title: Capillarization in skeletal muscle of rats with cardiac hypertrophy.
abstract: OBJECTIVE
  Exercise intolerance during chronic heart failure (CHF) is localized mainly in skeletal muscle. A decreased capillarization may impair exchange of oxygen between capillaries and muscle tissue and in this way contribute to exercise intolerance. We assessed changes in capillary supply in plantaris and diaphragm muscles of a rat aorta-caval fistula (ACF) preparation, a volume overload model for CHF.
  
  
  METHODS
  An ACF was created under equithesin anesthesia. Plantaris and diaphragm muscles were removed 6 wk postsurgery and examined for myosin heavy chain (MyHC) content and capillary supply.
  
  
  RESULTS
  Cardiac hypertrophy was 96% (P < 0.002) after ACF. The Type IIb MyHC content of the plantaris muscles increased (33.9 +/- 3.3 vs 49.8 +/- 3.8%; mean +/- SEM) at the expense of Type IIa MyHC (17.6 +/- 1.8 vs 11.2 +/- 1.7%) in ACF rats (P < 0.05). In the diaphragm, the number of Type I (32.1 +/- 2.3 vs 40.6 +/- 2.7%) and IIb fibers (40.6 +/- 1.9 vs 49.6 +/- 3.6%) increased at the expense of Type IIa fibers (26.8 +/- 2.5 vs 9.4 +/- 0.9%) (P < 0.05). The capillary number per fiber did not change, and this indicated that no capillary loss occurred with ACF. Also, the capillary density was maintained in the diaphragm and plantaris muscles of ACF rats. Furthermore, the coupling between fiber type, size, and metabolic type of surrounding fibers, with the capillary supply to a fiber, was maintained in rats with an ACF.
  
  
  CONCLUSIONS
  The cardiac hypertrophy induced by volume overload seems adequate to prevent atrophy and changes in the microcirculation of limb and diaphragm muscles.
authors.affiliation: Department of Anatomy, University of South Florida, Tampa, FL 33612, USA.
authors.forename: Hans
authors.initials: H
authors.lastname: Degens
authors.forename: Rebecca K
authors.initials: RK
authors.lastname: Anderson
authors.forename: Stephen E
authors.initials: SE
authors.lastname: Alway
mesh_terms: D000818:Animals; D001166:Arteriovenous Shunt, Surgical; D002196:Capillaries / Q000473:pathology*; D002306:Cardiac Volume; D006332:Cardiomegaly / Q000473:pathology* / Q000503:physiopathology*; D003238:Connective Tissue / Q000473:pathology; D003964:Diaphragm / Q000098:blood supply* / Q000473:pathology; D006333:Heart Failure / Q000473:pathology; D008297:Male; D023421:Models, Animal; D018485:Muscle Fibers, Skeletal / Q000473:pathology; D009124:Muscle Proteins / Q000032:analysis; D018482:Muscle, Skeletal / Q000098:blood supply* / Q000737:chemistry / Q000473:pathology*; D018995:Myosin Heavy Chains / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D009124:Muscle Proteins; D018995:Myosin Heavy Chains