Oxytalan elastic and collagen fibers during the repair process in experimental nitric oxide inhibition.
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Resumo
OBJECTIVE
To evaluate the repair process in rats with experimentally induced arterial hypertension. This study aimed to evaluate lesions in the ventricular myocardium and the repair process during experimental hypertension induced by systemic blockage of nitric oxide using N-omega-nitro-L-arginine methyl ester hydrochloride (L-NAME). Nitric oxide is an endothelial vasorelaxing factor and is necessary for the maintenance of normal arterial pressure, and L-NAME is an analog and antagonist of L-arginine, the substrate of the nitric oxide synthase.
METHODS
We used 26 normotensive young male Wistar rats belonging to several litters. Animals were treated with oral administration of L-NAME dissolved in water (75 mg/100 mL) for 43 days. Hearts were weighed and processed by routine methods. Special stains utilized were Gomori's trichrome (aniline blue), picrosirius red polarization to identify fibrillar collagen, alcian blue technique (pH 0.5 and pH 2.5) to identify glycosaminoglycans, periodic acid-Schiff technique (with and without amylases) to identify proteoglycans, and Weigert's resorcinol fuchsin solution (with and without oxone) to identify elastic fibers.
RESULTS
The results showed significant elevation of the arterial pressure (P <0.01) and significant increase of cardiac weight (P <.0001) in the L-NAME (hypertensive) treated group, as compared to an untreated control group. The histological analysis demonstrated wide infarcted myocardial areas in animals with nitric oxide blockade; several vascular changes such as thickening of the muscular tunica with fibrosis; thickening in the wall of small arteries and arterioles; and fibrinoid necrosis in the wall to nearly complete luminal obliteration. Reparative fibrosis involved mainly oxytalan elastic and collagen fibers.
CONCLUSIONS
Oxytalan elastic and collagen fibers are of great importance for the postinfarct repair process occurring during experimental nitric oxide inhibition.
