Avalia??o da resposta inflamat?ria cardiovascular em ratos com hipertens?o renovascular (2R1C) infectados pelo Trypanosoma cruzi.

Programa de P?s-Gradua??o em Ci?ncias Biol?gicas. N?cleo de Pesquisas em Ci?ncias Biol?gicas, Pr?-Reitoria de Pesquisa de P?s Gradua??o, Universidade Federal de Ouro Preto.A Hipertens?o Arterial Sist?mica (HAS), caracterizada pelo aumento de Angiotensina II plasm?tica/tecidual, ? uma das doen?as com maior preval?ncia no mundo moderno. Evidencias apontam para o envolvimento da inflama??o vascular no processo inicial da HAS. A cardiopatia chag?sica ? causada pelo protozo?rio Trypanosoma cruzi, capaz de desencadear uma resposta inflamat?ria progressiva gerando importantes altera??es el?tricas e morfo-funcionais ao cora??o. Nosso objetivo neste estudo foi avaliar a associa??o da HAS e os aspectos inflamat?rios cardiovasculares em animais infectados pela cepa Y do T. cruzi. Ratos Wistars machos foram submetidos ? cirurgia renovascular (modelo Goldblatt ? 2Rins/1CLIP) ou ? cirurgia fict?cia (SHAM) e divididos e agrupados de acordo com a infec??o ou n?o pelo T. cruzi. Foram realizados tr?s experimentos em diferentes momentos da ?infec??o e cirurgia? para avalia??o da HAS e do patol?gico induzido pelo parasito sendo (I) indu??o da HAS + infec??o pelo T.cruzi (ao mesmo tempo), experimento teve dura??o de 1 semana; (II) indu??o da HAS + infec??o com o T. cruzi 3 semanas ap?s a cirurgia e (III) indu??o da HAS + infec??o pelo T.cruzi (ao mesmo tempo) e experimento teve dura??o de 8 semanas. Nesse estudo, avaliou-se par?metros fisiol?gicos e inflamat?rios como pletismografia, Ang II e mediadores inflamat?rios plasm?ticos, parasitemia e achados histopatol?gicos no tecido card?aco. Ap?s a 3? semana de cirurgia os animais apresentaram picos press?ricos havendo concord?ncia com a produ??o de Angio II plasm?tica nas primeiras semanas, mas n?o se observando rela??o direta entre o aumento da press?o arterial e o numero de parasitos circulantes. No entanto, o T. cruzi exerceu papel definidor na alta produ??o de TNF-alfa e da CX3CL1/Fractalkine e, em associa??o com a cirurgia renovascular, observou-se maior eleva??o nesses mediadores inflamat?rios em diferentes etapas do estudo. Por outro lado, o aumento da press?o arterial n?o exerceu interfer?ncia no processo inflamat?rio tecidual nem na invas?o tecidual pelo parasito, mas contribuiu para a manuten??o do n?mero de vasos sangu?neos ap?s 8 semanas de experimento, quando houve diminui??o no grupo de animais normotensos. Com este estudo conclui-se que o tempo de infec??o pelo T. cruzi e o tempo de desenvolvimento da hipertens?o interferem, mutualmente, no perfil inflamat?rio induzido pelo hospedeiro mam?fero. No entanto, acredita-se tamb?m, que esse estudo fosse reproduzido em outro modelo experimental mais suscept?vel ? infec??o pelo T. cruzi, as les?es cardiovasculares seriam mais evidenciadas principalmente numa etapa cr?nica de ambas as doen?as.Systemic arterial hypertension (SAH) is characterized by the increase of plasma/tissue Angiotensin II (Angio II) and presents high prevalence in the world. There are evidences suggesting the involvement of vascular inflammation in the initial phase of SAH. Chagas cardiomyopathy is a disease caused by Trypanosoma cruzi infection that triggers a progressive inflammatory response with prominent fibrosis and, as a consequence, there are important cardiac electrical and functional disturbances and/or hypertrophy in this organ. Our aim in this study was evaluate SAH and the cardiovascular inflammation in Wistar rats infected by Y strain of T. cruzi. Male rats were submitted to renovascular surgery (Goldblat model ? 2Kidneys/1CLIP) or to a fictional surgery (SHAM) and grouped according to infection or not by T. cruzi. It was proposed 3 experiments in different times of infection and surgery to evaluate the SAH and the pathological aspects induzed by the parasite: (I) SAH induction and T.cruzi infection at same time ? experiment occurred in one week; (II) SAH induction + T.cruzi infection after 3 weeks of surgery and (III) SAH induction and T.cruzi infection at same time ? experiment occurred during 8 weeks. For these sets of experiments, there was evaluation of physiological, parasitological, inflammatory and histological parameters in the plasma and/or cardiac tissue. After the 3rd week of the renovascular surgery, animals presented high pressoric levels in accordance with high plasma Angio II on the first weeks. However, there were not observed relation between the increase of SAH and the number of circulating parasites. In our data, T. cruzi exerted an important role in the production of TNF-alpha and CX3CL1/Fractalkine by host cells and we observed high plasma release of these mediators when associated with SAH, in distinct times of this study. On the other hand, SAH does not exerted influence on cardiac inflammatory infiltration neither in the amastigote proliferation, but contributed to the maintenance of the number of blood vessels after 8 weeks of the experiment in comparison with the reduction observed in the control group (without SAH). Together, these data suggest that the time of T.cruzi infection and the time of SAH development interfere, mutually, in the inflammatory profile induced by host mammalian. However, other studies performed in other T.cruzi-susceptible experimental model might develop cardiovascular lesions with high magnificence as well as inflammatory process in heart tissue during chronic stages of both diseases