Differences in ischaemic dysfunction after gradual and abrupt coronary occlusion: effects on isovolumic relaxation.
The effects of both gradual and abrupt coronary occlusion on regional wall function (sonomicrometry) and left ventricular relaxation were studied in the intact dog heart. The ischaemic dysfunction observed in the two interventions as assessed by pressure-length loops showed considerably different patterns. The regional ischaemia after abrupt occlusion of the left anterior descending coronary artery was characterised by a bulge during isovolumic relaxation in contrast to the pattern observed during gradual occlusion, which was characterised chiefly by early systolic lengthening and post-systolic shortening. The effect of regional dysfunction on left ventricular relaxation was evaluated using peak negative dP/dt and tau, the time constant of isovolumic pressure decline. Abrupt occlusion had a more profound effect on relaxation than did gradual occlusion, though there were no significant changes in either pressure or flow derived indices of systolic ventricular function with abrupt occlusion of the left anterior descending artery. Two distinct patterns of regional dysfunction were produced at zero coronary flow depending on the time course of the occlusion. The regional dysfunction observed during abrupt occlusion may in part be explained by the mechanical effect of abrupt cessation of coronary flow, which in turn influences relaxation. With gradual occlusion tau was less affected even though substantial regional dysfunction was observed. This may reflect the development of collateral flow. Thus the patterns of regional dysfunction and ventricular relaxation depend on the time course of ischaemia.
Doyle
R L
RL
Nuffield Department of Anaesthetics, Radcliffe Infirmary, University of Oxford.
Foëx
P
P
Ryder
W A
WA
Jones
L A
LA
D000818:Animals; D001157:Arterial Occlusive Diseases / Q000503:physiopathology*; D003326:Coronary Circulation; D003327:Coronary Disease / Q000503:physiopathology*; D004285:Dogs; D006321:Heart / Q000503:physiopathology*; D006352:Heart Ventricles / Q000503:physiopathology; D006439:Hemodynamics; D009200:Myocardial Contraction; D013997:Time Factors