RESUMO
BACKGROUND: Brain death (BD) induces hemodynamic instability with microcirculatory hypoperfusion, leading to increased organ inflammation and dysfunction. This study investigated the effects of 7.5% hypertonic saline solution (HSS) on mesenteric microcirculatory dysfunction and inflammation in a rat model of BD. METHODS: Male Wistar rats were anesthetized and mechanically ventilated. BD was induced by rapidly inflating an intracranial balloon catheter. The rats were randomly divided into: SH, sham-operated rats subjected to trepanation; NS, rats treated with NaCl 0.9%, 4âmL/kg immediately after BD; T1, rats treated with HSS (NaCl 7.5%, 4âmL/kg) immediately or 60âmin after BD, T60. All groups were analyzed 180 min after the start of the experiment. RESULTS: Rats in BD groups presented with a similar hypertensive peak, followed by hypotension. Proportion of perfused small vessels was decreased in the NS group (46%) compared with the SH group (74%, Pâ=â0.0039). HSS restored the proportion of perfused vessels (T1â=â71%, Pâ=â0.0018). The anti-endothelial nitric oxide synthase (eNOS) protein expression significantly increased in rats given HSS (T1, and T60, Pâ=â0.0002). Similar results were observed regarding endothelin-1 (Pâ<â0.0001). Increased numbers of rolling (Pâ=â0.0015) and migrated (Pâ=â0.0063) leukocytes were observed in the NS group compared with the SH group. Rats given HSS demonstrated an overall reduction in leukocyte-endothelial interactions. The ICAM-1 levels increased in the NS group compared with the SH group, and decreased in the HSS-treated groups (Pâ=â0.0002). CONCLUSIONS: HSS may improve the density of mesenteric perfused small vessels due to its effects on eNOS and endothelin-1 protein expression, and reduces inflammation by decreasing leukocyte adhesion and migration in a rat model of BD.