Observations have been made regarding the effects of long-term exercise training on blood pressure, renal sodium handling and renal renin-angiotensin-aldosterone (RAS) intracellular pathways in conscious, trained Okamoto-Aoki spontaneously hypertensive rats (SHR) and Wistar Kyoto (WKy) normotensive rats, compared with appropriate agematched sedentary SHR and WKy. To evaluate the influence of exercise training on renal function and RAS, receptors and intracellular angiotensin II (AngII) pathway compounds were used respectively, and lithium clearance and western blot methods were utilised. The current study demonstrated that increased blood pressure in SHR was blunted and significantly reduced by long-term swim training between the ages of 6 and 16 weeks. Additionally, the investigators observed an increased fractional urinary sodium excretion in trained SHR (SHR T ) rats, compared with sedentary SHR (SHR S ), despite a significantly decreased creatinine clearance (C Cr ). Furthermore, immunoblotting analysis demonstrated a decreased expression of AT1 R in the entire kidney of T SHR rats, compared with S SHR . Conversely, the expression of the AT2 R , in both sedentary and trained SHR, was unchanged. The present study may indicate that, in the kidney, long-term exercise exerts a modulating effect on AngII receptor expression. In fact, the present study indicates an association of increasing natriuresis, reciprocal changes in renal AngII receptors and intracellular pathway proteins with the fall in blood pressure levels observed in T SHR rats compared with age-matched S SHR rats.

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1 Theophylline is commonly used to relieve symptoms of chronic asthma. Since neutrophil and mononuclear cell activation are associated with late phase asthmatic reactions, effects of theophylline on these cells may be of importance. 2 In the present investigation we compared neutrophil and mononuclear cell chemotaxis from chronic asthmatic children during and after theophylline therapy. 3 Thirty patients were recruited for the study. Each patient received theophylline orally for 10 days. The theophylline dose was 20 mg kg-1 day-1 given in four divided doses. On the tenth day, blood was collected into heparinized (100 u ml-1) and siliconized tubes 2 h after the last theophylline dose for chemotactic assays, cAMP and theophylline plasma determinations. When clinical conditions allowed, theophylline was discontinued for 7 days and the chemotactic assays, cAMP and theophylline plasma concentrations repeated. Serum complement and IgE levels were also determined. 4 Theophylline therapy clearly inhibited both spontaneous and stimulated neutrophil and mononuclear cell chemotaxis. Twenty-seven patients had therapeutic plasma concentrations of theophylline (5-20 ,ug ml-'). Discontinuation of theophylline therapy caused a significant decrease in plasma cAMP levels (44 and 31 pmol ml1 respectively during and after treatment, n = 30, P < 0.001).5

-Neurogenic pulmonary edema is a serious and always life-threatening complication following several lesions of the central nervous system. We re p o rt an experiment with 58 Wi s t a r-Hanover adult male rats. Two gro u p s w e re formed: control (n=4) and experimental (n=54). The experimental group sustained acute midthoracic spinal c o rdinjury by Fogart y 's balloon-compression technique containing 20µL of saline for 5, 15, 30 or 60 seconds. The rats w e reanesthetized 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 diff e rent gro u p s . Poor outcome occurred with 60 seconds of compression. Six animals died suddenly with pulmonary edema. Using the pro c e d u re to investigate the pulmonary edema during 60 seconds of compression, followed by decompre s s i o n 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 ru p t u res and acute hemorrh a g e . Comparison of the pulmonary index with morphometric evaluation of edema fluid-filled alveoli by light micro s c o p y showed that relevant intra-alveolar edema occurred only for index values above 0.55. The results suggest that the p u l m o n a ryedema induced by spinal compression is of neurogenic nature and that the type of anesthesia used might be important for the genesis of lung edema.KEY WORDS: spinal cord injury, neurogenic pulmonary edema, central nervous system lesions. P a r â m e t ros hemodinâmicos e edema pulmonar neurogênico após traumatismo raquimedular: modelo experimental RESUMO -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 torá-cico 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 re l a ç ã o e n t re 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 ocorre u 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, an...

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