No abstract

Carbon monoxide (CO) intoxication is one of the most common types of poisoning worldwide, and may result in neuropathologic sequelae, yet its pathogenesis is not clear and there is no optimal management strategy for patients with CO poisoning. In this study, the rat model of CO poisoning was established in a hyperbaric chamber by CO exposure. Rats were administered orally N-Butylphthalide (NBP) at a dose of 1 ml/100g. Neuronal apoptosis was assessed by TUNEL stain and flow cytometry. The expressions of neurite outgrowth inhibitor (Nogo), myelin-associated glycoprotein (MAG) and Nogo receptor-1 (NgR1) were observed in rat brain tissue by immunohistochemistry and double immunofluorescence staining. As we expected, CO poisoning could start the mechanism of apoptosis. The number of apoptotic cells and the early neuronal apoptosis percentage (EAR) were significantly increased at 1 day, 3 day after CO exposure. NBP treatment obviously reduce neuronal apoptosis and the EAR (P<0.05). CO poisoning could induce Nogo, MAG and NgR1 expressions. The increased Nogo, MAG and NgR1 proteins were still observed at 4 week after CO poisoning. NBP could significantly reduce the levels of Nogo and NgR1 proteins. Then we suspected that the expressions of Nogo, MAG and NGR1 proteins might be associated with brain injury and demyelination induced by CO poisoning. NBP might inhibit neuronal apoptosis and the EAR, down-regulate the expressions of Nogo and NgR1 proteins (but not MAG), and play a neuro-protective role in brain damage after acute CO poisoning.

Objectives: To investigate the clinical value of B-type natriuretic peptide (BNP) in the assessment of severity and prognosis in acute lung injury/acute respiratory distress syndrome (ALI/ARDS). Methods: Plasma BNP level, arterial blood gases, serum C-reactive protein level, alveolar-arterial oxygen tension difference and oxygenation index were measured in patients with and without ALI/ ARDS within 24 h of admission to an intensive care unit. Patients with ALI/ARDS were divided into mild, moderate or severe groups according to the degree of hypoxaemia. Survival >28 days was recorded.Results: A total of 59 patients with ALI/ARDS and 14 patients without ALI/ARDS were included in the study. Of the patients with ALI/ARDS, 18 had mild hypoxaemia, 20 had moderate hypoxaemia and 21 had severe hypoxaemia. The mean AE SD BNP level was significantly higher in all three ALI/ ARDS groups (92.41 AE 28.19 pg/ml, 170.64 AE 57.34 pg/ml and 239.06 AE 59.62 pg/ml, respectively, in the mild, moderate and severe groups) than in the non-ALI/ARDS group (47.27 AE 19.63 pg/ml); the increase in BNP level with increasing severity was also statistically significant. When divided according to outcome, the BNP level in the death group (267.07 AE 45.06 pg/ml) was significantly higher than in the survival group (128.99 AE 45.42 pg/ml). Conclusions: The BNP level may be of value in evaluating severity and prognosis in patients with ALI/ARDS.