Cardiac morphometric changes associated with decreased
contractility after endotoxin.
Goddard, Christopher M., Michael F. Allard, James C. Hogg, Keith R.
Walley.
Pulmonary Research Laboratory, St. Paul's Hospital, University of
British Columbia, Vancouver, B.C., Canada
APStracts 2:0462H, 1995.
Myocardial depressant factor is rapidly reversible in vitro and
therefore may not account for all of the prolonged decrease in left
ventricular contractility during sepsis. Our hypothesis is that blood
borne factors also cause myocardial damage associated with decreased
contractility. This could then account for the prolonged time course.
We utilized a preparation consisting of an isolated rabbit heart
perfused by a support rabbit. Support rabbits received 1 mg/kg
endotoxin I.V. over 30 minutes (endotoxin group, n=7) or vehicle
(control group, n=6). The slope of the end-systolic pressure-volume
relationship, Emax, was used to measure contractility of the isolated
heart. Five hours after endotoxin infusion Emax decreased by 17 +/-
7% (p<0.03) in the endotoxin group but was unchanged in the
control group (0 +/- 2%). Quantitative morphometric analysis of
hearts from the endotoxin group demonstrated an increased volume
fraction of abnormal myocytes (7.6 3.6% versus 0.8 0.4% in controls,
p < 0.01), interstitial edema (23.2 5.2% versus 14.3 21.5 in
controls, p < 0.05), and myocardial capillaries occupied by
leukocytes (15.7 3.5% versus 3.0 0.7% in controls, p < 0.05) We
conclude that blood borne factors alone can cause myocardial
morphometric changes and decrease left ventricular contractility
during sepsis.
Received 2 December 1994; accepted in final form 12 September
1995.
APS Manuscript Number H1056-4.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 November 95