AJP - Heart Journal of Neurophysiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Heart Circ Physiol 254: H1065-H1073, 1988;
0363-6135/88 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Hoit, B. D.
Right arrow Articles by Lew, W. Y.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hoit, B. D.
Right arrow Articles by Lew, W. Y.

AJP - Heart and Circulatory Physiology, Vol 254, Issue 6 1065-H1073, Copyright © 1988 by American Physiological Society


ARTICLES

Functional consequences of acute anterior vs. posterior wall ischemia in canine left ventricles

B. D. Hoit and W. Y. Lew
Department of Medicine, Veterans Administration Medical Center, San Diego, California.

We compared the consequences of acute anterior and posterior wall ischemia on regional left ventricular function in seven open-chest dogs. Circumferentially oriented sonomicrometers were implanted in the midwall of the anterior and posterior left ventricle. The left anterior descending (LAD) and left circumflex (LCX) coronary arteries were each occluded for 3 min, with 45 min of reperfusion between the two occlusions. The ischemic areas at risk, as assessed by postmortem perfusion techniques, were similar for anterior (34.5 +/- 12.5 g) and posterior (32.3 +/- 9.4 g) wall ischemia. Both occlusions produced a similar increase in end-diastolic pressure. After LAD occlusion, total segment shortening (end diastole to aortic valve closure) in the nonischemic posterior wall increased from 8.0 +/- 3.9 to 10.8 +/- 4.4%, solely caused by increased isovolumic shortening. In contrast, with LCX occlusion, total segment shortening in the nonischemic anterior wall increased significantly more, from 10.5 +/- 3.8 to 14.6 +/- 4.2% caused by nearly equal increases in isovolumic and ejection phase shortening. Thus, with both LAD and LCX occlusions, there was increased shortening in nonischemic areas during isovolumic systole, which was "wasted" in paradoxically stretching the ischemic zone. However, a compensatory increase in nonischemic area ejection phase shortening occurred only with LCX occlusions. These findings may explain the greater functional impairment that occurs with LAD than LCX occlusions.





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online