with EL (p<0.007) and ca. 69% in the KH buffer-treated group(p<0.007). Q10-L may provide an effective exogenous sourceof coenzyme Q10 in vivo to protect ischemically damagedmyocardium.

Keywords: Coenzyme Q10; Liposomes; Ischemia

doi:10.1016/j.yjmcc.2007.03.648

Protective effect of ocotillol on acute myocardial injuryinduced by LAD in ratChen Yu, Fenghua Fu, Xin Yu, Mei Zhu. Department ofPharmacology, School of Pharmacy, Yantai University, Yantai,264005, China

Ocotillol is a ginsenoside-derivate in gastrointestinal tract invivo or alkaline degradation product from ginsenoside F11 invitro. So far, there are no data available in the literature withregard to the cardioprotective effect of ocotillol. In this studythe effect of ocotillol on acute myocardial ischemia wasinvestigated.

Male Sprague–Dawley rats (150±20 g) were randomlydivided equally into six groups including control, model, pro-pranolole groups and treatment groups at three different doses.Acute myocardial ischemia model was performed with leftanterior descending (LAD) occlusion in rat heart. The effects ofocotillol on myocardial infarction and the activity of LDH inserum of rats with myocardial ischemia were observed. Theglass-slide method was used to determine the clotting-time ofmice.

The results showed that the myocardial ischemia extent andthe level of LDH in serum were markedly decreased by ocotillolin dosage of 5 mg/kg, 10 mg/kg and 20 mg/kg, ocotillol at doseof 5 mg/kg and 10 mg/kg could significantly prolong theclotting-time of mice.

It suggests that octillol has a protective action on myocardialischemia.

Keywords: Cardiovascular diseases; Myocardial ischemia;Cardioprotective

doi:10.1016/j.yjmcc.2007.03.649

The reduction in infarct size produced by cannabinoids inrats in vivo is mediated by CB2-receptorsDaniel Lamontagne, Philippe Lepicier. Faculty of Pharmacy,University of Montreal, Canada

Cannabinoids have been shown to exert marked cardiopro-tective effects in ischaemic hearts, in terms of reduced infarctsize, fewer arrhythmias, and improved post-ischaemic ventri-cular recovery. However, controversies remain on the receptorsinvolved in these effects, whether they are CB1, CB2, or novel

cannabinoid sites of action. The objective of the present studywas to assess the contribution of CB1 and CB2 receptors in thecardioprotective effects of a non-selective cannabinoid agonistin anaesthetised rats.

The non-selective cannabinoid agonist CP55940 (0.1 mg/kgiv) induced a marked reduction in blood pressure (by 42%),which significantly reduced the rate-pressure product. Infarctsize, measured by TTC staining after 30 min of LAD coronaryocclusion and 60 min reperfusion, was reduced by 37%(p<0.05, n=9) in CP55940-treated rats. The CB1-receptorantagonist, AM251 (1 mg/kg ip), partially prevented the re-duction in blood pressure and rate-pressure product induced byCP55940, but had no effect on its ability to reduce infarct size.In contrast, CP55940 was no longer able to reduce infarct size inthe presence of the CB2-receptor antagonist, SR144528 (1 mg/kg ip), despite a similar reduction in blood pressure and rate-pressure product.

In conclusion, although the hemodynamic effects of canna-binoids are mediated mainly by CB1-receptors, CB2-receptorsare involved in the cardioprotective effects of cannabinoids inrats in vivo.

Keywords: Cannabinoids; Myocardial infarction; Rats in vivo

doi:10.1016/j.yjmcc.2007.03.650

Ceiling of cardioprotection with the pharmacologicalpostconditioning induced by the phytoestrogen genisteinN. Couvreur, R. Tissier, X. Waintraub, M. Gervais-Taurel, S.Pons, R. Zini, A. Berdeaux, B. Ghaleh. INSERM, U 841,Creteil, France

We previously demonstrated that estrogens are able toinduce a pharmacological postconditioning involving PI3K-Akt in rabbits subjected to 20 min of coronary arteryocclusion (CAO). The goal of this study was to investigatewhether such a protection is subjected to a ceiling ofcardioprotection when the duration of ischemia is extended.Accordingly, pentobarbital-anesthetized male rabbits under-went either a 20 min (protocol A) or a 30 min CAO (protocolB) followed by 4 h of coronary artery reperfusion (CAR).Prior to CAR, animals randomly received an i.v. injection ofeither saline (Control), 100 or 1000 μg/kg of genistein(Geni100 and Geni1000, respectively), and 10 or 100 μg/kgof 17β-estradiol (17β10 and 17β100, respectively). Theselow doses of genistein were used in order to avoid tyrosinekinases inhibition. Myocardial infarct size (IS) was measuredby triphenyltetrazolium chloride staining and expressed aspercentage of the area at risk. In protocol A, IS wassignificantly reduced in Gen100 (n=5), Gen1000 (n=5)and 17β100 (n=6) but not in 17β10 (n=5) vs. Control(n=9) (5±2, 13±5, 11±3 and 28±8% vs. 35±5%, respec-tively). In protocol B, IS did not decrease significantly inGen100 (n=8), Gen1000 (n=5), 17β100 (n=5) and 17β10(n=9) vs. Control (n=11) (46±4, 55±6, 51± , 47±6% vs. 54±

S215ABSTRACTS / Journal of Molecular and Cellular Cardiology 42 (2007) S190–S218