current study demonstrates that in the isolated rat heart, propofol attenuates mechanical, biochemical, and histological changes causes by ischemia and reperfusion.