Effects of changes in afterload on regional wall motion in acute ischemic canine heart.
The aim of the present study was to examine effects of changes in afterload on regional myocardial motion in acute ischemia. Ischemic and non-ischemic segment lengths of the left ventricular free wall were measured by miniature ultrasonic gauges in eleven open chest dogs with the pericardium preserved. In a stable state after left anterior descending coronary artery occlusion, peak left ventricular pressure was varied by the infusion of angiotensin II (n = 8) and sodium nitroprusside (n = 8). To exclude effects of preload on the responses, end-diastolic lengths of the non-ischemic region before and during infusion of each drug were matched with vena caval occlusion. When peak left ventricular pressure elevated from 113 +/- 2 (mean +/- S.E.)mmHg to 145 +/- 6, in isovolumetric contraction phase, degree of active shortening in the non-ischemic region and that of paradoxical expansion of the ischemic region did not change. In ejection phase, active shortening of the non-ischemic region decreased from 1.38 +/- 0.11 mm to 1.06 +/- 0.10 but that of the ischemic region remained unchanged. Stroke volume decreased from 14.5 +/- 1.3 ml to 10.8 +/- 1.0. When peak left ventricular pressure decreased from 111 +/- 4 mmHg to 101 +/- 6, in isovolumetric contraction phase, active shortening of the non-ischemic region decreased from 0.90 +/- 0.13 mm to 0.76 +/- 0.15 and paradoxical expansion of the ischemic region reduced from -0.95 +/- 0.11 mm to -0.80 +/- 0.11. In ejection phase, shortening of the non-ischemic region increased from 1.05 +/- 0.13 mm to 1.31 +/- 0.15 but that of the ischemic region did not change. Stroke volume increased from 11.5 +/- 1.3 ml to 14.0 +/- 1.4. These results indicate that in acute ischemia, changes in isovolumetric shortening of the non-ischemic region and paradoxical expansion of ischemic region are related with each other in isovolumetric contraction phase when afterload is altered and suggest that stroke volume is affected by the shortening of ejection phase in the non-ischemic region.
Sakuma
M
M
First Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
Shirato
K
K
Oikawa
Y
Y
Katoh
A
A
Nakagawa
M
M
Ishigaki
H
H
Takishima
T
T
D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D003331:Coronary Vessels / Q000502:physiology; D004285:Dogs; D005260:Female; D006321:Heart / Q000187:drug effects / Q000503:physiopathology*; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology; D017202:Myocardial Ischemia / Q000503:physiopathology*; D009599:Nitroprusside / Q000494:pharmacology; D013318:Stroke Volume / Q000187:drug effects; D017725:Ventricular Pressure / Q000187:drug effects
D000804:Angiotensin II; D009599:Nitroprusside