The American journal of physiology
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Unilateral pneumonectomy in rats causes compensatory growth of the remaining lung. This growth involves rapid production of collagen and noncollagen proteins, but the mechanisms for these changes have not been fully investigated. Rates of collagen metabolism were measured using previously validated in vivo methods. ⋯ Noncollagen protein synthesis and degradation rates both increased by approximately 80% (control 44.3 +/- 3.4%/day, pneumonectomy 80.3 +/- 10.2%/day) with a slightly greater increase in synthesis that led to an 85% increase in noncollagen protein content 28 days after pneumonectomy. The data obtained show dramatic changes in protein synthesis and degradation during compensatory lung growth and indicate extensive remodeling of structural elements in lung tissue. The changes for intracellular collagen degradation provide further evidence that this pathway may have an important role in regulating collagen deposition.
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We used awake, unsedated rats with indwelling cardiovascular catheters to study the role of endothelial injury and increased pulmonary vascular reactivity in the pathogenesis of monocrotaline (MC)-induced pulmonary hypertension. Hemodynamic findings were correlated with morphometric analyses of alterations in the vascular endothelium assessed by electron microscopy and of muscularization of pulmonary arteries assessed by light microscopy. Male Sprague-Dawley rats (200-250 g) were injected with MC (60 mg/kg) or with saline vehicle. ⋯ Endothelial injury was observed as early as 4 days postinjection with pallor and swelling evident qualitatively and by a decreased proportion of microfilaments (P less than 0.05) assessed quantitatively. By light microscopy, extension of smooth muscle into normally nonmuscularized pulmonary arteries was evident by 8 days postinjection. By 12 days postinjection there was marked extension of smooth muscle present (P less than 0.01) with medial hypertrophy of muscular arteries.(ABSTRACT TRUNCATED AT 250 WORDS)