Development and prevention of skeletal muscle structural alterations after experimental myocardial infarction. Schieffer, Bernhard, Kai C. Wollert, Michael Berchtold, Kristina Saal, Elisabeth Schieffer, Burkhart Hornig, Urs N. Riede, and Helmut Drexler. From the Medizinische Klinik III and the Pathologische Institut (U.N.R.) Albert-Ludwigs Universit[umlaut]at, Freiburg, Germany.
APStracts 2:0223H, 1995.
The present study was designed to assess whether structural alterations develop within skeletal muscle one year after myocardial infarction (MI) and failure and, if so, whether these structural alterations can be prevented by angiotensin-converting enzyme (ACE) inhibition. Infarcted rats were randomized and treated for one year with either placebo (IP, n=9), low dose lisinopril (LL, 0.5 mg/kg/d, n=12) or high dose lisinopril (LH, 5 mg/kg/d, n=9). Sham operated animals served as controls (SH, n=14). One year after MI, in situ fixation of rat hindlimb was performed to investigate interstitial collagen fraction (CVF%), capillary density and media thickness of resistance vessels (80-200[mu]m) of musculus quadriceps femoris muscle. Infarct size was similar in all infarct groups and averaged 26+/-4%. Right ventricular weight was increased in IP as compared to SH, LL and LH. Both, left ventricular (LV) CVF% and skeletal muscle CVF% were increased in IP. LV CVF and skeletal muscle CVF were closely related to each other (N=44, r= 0.5377, p<0.002). In infarcted rats, high dose ACE-inhibition significantly reduced skeletal muscle and LV CVF. Skeletal muscle capillary density and capillary to muscle fiber ratio were significantly decreased in infarcted rats, but were restored by low and high dose ACE -inhibition. Media thickness of intramuscular resistance vessels was increased in the IP group and significantly reduced by high dose ACE -inhibition. In summary, structural interstitial and vascular alterations develop within the skeletal muscle in chronic heart failure after MI and may contribute to the impaired exercise induced vasodilatation and skeletal muscle hypoperfusion. High dose ACE -inhibition completely prevented these structural alterations. 

Received 31 January 1995; accepted in final form 17 May 1995.
APS Manuscript Number H88-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 May 1995.