[Experimental anatomo-pathologic study in the myocardium of animals with arterial hypertension caused via a nitric oxide synthesis blocker].
BACKGROUND
Cardiac hypertrophy and reactive (including perivascular) and reparative fibrosis in L-NAME model are similar to that of hypertensive and cardiomyopathic patients.


OBJECTIVE
To qualitatively evaluate the reactive (including perivascular) and reparative fibrosis, on days 21 and 35, occurring in hearts submitted to the L-NAME model, using special staining.


METHODS
We utilized 33 normotensive Wistar rats. L-NAME was administered orally--in a concentration of 75 mg x 100 ml-1 in drinking water. Six rats were submitted during 21 days and an other 15 rats during 35 days. The arterial pressure was obtained on days 12, 20 and 34 using hydraulic plethysmography. On days 21 and 35 during the experiment the animals were anesthetized and submitted to cardiotomy. The hearts were fixed in Bouin fixative during 48 hours and processed using routine methods, emblocked in paraplast and cut in slices 4 to 7 microns thick. The special staining utilized were: Gomori's trichrome (aniline blue) or Masson trichrome, picro-sirius red-polarization, alcian blue technique (pH 0.5 and pH 2.5), periodic acid-Schiff technique (with and without amylases) and Weigert's resorcinol fuchsin solution (with and without oxon).


RESULTS
Our results demonstrated an increase in the arterial pressure in animals submitted to the model. On day 21 of submission we observed modest to extensive infarct areas in the right and left ventricular myocardium. On day 35 the wide reparative areas were from old infarct areas. In some cases at day 35 the lesions reached the totality of the right ventricle in several histological slices. The right ventricle was much more affected than the left one. In both groups perivascular fibrosis was observed, nevertheless, on day 21 it was very reduced.


CONCLUSIONS
The degree of direct influence of NO or hypertension produced by NO on hypertension and cardiac lesions during L-NAME model is discussed nowadays. Nevertheless, the fact is that NO deficit has great influence in several cases of cardiac lesions occurring in hypertension and also in cardiomyopathies.
Xavier-Vidal
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Laboratório de Anatomia Patológica, Instituto de Puericultura e Pediatria Martagão Gesteira. rxavier-vidal@interclub.com.br
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D000818:Animals; D004791:Enzyme Inhibitors; D005355:Fibrosis; D006325:Heart Atria / Q000473:pathology; D006352:Heart Ventricles / Q000473:pathology; D006973:Hypertension / Q000139:chemically induced / Q000473:pathology*; D009203:Myocardial Infarction / Q000209:etiology / Q000473:pathology*; D019331:NG-Nitroarginine Methyl Ester; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors
D004791:Enzyme Inhibitors; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester
Estudo anátomo-patológico experimental em miocárdio de animais submetidos a hipertensão arterial via bloqueador da síntese do óxido nítrico.