A possible mechanism of ventricle fibrillation

56 FEEDBACK REGULATION OF ENDOGENOUS LIPOLYSIS H. Stam & W.C. Hiilsmann, Dept. of Biochemistry P.O.Box 1738, Rotterdam, The Netherlands.

IN LIPID-ENRICHED RAT HEARTS I, Erasmus University

The rate of endogenous triglyceride (TG) hydrolysis, providing fatty acids (FA) for energy metabolism, is controlled by numerous factors, e.g. catecholamines, exogenous substrates, fasting and diabetes. The TG stores in normal hearts are only limited available during perfusion and therefore endogenous lipolysis was studied in TG-enriched hearts obtained from rats fed for 3 days with 50 cal% of a 2:l mixture of trierucate and sunflower oil. Hydrolysis of endogenous TG during in vitro perfusion was determined as glycerol and FA release and lactate production was used as a marker for glycogenolysis. We observed that a) basal and glucagon-stimulated glycerol release is enhanced in TGenriched hearts, while FA release was low and not affected by glucagon, b) stimulation of FA oxidation by dinitrophenol leads to an increase in glycerol release, and c) inhibition of basal and glucagon-stimulated glycogenolysis by 5gluconolactone during substrate-free perfusion is followed by a marked inhibition of endogenous TG hydrolysis, which was partially restored by the addition of 11 mM glucose. endogenous TG hydrolysis is Our experiments indicate that myocardial subject to product inhibition and is regulated by the removal of the liberated FA as a consequence of increased rates of 8-oxidation and reesterification.

STEENWIJK, R. van and SCHNEIDER, if. Laboratory for Medical Physics, Faculty Free University, Van der Bocchorststraat -6 Dossiblc

mechanism

of vcntriclc

The rosfarch of vcntriclc perfusion system. Fibrillation

of Mcaicinc 7, 1081 BT

Amsterdam

fibrillation. fibrillation is initiated

is

carried by means

out on RR isolated of a weak current

First, a film of the phenomenon will bc shorn, after which, succession of the contraction patterns will bc msdc visible Yapping these contractions gives a basis for B hotter insight ions and their mutual interaction. 3econdly. a rcscarch program is discussed conccminr: ncrpcndicular to the ventricle wall during vcntriclc fibrillation wavcfronts cover the entire thickness
dog's heart of 50 Hz.

by Langendorff's

using marking points and to the human cyc. in the pathway process

the correlation fibrillation, of the wall

slow

If

motion,

the

ttc

contract-

of the clcctricai activations, from which will a?piar that the and pass the registration points in

Thirdly, intreccllular registrations will bc shown of intact. fibrillotine hcnrts, iwintcd vcntr:clo walls and parts thcrcof. From thcsc registrations it appears that the fern: of thcsc intrnccllular complcxcs aren't by far &B random BS is usually supposed, but mny bc divided in two definite classes, whereas the decrcasc of the quantity of the fibrillating miss is followed by 8n increasing rcpularity sf thcsc intracellular complcxcs. Thcsc results are in accordance with those of Carry, Levis, Hoffman and Crulcficld 11s well as Alcssic and Van Capelle (The ralc of ccl1 coupling in the synchronisntion and conduction of thc.cardial impulse). ?rom thcsc results, a preliminary model The fibrillation phcnomcnon may bc seen motions around moving vortices.

may bc acrivcd as 8n intricotc

BS follows: ~8.m~ of scvcral

mutually

intc rfcrinr

circular