Decreased regional contractility in nonischemic myocardium during acute coronary artery occlusion in conscious pigs.
The purpose of this study was to use the relationship between end-systolic left ventricular pressure and segment length to assess the inotropic state of nonischemic myocardium during acute coronary artery occlusion in the conscious pig. Eight pigs were chronically instrumented with sonomicrometers to measure midwall segmental shortening and a micromanometer to measure left ventricular pressure. Occlusion of the inferior vena cava with a pneumatic occlusive cuff caused transient decreases in left ventricular pressure so that the relationship of left ventricular pressure and segment length at end systole could be determined over a range of pressures. In preliminary studies using open-chest pigs, this relation was shown to be highly linear and best quantified using a calculated segment length at a left ventricular pressure of 100 mm Hg (ESL100). During acute, 1-min occlusion of the left anterior descending coronary artery, the ESL100 of the nonischemic lateral and posterior walls was significantly increased from 8.75 +/- .18 mm to 9.64 +/- .21 mm (mean +/- SD, p less than .01), indicating a decreased inotropic state. Similarly, during occlusion of the left circumflex coronary artery, the ESL100 of the nonischemic anterior wall increased from 8.44 +/- 2.53 mm to 9.26 +/- 3.12 mm (p less than .05). This was not associated with a change in the amount of shortening during systole. Pharmacological autonomic blockade using atropine and propranolol failed to alter the response of nonischemic zones to acute coronary artery occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)
Guth
B D
BD
Department of Medicine, University of California, San Diego.
White
F C
FC
Widmann
T
T
Lew
W
W
Bloor
C M
CM
D000818:Animals; D001158:Arteries / Q000473:pathology / Q000503:physiopathology; D003327:Coronary Disease / Q000473:pathology / Q000503:physiopathology*; D003331:Coronary Vessels / Q000473:pathology / Q000503:physiopathology*; D004195:Disease Models, Animal; D006321:Heart / Q000503:physiopathology*; D006439:Hemodynamics; D009200:Myocardial Contraction; D013552:Swine