Edema pulmonar neurogênico é complicação séria e aumenta o risco de vida em pacientes com várias lesões do sistema nervoso central. Apresentamos uma experiência com 58 ratos Wistar machos e adultos. Foram formados dois grupos: controle (n=4) e experimental (n=54). O grupo experimental sofreu trauma raquimedular torácico médio com o cateter-balão de Fogarty contendo 20µL de salina por 5, 15, 30 ou 60 segundos de compressão. Os ratos foram anestesiados com pentobarbital sódico (p.s.), 60 mg/Kg intraperitoneal (i.p.). Foi investigada a relação entre a lesão medular e o tempo de compressão. A evolução neurológica foi quantificada e apresentada com 4, 24 e 48 horas da compressão para caracterizar a graduação da lesão nos diferentes grupos. A pior evolução ocorreu com 60 segundos de compressão. Seis animais morreram subitamente com edema pulmonar. Vinte ratos foram randomicamente distribuídos em um dos seguintes grupos: controle (1, n=4, anestesiados com p.s. i.p., 60 mg/Kg, mas sem compressão) e experimental (2, n=7, anestesiados com xilasina 10 mg/Kg e ketamina 75 mg/Kg) e (3, n=9, anestesiados com p.s. i.p., 60 mg/Kg). O índice pulmonar (100 x peso pulmonar / peso corporal) foi 0,395 ± 0,018 no grupo controle, 0,499 ± 0,060 no grupo 2, e 0,639 ± 0,14 no grupo 3. O exame histológico da medula espinhal mostrou rupturas no parênquima e hemorragia aguda. Comparando-se o índice pulmonar com o índice morfométrico através da microscopia óptica, evidenciou-se que ocorreu edema intra-alveolar relevante para índices acima de 0,55. A presente experiência sugere que o edema pulmonar induzido pela compressão medular é de natureza neurogênica e que o tipo de anestesia utilizada no experimento poderia ter participação na gênesis do edema pulmonar.

Neurogenic pulmonary edema is a serious and always life-threatening complication following several lesions of the central nervous system. We report an experiment with 58 Wistar-Hanover adult male rats. Two groups were formed: control (n=4) and experimental (n=54). The experimental group sustained acute midthoracic spinal cord injury by Fogarty’s balloon-compression technique containing 20µL of saline for 5, 15, 30 or 60 seconds. The rats were anesthetized by intraperitoneal (i.p.) sodium pentobarbital (s.p.) 60 mg/Kg. The quantitative neurological outcome was presented at 4, 24 and 48 hours from compression to characterize the injury graduation in different groups. Poor outcome occurred with 60 seconds of compression. Six animals died suddenly with pulmonary edema. Using the procedure to investigate the pulmonary edema during 60 seconds of compression, followed by decompression and time-course of 60 seconds, 20 rats were randomly asigned to one of the following groups: control (1, n=4, anesthetized by i.p. s.p., 60 mg/Kg but without compression) and experimental (2, n=7, anesthetized by i.p. xylazine 10 mg/Kg and ketamine 75 mg/Kg) and (3, n=9, anesthetized by i.p. s.p., 60 mg/Kg). The pulmonary index (100 x wet lung weight / body weight) was 0.395 ± 0.018 in control group, rose to 0.499 ± 0.060 in group 2, and was 0.639 ± 0.14 in group 3. Histologic examination of the spinal cord showed parenchymal ruptures and acute hemorrhage. Comparison of the pulmonary index with morphometric evaluation of edema fluid-filled alveoli by light microscopy showed that relevant intra-alveolar edema occurred only for index values above 0.55. The results suggest that the pulmonary edema induced by spinal compression is of neurogenic nature and that the type of anesthesia used might be important for the genesis of lung edema.

