274 BIOCHl!UICAL EVIDENCE FOR CARDIOPROTECTION BY R 51 469 AFTER 1 HOUR OF NOFMOTHERMIC GLOBAL ISCHEMIA IN DOGS. H. Van Belle, R. Xhonneux, W. Flameng. Janssen Pharmaceutics Research Laboratories, B-2340 Beerse, Belgium. Aortic clamping for 60 min was used as a means to induce global ischemia in 23 dogs in situ. Eleven animals served as controls, the others received 2.5 mpk of F 51 469 orally, two hours before the start of the experiment. Biopts of heart tissue were taken before clamping, at 59 min of ischemia and after reperfusion (from 1 min up to 30 min depending on the heart's function). In the control group 9 hearts failed within 12 min whereas in the treated animals 10 out of 12 survived for 25 min or more. All biopts were analyzed for inorganic phosphate and glycogen for CrP and A!CP (luminometry) and for nucleotides and (spectrophotometry), nucleosides (HPLC). The vast amount of data, thus produced, was analyzed using because of a relatively large scatter in the absolute values computer programs. differences between both groups were not apparent except for ATP, AMP and hypoxanthine content. However, when looking at several ratios, highly significant differences were noted all indicating that R 51 469, even during ischemia, maintains somehow a better energy status of the heart tissue. It became also apparent that several ratios are much more valuable in reflecting the heart's function than any absolute figure.
275THE ROLE OF COENZYME Qio FOR PRESERVATION OF MYOCARDIUM. J.Amano, T.Okamura, M.Sunamori, A.Suzuki. Department of Thoracic and Cardiovascular Surgery, Tokyo Medical and Dental University, Tokyo, Japan. electron Coenzyme Qlo(CoQlo) is known to act as a component of mitochondrial transport of oxidative phosphorylation and antioxidant to stabilize tissue lipids. This study was undertaken to characterize the relationship between tissue CoQlo, myocardial contractility and metabolism following global ischemia. 120 min of aortic cross-clamping was employed in 10 mngrel dogs under cardiopulmonary bypass and myocardial temperature was kept at 2O'C. Left.ventricular function (peak LVP, Max dp/ dt, LVEDP, CI, LVSWI), coronary blood flow, MVO2, myocardial enzymes (m-AST,CK-MB), and water content (WC) of the subendocardium myocardial ATP and creatine phosphate, Data was obtained at 60 min of reperfusion priod of the left ventricle were measured. Significant negative relati(R). CoQlo content of subendocardium was 240.&22.7pg/g. ons were obtained between CoQlo content and LVEDP(R=-0.8073, p(O.O2), WC(R=-0.7854, p
NONSIGNIFICANT MYOCARDIAL PROTECTION BY COENZYME Ql IN CORONARY BYPASS SURGERY. Takao Okamura, Makoto Sunam,ri, Jun Amano, Akio !?uzuki. Thoracic-Cardiovasc Surg., Tokyo Med & Dent. Univ., School of Med., Tokyo, Japan. This study was aimed to define the protective effect of pretreatment of coenzyme QlO(CoQ) on the heart in clinical open heart surgery in assessment of tissue CoQ content, serial myocardial enzyme release and cardiac function. 39 pts were selected at random in the cases operated upon by coronary artery bypass surgery(CABG). CoQ was given in 21 pts with 5 mg/kg IV a night before surgery and additional dose of 5 mg/kg IV at 2 hrs prior to cardiopulmonary bypass(CPB) comparing with 18 pts without lidocaine(lmg/min drip infusion) and aprotinin(lO,OOO treatment(C). In both groups, was performed under CPB with eKU/kg,IV, pretreatment) were added to CoQ. Operation cardioplegia associated with moderate systemic hypothermia. Tissue CoQ content was studied by sampling the right atria1 appendage taken just before CPB. Serum MB-CK and mitochondrial aspartate aminotransferase(m-AST)were examined at before CPB,0,6,18 hrs of reperfusion(R). Left ventricular stroke work index(LVSW1) was studied at before CPB,3,6,10 and 18 hrs in R. MB-CK at 6 hrs of R ws 22.2+2.5 IU(C) and 7.8+1.8(CoQ), pc.05. LVSWI at 6 hrs of R was 35.7+2.8 g.m/beat/m2(C) and 45.8+2.4(CoQ),p<.05. Dose of catecholamine in R was less in-CoQ than that in C. CoQ content was 4.350.5 pg/g(C) and 7.5+2.0 (CoQ),p<.O5. These results suggest that CoQ was in effective level by our pretreaEment to provide myocardial protection during CABG.