In vivo determination of the left ventricular wall stress
-shortening relationship in normal mice.
Hoit, Brian D., Zia U. Khan, Corinn M. Pawloski-Dahm, Richard A.
Walsh.
Division of Cardiology, University of Cincinnati, 231 Bethesda
Ave., ML 0542, Cincinnati, OH 45267 0542, (513) 558-3070, FAX: (513)
558-3116
APStracts 3:0355H, 1996.
Although targeted alterations of the mouse genome are used
increasingly to identify the mechanisms underlying cardiac function,
the methods used to study the phenotypic expression of these
alterations in vivo are limited. In order to derive a relatively
noninvasive, load-independent measure of LV contractility in mice, we
cannulated the femoral artery and performed 2-D directed M-mode echo
studies in 28 anesthetized FVB/N mice using a 9 MHz transducer
(Interspec - ATL CX 200). Loading conditions were altered by
intraarterial methoxamine (3-12 [mu]g/g), and LV shortening fraction
was determined at several steady states both before and after
myocardial contractility was altered either by 4 [mu]g/gm
intraperitoneal dobutamine (n=16) or 1-2 [mu]g/gm verapamil (n=12).
The relation between LV systolic meridional stress and fractional
shortening derived from pooled baseline data was inverse and linear
(r=.80, slope=-0.19%/g/cm2, intercept=48%, SEE=5.5%, p <0.001).
Dobutamine produced a parallel upward shift of the relation (r=.87,
slope=-0.21%/g/cm2, intercept=61%, SEE=4.5%, p< 0.001), and
verapamil produced a downward shift of the relation (r=.48, slope=
-0.05% g/cm2, intercept=24%, SEE=3.7%, p<0.05). At matched levels
of end systolic stress, dobutamine increased, and verapamil decreased
the LV shortening fraction. We conclude: 1) inverse stress-shortening
relations can be assessed noninvasively in mice; 2) these relations
are sensitive to alterations in inotropic state, independent of
loading conditions.
Received 16 April 1996; accepted in final form 2 August 1996.
APS Manuscript Number H338-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 29 August 1996