Effects of diabetes on isometric tension as a function of [ca2+[
cb] and ph in rat skinned cardiac myocytes..
Hofmann, Polly A., Vandana Menon, and Karen F. Gannaway.
Dept. of Physiology and Biophysics, University of Tennessee,
Memphis TN 38163
APStracts 2:0206H, 1995.
In diabetes a primary myocardial defect occurs which is characterized
by decreases in systolic pressure and cardiac output. The present
study investigates if diabetes causes a decreased maximum tension
generating ability, decreased Ca2+ sensitivity of myofilaments or no
change in cardiac myofilament contractile properties at pH 7.0 and
6.6. Hearts from Wistar rats were excised and mechanically disrupted
6-10 weeks post injection of streptozotocin. The resulting myocyte
-size preparations of skinned myocardium were used to determine the
steady state tension-pCa relation. Maximum tension was unchanged and
the pCa of half maximum tension generation was 0.14 pCa units lower
than control for skinned myocytes from diabetic rats at pH 7.0. A
significantly lower-than-normal maximum tension was observed at pH
6.6 for cardiac myocytes from diabetic rats. Increased expression of
[beta]-myosin heavy chain (MHC) occurred in hearts from diabetic
rats. Two troponin T (TnT) isoforms in myocardium of adult rats were
identified by Western blots. The ratio of the two TnT isoforms was
altered in diabetes. Changes in cardiac MHC and TnT expression may
contribute to the observed decrease in Ca2+ sensitivity of
myofilaments at pH 7.0 and decreased maximum tension generating
ability at pH 6.6 in diabetes.
Received 22 August 1994; accepted in final form 10 May 1995.
APS Manuscript Number H754-4.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 26 May 1995.