title: 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)
authors.affiliation: Medizinische Klinik III, Albert-Ludwigs Universität, Freiburg, Germany.
authors.forename: B
authors.initials: B
authors.lastname: Schieffer
authors.forename: K C
authors.initials: KC
authors.lastname: Wollert
authors.forename: M
authors.initials: M
authors.lastname: Berchtold
authors.forename: K
authors.initials: K
authors.lastname: Saal
authors.forename: E
authors.initials: E
authors.lastname: Schieffer
authors.forename: B
authors.initials: B
authors.lastname: Hornig
authors.forename: U N
authors.initials: UN
authors.lastname: Riede
authors.forename: H
authors.initials: H
authors.lastname: Drexler
mesh_terms: D000818:Animals; D001808:Blood Vessels / Q000473:pathology; D006332:Cardiomegaly / Q000209:etiology / Q000473:pathology; D003094:Collagen / Q000378:metabolism; D005355:Fibrosis; D006352:Heart Ventricles; D006614:Hindlimb / Q000098:blood supply; D008297:Male; D024510:Muscle Development; D018482:Muscle, Skeletal / Q000098:blood supply / Q000254:growth & development* / Q000473:pathology*; D009132:Muscles / Q000378:metabolism; D009203:Myocardial Infarction / Q000150:complications / Q000473:pathology* / Q000503:physiopathology*; D009206:Myocardium / Q000473:pathology; D007703:Peptidyl-Dipeptidase A / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D003094:Collagen; D007703:Peptidyl-Dipeptidase A