Angiotensin II (AII), a product of rennin-angiotensin system, exerts an important role on the function of immune system cells. In this study, the effect of AII on the phagocytic activity of mouse peritoneal macrophages was assessed. Mice peritoneal macrophages were cultured for 48 h and the influence of different concentrations of AII (10-14 to 10-7 M) and/or losartan, 10-16 to 10-6 M), an AT1 angiotensin receptor antagonist, on phagocytic activity and superoxide anion production was determined. Dimethylthiazoldiphenyltetrazolium bromide reduction and the nucleic acid content were used to assess the cytotoxicity of losartan. A stimulatory effect on phagocytic activity (P < 0.05) was observed with 10-13 M and 10-12 M AII concentrations. The addition of losartan (up to10-14 M) to the cell cultures blocked (P < 0.001) the phagocytosis indicating the involvement of AT1 receptors. In contrast, superoxide anion production was not affected by AII or losartan. The existence of AT1 and AT2 receptors in peritoneal macrophages was demonstrated by immunofluorescence microscopy. These results support the hypothesis that AII receptors can modulate murine macrophage activity and phagocytosis, and suggest that AII may have a therapeutic role as an immunomodulatory agent in modifying the host resistance to infection.

OBJETIVO: Caracterizar a associação entre doença de Chagas e hipertensão arterial primária. MÉTODOS: Estudaram-se os chagásicos crônicos acompanhados pelo Grupo de Estudos em Doença de Chagas (Unicamp), no período de 15 anos, considerando-se: hipertensão arterial, forma clínica da doença, sexo, idade e raça. Confrontaram-se dados dos chagásicos hipertensos com os dos não hipertensos. RESULTADOS: Constatou-se que entre 878 chagásicos, 37% eram também hipertensos, dos quais 65% tinham cardiopatia, contra 49% do grupo normotenso; 31% dos chagásicos hipertensos apresentavam descompensação hemodinâmica, contra 24% dos não hipertensos. Entre os chagásicos hipertensos 41% eram negróides e 35% caucasóides; 50% dos chagásicos hipertensos tinham mais de 45 anos contra 29% dos não hipertensos. CONCLUSÃO: A associação entre moléstia de Chagas e hipertensão arterial primária cursou com um freqüente e mais grave comprometimento cardíaco, sendo esta mais prevalente nas faixas etárias mais elevadas.

PURPOSE: To evaluate the clinical relationship between Chagas' disease and primary arterial hypertension. METHODS: The study involved 878 chronic chagasic outpatients followed by the Chagas' Disease Study Group of the University Hospital (Unicamp), over a 15-year period. Initially, the age, gender, race, clinical form of Chagas' disease and the presence of hypertension were noted for each patient. Subsequently, the data for matched hypertensive and normotensive chagasic patients were compared. RESULTS: Of the chagasic patients 37% were hypertensive, of those, 65% had some form of heart disease compared to 49% in the normotensive group. Of those patients with Chagas' disease and arterial hypertension, 41% were blacks and 35% were caucasians. Fifty percent of the hypertensive chagasic patients were over 45 years old compared to only 29% of the non-hypertensive patients. CONCLUSION: Most of the hypertensive chagasic patients were 45 or more years old and showed some degree of heart failure compared to the normotensive group.

Neste estudo foram avaliados 16 pacientes chagásicos e 28 indivíduos normais, em termos de respostas pressórica e cronotrópica pós sobrecarga oral de glicose. Essas respostas foram apreciadas através das medidas de pressão arterial e frequência de pulso. A resposta cardiovascular foi correlacionada com os níveis de insulinemia e glicemia. O experimento detectou um subgrupo de chagásicos (N=8) com padrão hipoinsulinêmico com atividades cronotrópicas e pressórica deprimidas quando comparadas ao grupo controle, o que indica um possivel déficit nas atividades insulínicas e/ou disfunção autonômica precoce neste subgrupo.

Cardiac chronotropic and pressor responses after an oral load of glucose were assessed in sixteen Chagasic subjects and 28 controls by means of blood pressure and pulse rate measurements. Cardiovascular response was correlated with serum insulin and glucose levels. The experiment identified a subgroup of Chagasic subjects (n=8) with a hypoinsulinemic behavior presenting less chronotropic and pressor responses than controls. This may indicate a lower insulin activity and/or an early Autonomic Nervous System dysfunction in this subgroup.