Regeneration and revascularization of a nerve-intact skeletal
muscle graft in the spontaneously hypertensive rat.
Carlsen, Richard C., Deborah Kerlin, and Sarah D. Gray.
Departments of Human Physiology and Surgery, University of
California, School of Medicine, Davis, California 95616
APStracts 2:0274R, 1995.
Skeletal muscles in hypertensive subjects develop an increased
resistance to insulin that reduces their ability to incorporate
glucose and synthesize glycogen. Insulin is an anabolic hormone in
muscle and muscle insulin receptors bind the growth factor, insulin
-like growth factor I (IGF I), an important contributor to muscle
development and regeneration. An increase in insulin resistance in
hypertensive subjects might produce muscle atrophy and weakness, or
limit regenerative growth following injury. Regenerative muscle
growth was assessed in 24-26 week old Spontaneously Hypertensive Rats
(SHR) and Wistar-Kyoto (WKY) rats by subjecting extensor digitorum
longus (EDL), an ankle flexor, to a nerve-intact graft procedure. The
procedure produces extensive muscle fiber and capillary degeneration,
but has little effect on the muscle nerve. Muscle morphology and
contractile function were examined in intact and regenerating EDL at
21, 42 and 63 days postgraft. Muscle revascularization was assessed
histologically at the same time points. Severe, established
hypertension did not prevent the reestablishment of a structurally
normal capillary network in injured muscles. SHR muscle fiber
regeneration and maturation, however, were significantly depressed
when compared to WKY grafts. The reduced regenerative recovery of SHR
EDL in adult animals with severe hypertension does not appear to be
due to a failure to restore the muscle nerve or capillary network,
but may reflect a reduced anabolic response to insulin or IGF I.
Received 30 June 1994; accepted in final form 11 October 1995.
APS Manuscript Number R355-4.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 14 November 95