PROPOFOL ATTENUATES ISCHEMIA-REPERFUSION INJURY IN THE ISOLATED RAT-HEART

The purpose of this study was to examine the direct effects of propofo l on ischemia-reperfusion injury using an isolated Langendorff rat hea rt preparation. Hearts were perfused with Krebs-Henseleit (K-H) soluti on (control); intralipid; or 10, 30, and 100 mu M propofol. Hearts wer e rendered globally ischemic for 25 min, then reperfusion was begun wi th K-H solution for 30 min. Treatment with 100 mu M propofol delayed t he onset of contracture during ischemia compared with control or intra lipid treatments (6.4 +/- 2.1 vs 4.4 +/- 1.4 or 4.1 +/- 0.7 min, respe ctively; P < 0.05). During reperfusion, 100 mu M propofol increased co ronary flow and reduced lactate dehydrogenase release compared with co ntrol or intralipid treatments. After 30 min of reperfusion, left vent ricular developed pressure (LVDP) returned to 55 and 76 mm Hg in the 3 0 and 100 mu M propofol-treated groups, respectively, whereas LVDP was 39 mm Hg in the control group. The hearts treated with 100 mu M propo fol showed significantly lower left ventricular end-diastolic pressure compared with the control or intralipid groups 30 min after reperfusi on (29 +/- 13 vs 48 +/- 5 or 48 +/- 11 mm Hg, respectively; P < 0.05). In histological evaluation, control and intralipid hearts had increas ed injury severity scores compared with hearts treated with 100 mu M p ropofol (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 an d during global myocardial ischemia has cardioprotective effects on is chemia-reperfusion injury. Implications: It is important to protect th e heart from injury by ischemia and reperfusion. The current study dem onstrates that in the isolated rat heart, propofol attenuates mechanic al, biochemical, and histological changes causes by ischemia and reper fusion.