Lysolecithin and experimental acute myocardial ischaemia

77 Lysolecithin and Experimental Acute R.A.Riemersma and B. Michorowski. Myocardial Ischaemia. Cardiovascular Research Unit, University of Edinburgh, U.K. and Postgraduate Medical School, Warsaw, POLAND. Lysolecithin extraction by the heart was examined in an open-chest anaesthetised dog model (n = 6). Acute myocardial ischaemia was induced by ligation of the left anterior descending coronary artery (Occl), Blood samples were collected simultaneously from the femoral artery (A), coronary sinus (CS) and from local vein (LV), draining the predominantly ischaemic myocardium, before and at 2, 6, 10, 15 and 20 min of Occl. Before Occl the percentage of the lysoform of lecithin (% lysolecithin) was higher in A than in LV and CS, compatible with 27 * 11 and 45 2 16 % extraction of A lysolecithin by the normoxic heart respectively (PtO.O1). Following Occl, A-LV and A-CS difference of % lysolecithin deminished in S/6 experiments. Ischaemia may therefore activate myocardial phospholipase both in the ischaemic and nonischaemic areas. However, resultant alteration in venous effluent plasma lysolecithin from 0.25 to 0.32 mmol/l is difficult to quantify, and is much lower than those inducing electrophysioloqical changes in superperfused canine Purkinje fibers and rabbit papilliary muscles. These results question the validity of previous in -- vitro work where electrophysioloqical abnormalities were induced by lysolecithin (3 mmole/l).

EFFECT OF c1AND@ADRENERGICBLOCKINGAGENTSON RELEASEOF MYOCARDIAL NOREPINEPHRINE AND VENTRICULARARRYTHMIASFOLLOWINGREPERFUSIONOF THE ISCHEMIC IS$LATED WORKING+RAT HEART. ~ L&*ROCHETTE, J.P. DIDIER , D. MOREAU, J. BRALET* and L.H. OPIE'! *University of Cape Town - Afrique du Sud Facultes de Medecine et de Pharmacie - DIJON - France Supported by a grant from DGRST. (80.7.0399). Isolated working rat hearts were prelabeled with 3H norepinephrine (NE) and submitted to coronary artery ligation during 10 min. In control preparations reperfusion was accompanied by a sudden release of radioactivity and long lasting ventricular arrhythmias. Reperfusion arrythmias (RA) were prevented by perfusion medium containing a high dose of Acebutolol (40 mq/l) or d Propranolol (4 mq/l). In return, Atenolol (40 mq/l) was ineffective in reducing the incidence of RA. In our model, Nicerqoline (2 mg/l) or Phentolamine (2 mg/l) were effective preventing RA but not an other c1blocking agent ; Prazosine (2 mq/l). Addition of Acebutolol, d Propranolol or c1blocking agents to perfusion liquid was accompanied by an increase of spontaneous release of 3HNE in the coronary effluent. The present results indicate that it is the membrane stabilisinq effects of Acebutolol which are preventing the RA. Concerning the antiarrhythmic effect of Nicerqoline and Phentolamine, it is not clear whether this is an effect of c1 blockade or a direct membrane effect of these drugs.