Peripheral blood‐flow restriction caused hypertrophy associated with decreased HSP‐72 and fibrosis in rat myocardium

Abstract

Introduction To obtain an insight into mechanisms of the myocardium hypertrophy, we developed a new animal model. Methods Male Wistar rats were randomly assigned into a group for sham operation (sham group) and a group for venous occlusion in the hindlimb (experimental group; n= 7 for each group). 14 days after the operation, heart was dissected out and weighed. The relative content of heat shock protein-72 (HSP-72) and heat shock cognate protein-70 (Hsc-70), and the expressions of IGF-1, mechano growth factor (MGF), a1(1) procollagen, myostatin, nitric oxide synthase-1 and 2 (NOS-1 and NOS-2) mRNA were examined. Also, myocardium nitric oxide (NO) concentration was measured. For histological analyses, Hematoxylin/ Eosin (H&E), Oil Red O, Van Gieson and Elastica stains were made. Results The venous occlusion caused hypertrophy of the cardiac muscle (left ventricle), in which the expressions of IGF-1, a1(1) procollagen, and NOS-2 increased, whereas that of MGF, and the relative content of HSP-72 and NO concentration decreased. Elastica stain exhibited dense regions in the hypertrophied cardiac muscle. Conclusion Increase in peripheral vascular resistance causes myocardial hypertrophy and fibrosis associated with changes in heat shock protein and growth factors.