Circulation, Vol 80, 1783-1794, Copyright © 1989 by American Heart Association
DA Kass, P Marino, WL Maughan and K Sagawa
The influence of extent and location of regional ischemia, baseline left
ventricular systolic function, and autonomic reflexes on in situ left
ventricular end-systolic pressure-volume relations (ESPVRs) during coronary
occlusion were studied in 13 open-chest dogs. Circumflex or left anterior
descending arteries were randomly occluded (at proximal or distal sites)
for 3 minutes in reflex-blocked (n = 6, hexamethonium/vagotomy) and
unblocked (n = 7) animals. Pressure-volume data were obtained by the
conductance-catheter technique, with ESPVRs determined by transient
inferior vena caval occlusion. Ischemic zone size was estimated for each
occlusion by radiolabeled microspheres. The relative influence of each
variable on ESPVR change with ischemia was determined by multiple
regression analysis. As in previous studies, regional ischemia displaced
ESPVRs to the right by an amount that varied directly with ischemic bed
size (y = +0.48x, r = 0.76, p less than 0.001). However, in contrast to
previous data, coronary occlusion also reduced the ESPVR slope
(end-systolic elastance, Ees) in the majority of cases. The extent of slope
change was primarily dependent on the baseline elastance (Eesbase), such
that the higher the initial elastance, the larger its subsequent reduction
for any amount of ischemia (delta Ees = -0.78Eesbase, r = 0.94, p less than
0.001). Active reflexes added an offset constant to this relation (+3.15 mm
Hg/ml, p less than 0.001). In addition, Ees fell slightly more with larger
ischemic regions. Thus, although previous studies have reported primarily
rightward parallel shifts in ESPVR with regional ischemia, the present data
also demonstrate that the slope of the relation is often reduced. Greater
baseline elastances typical of in situ, as opposed to isolated, ventricles
probably explain the differences in apparent responses.
ARTICLES
Determinants of end-systolic pressure-volume relations during acute regional ischemia in situ
Department of Internal Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland.
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