ccMETABOLIC DIFFERENTIATION OF CARDIAC MYOCYTES Christophe Montessuit, hiathalie Velin, IrPne Papageorgiou & Rem5 Lerch. Cardiology, University Hospital of Geneva. Switzerland.

The phenotypic dedifferentiation of adult rat cardiac myocytcs (ARC) in pf-irnary culture includci downregulation of the ins&-wnsitive &lCcl\~ transporter GLUT4 and of enzymes 01’ fatty acids metabolism. as well 3’; transient imutin reststance 9-h and all-tranr ( ATf retinoic acids {RA) are hear! morphogens and induce differenttation of vwiou~ cell types. RA restored GLUT4 protein and mRNA efxpression in ARC. The dose-response cww5 for GLUT4 protein expression showed 9-&s KA to be IW- fold more potent than ATRA. wggesting a role of retinoid X receptors (KXR) rather than retinoic acid receptor\ (KAR). However. 9-cis HA and ATRA were roughly quipotcnt in incwsing GLC’T4 mR.VA expression ‘ITCH, a selective RAR agonist. increased both GLIJT4 protein and mRNA expression. KA enhanced insulin cignaling and stimulation of gIucosc transpon in paniallk insulin-resistant ARC. RA also ilightly increased expression of the proteins of fatty acid oxidation MCAD. LCAD and VLCAD. Expression of a-w~ooth muscle win. a marker of dcdifferentiation and hypertrophy. NW increased by RA treatment. Thus RA-induced preservation of metabolic differentiation of cardiac myocqTcs is not necessarily associated with a mow differentiated contractile or morphological phenotype

ISCHAEMlC PRECOP(DiTIOWW POTEhTL~TES lIEA STRESS INDUCED CARBIOPROTECTION

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Conclusioas: PC Induced cardiopmtKbon ts mtated with d-reared aclrvatlon ofJ?% during r~prfus~on

MITOCHONDRIAL K*rpCHANNELS ARE POSSlBLE TRIGGERS OF ISCHEYtC PRECOHOlTtOWNG PROTECTIVE EFECf AGAtNST RPIPERNSION ARRRYTHM~AS Dantna M. Munmn, AJexmdru Cffrtgcu, Ovkftu flfwYI8dtrmacu, Dan Mthhula’, betal Llg#m?.an”. mmmnt ot Palhophy&ology. ‘Oqa8rIment d Pneumm, -v ol Muad sanwlogy. Unlvarrlty of Msdlclne ~14 PM-y, TImi-, Ronunla

The goes ol thth sttidy we:e lo evaluate the dntiarrtiythmlc role 01 IscherPlc precond#loning [IPC) and to lnvestlgate 11 the mdochondnal K.r- cha?nels arc poss~bls trlggsrtimedtators of Ihls effect Aneslhenzed. ~~~n~cnesteo rabbns were sdqecroa to one c! f&r protocol In group I (control). rabbits were su~lad to 30 mm reglonal Ischemm my cccludq a coronary artery lollowed by 45 ITIP. 01 reporfuson In Grwp 11, PC was al!ciled by 5 mln ccclusion plus :0 mm reperfuson pm to the test NEhemra. In group 111, a saloct~ua m1t0 KATP blocker, 5.ayaroqdecanoate (5-H@ was given as a bonus 5 rr@kg mtraventncularly 2 mm balore tha IPC episode and I” group IV tne same dose was ic‘tected 5 mm pnor ttx last IXhemta Iol:0wtng the IPC episode. We monrtorsd teed I or iI 01 !he ECG and we recorded the @D~Cardal mOnoph%ic aCtrOn potantl8ls (MAPS). The 1861 fschema el:c~ied maiignant tachyarrhy?hmlas In the contrd group with he time to mset between 17-25 mn and m the flrsl 3 minutes of reparfus~on IPC had anti-etiythrmc &act both agarnsi (schema and reparfu510~- arrhythmras and induced a shoRening or the xiron potential duratloo rAPD: 5YD giver, 2 TIC prior Ihe iPC aboished cardlopfotecttoll against reperlusron arrhylhmias. wrthout mfluencmg n6ittw the tnclderce 01 Ihe rschemfa reLaled atmythmias nor tha lschernla tnduced shonenmg of APD. Ftve rmn przor the test ly;hemta the antl-artiythmtc clfec! o! IPC was not stgnhcanrly tnfluenced by 5.WD Our resulls snow that mlto KarF are pos.slble mggera ot IPC card~o$rotective etiecr agalnsl repedus~on maucRd arrhylhmdas