Hydralazine reduces myocardial tissue damage in rats submitted to chronic inhibition of systemic nitric oxide synthesis during 4, 14 and 28 days

Jornal Brasileiro de Patologia e Medicina Laboratorial

Ricardo Xavier-vidal²  Kalil Madi²  Aline De Abreu Reis¹  Leandra Da Silva Paes¹  Ana Carolina De Azevedo Carvalho¹  Nádia Maria S. Marques¹  Marcelo Guimarães¹  Marcelo Aranha Gardel¹  Sonia Oliveira Souza¹  Simone Marques Fernandes¹  Fernanda Oliveira Laranjeira¹ 

[1],Universidade Federal do Rio de Janeiro Post-Graduate Program on Morphologic Sciences

关键词: Nitric oxide;    L-Name;    Arterial hypertension;    Cardiac hypertrophy;    Heart morphology;    Cardiomyopathy;    Arteriosclerosis;    Óxido nítrico;    L-Name;    Hipertensão arterial;    Hipertrofia cardíaca;    Morfologia cardíaca;    Cardiomiopatia;    Arteriosclerose;   

DOI  :  10.1590/S1676-24442003000300012

来源: SciELO

【 摘 要 】

The aim of the present work was to develop a qualitative chronopathological study concerning abnormalities in myocardium, due to nitric oxide (NO) blockage. We used 60 Wistar normotensive young male rats from several breeds. Groups of rats were submitted to L-Name (L) via oral administration dissolved in water (750mg/l) during days 4, 14 and 28. Other groups were submitted concomitantly to L-Name and hydralazine hydrocloride (L + H) (120mg/l). On days 4 and 14 (L group) we have found myocardial abnormalities and lesions while in L + H we could not identify abnormalities. Considering L group on day 28, the myocardium presented characteristic fibrosis (reactive and reparative), vascular damage with increasing wall thickness due mainly to proliferation of the arterial smooth muscle cell. Total obliteration of vessels was noted only in this period. We also observed reactive fibrosis between muscle cells of the vascular wall and proliferation of cells in the intimal layer. In L + H (day 28), similar vascular abnormalities described for L group (less frequent and less apparent) were also observed. In L + H we did not identify total vascular obstructions. In L + H, infarct areas were not observed. Control groups did not present any abnormalities. Our results support the idea that, at least in some cases, hypertrophy vascular abnormalities and myocardial lesions in arterial hypertension can occur because of the reduction in organic nitric oxide production. Our results also suggested that these morbid processes can be postponed by the use of hydralazine which, however, does not avoid abnormalities after long-term experimental blockage of NO.

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