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

3%, respectively). In additional experiments, pre-ischemicadministration of 17 β-estradiol reduced IS following 30 minCAO. In conclusion, estrogens administered prior to reperfu-sion induce a cardioprotection that vanishes when duration ofischemia is increased, i.e., demonstrating a “ceiling” effectcontrasting with their preventing effect.

Keywords: Cardioprotection; Infarct size; Pharmacology

doi:10.1016/j.yjmcc.2007.03.651

Adequate pre-ischemic myocardial glycogen content iscritical for ischemic preconditioning effectJ.S. Seo1, H.-d. Kim2. 1Dept of Forensic Medicine, Nat'l InstSci Invest, Seoul. 2Dept of Anatomy Cardiovasc Res Unit,SKKU School of Medicine, Suwon, Korea (South)

Effect of pre-ischemic myocardial glycogen content (PMGc)on ischemic preconditioning (IPC) has not been well docu-mented. To assess the effect of low or high PMGc before IPCand subsequent long period of ischemia (I), left ventricle func-tion (LVF), infarct size, ADP/ATP, lactate production, proteinkinase C (PKC) and KATP channel were considered in isolatedLangendorff-perfused rabbit heart. Hearts received 45-min Ifollowed by 120-min reperfusion (R) with IPC (n=10, 3 cyclesof 3-min I and 2-min R) or not (n=9). IPC increased LVFrecovery (p<.05) and reduced the infract size (mean±SEM,from 38.0±2.3 to 14.2±2.5% of the left ventricle, p<.01). IPCincreased membrane PKC activity (from 1.25± .14 to 2.01±.11 nmol/g tissue, p<.05) and expression of membrane εPKCand Kir6.2 protein (37 kDa) of KATP channel, but ADP/ATP andlactate production were not significantly different betweengroups. However, IPC effects were abolished by concurrent lowPMGc (n=10, 10.03± .50 mmol/g tissue, by 5 mg/L sodiumacetate, p<.05 vs. baseline PMGc, 15.87± .63 mmol/g tissue)or high PMGc (n=10, 23.49±1.37 mmol/g tissue, by 1 unit/Linsulin, p<.01 vs. baseline) before IPC. It is likely that anadequate PMGc is critical for the cardioprotective effect of IPC.Low or high PMGc before IPC could not activate IPC-mem-brane εPKC-KATP channel signal pathway.

Keywords: Preconditioning; Infarct size; Protein kinase C

doi:10.1016/j.yjmcc.2007.03.652

Effect of hydroxysafflor yellow a combined withnitroglycerin on acute myocardial infarctionT. Wang, F. Fu, B. Han, X. Yu, M. Zhu, L. Zhang. School ofPharmacy, Yantai University, 264005, China

Previous studies from our laboratory showed that HSYAsignificantly reduced the myocardial infarct size. The aim of thisstudy is to evaluate effect of HSYA combined with nitroglycerin

on acute myocardial infarction. Fifty SD rats were randomlydivided into five groups with ten rats in each group: controlgroup (NS 1 ml/100 g), model group (NS 1 ml/100 g), HSYAgroup (10 mg/kg), nitroglycerin (NTG) group (0.3 mg/kg) andHSYA+NTG group (10 mg/kg+0.3 mg/kg). After the left an-terior descending branch of the coronary artery ligation exceptthe sham group the rats were administered immediately the drugby intraperitoneal injection. Six hours later, the myocardialinfarct size (MIS), creatine kinase activity (CK-MB), endothe-lial nitric oxide synthase activity (eNOS), superoxide dismutaseactivity (SOD), malondialdehyde content (MDA), nitric oxidecontent (NO) were measured. The results showed that HSYA,NTG had significant cardioprotective effects. Compared withHSYA group or NTG group, the rats treated with HSYA andNTG produced a marked reduction in MIS (P<0.01). HSYAand NTG significantly inhibited the elevation of the activity ofCK-MB and the content of MDA (P<0.05 or P<0.01). HSYAand NTG also showed an obviously capacity to increase theactivity of SOD, eNOS and NO content (P<0.05 or P<0.01).The findings suggested that the therapeutic action of HSYAcombined with NTG on acute myocardial infarction is betterthan treat with HSYA or NTG alone. (NO) was measured. Theresults showed that HSYA, NTG had significant cardioprotec-tive effects. Compared with HSYA group or NTG group, therats treated with HSYA and NTG produced a marked reductionin MIS (P<0.01). HSYA and NTG significantly inhibited theelevation of the activity of CK-MB and the content of MDA(P<0.05 or P<0.01). HSYA and NTG also showed anobviously capacity to increase the activity of SOD, eNOS andNO content (P<0.05 or P<0.01). The findings suggested thatthe therapeutic action of HSYA combined with NTG on acutemyocardial infarction is better than treated with HSYA or NTGalone.

Keywords: Hydroxysafflor yellow A; Nitroglycerin; Acutemyocardial infarction

doi:10.1016/j.yjmcc.2007.03.653

Cardioprotective actions of the novel adipocytokine visfatinDerek J. Hausenloy, Shiang-Yong Lim, Ajeev J. Paramanathan,Sean M. Davidson, Derek M. Yellon. The Hatter Institute,UCL, London, UK

In this study we investigated the cardioprotective potential ofthe novel adipocytokine, visfatin, which has been demonstratedto act as an insulin-mimetic and activate Akt. This protein ki-nase has been linked to closure of the mitochondrial perme-ability transition pore (mPTP), a channel whose opening at thetime of reperfusion mediates cell death. In this study we hypo-thesized that visfatin elicits cardioprotection through the inhi-bition of mPTP opening. Three different experimental modelswere used: (1) Using anesthetized C57BL/6 male mice sub-jected to in situ 30 min of myocardial ischemia and 120 min ofreperfusion, Visfatin (50pmol) given as an intravenous bolus at

S216 ABSTRACTS / Journal of Molecular and Cellular Cardiology 42 (2007) S190–S218