Myofibroblast accumulation in healing rat myocardium due to long-term low-dosage nitric oxide synthesis inhibition.
Inhibition of nitric oxide synthesis causes hypertension, myocardial damage and repair in rats. The myocardial healing process includes changes in extracellular matrix composition associated with the phenotypic modulation of fibroblasts. Early and later lesion areas showed a population of spindle-shaped cells expressing alpha-smooth muscle actin content. These cells apparently are associated with type III collagen and fibronectin accumulation in the ischemic lesion areas contributing to maintaining of the mechanical performance of the heart through out the healing process.
Laboratory of Morphometry and Cardiovascular Morphology, Biomedical Center, Institute of Biology, State University of Rio de Janeiro, Rio de Janeiro, Brazil. mandarim@ueri.br
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Pessanh
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Mandarim-de-Lacerda
D000818:Animals; D009202:Cardiomyopathies / Q000139:chemically induced* / Q000473:pathology*; D003094:Collagen / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D005260:Female; D005347:Fibroblasts / Q000473:pathology*; D005353:Fibronectins / Q000378:metabolism; D008297:Male; D009206:Myocardium / Q000473:pathology; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors*; D051381:Rats; D017208:Rats, Wistar
D004791:Enzyme Inhibitors; D005353:Fibronectins; D003094:Collagen; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester