Development and prevention of skeletal muscle structural alterations after experimental myocardial infarction.

Abstract

The present study was designed to assess whether structural alterations develop within skeletal muscle 1 yr 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 1 yr with either placebo (MI-IP, n = 9), a low dose of lisinopril (MI-LL, 0.5 mg.kg-1.day-1, n = 12), or a high dose of lisinopril (MI-LH, 5 mg.kg-1.day-1, 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 volume fraction (CVF), capillary density, and media thickness of resistance vessels (80-200 microns) of musculus quadriceps femoris muscle. Infarct size was similar in all infarct groups and averaged 26 +/- 4%. Right ventricular weight was increased in MI-IP compared with SH, MI-LL, and MI-LH. Both left ventricular (LV) CVF and skeletal muscle CVF were increased in MI-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 MI-IP group and significantly reduced by high-dose ACE inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)