Hypertonic Saline Solution Reduces Microcirculatory Dysfunction and Inflammation in a Rat Model of Brain Death

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Abstract

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: (1)SH, sham-operated rats subjected to trepanation; (2)NS, rats treated with NaCl 0.9%, 4 mL/kg immediately after BD; (3)T1, rats treated with HSS (NaCl 7.5%, 4 mL/kg) immediately or 60 min after BD, (4)T60. All groups were analyzed 180 minutes 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%, p = 0.0039). HSS restored the proportion of perfused vessels (T1 = 71%, p = 0.0018). The eNOS protein expression significantly increased in rats given HSS (T1, and T60, p = 0.0002). Similar results were observed regarding endothelin-1 (p < 0.0001). Increased numbers of rolling (p = 0.0015) and migrated (p = 0.0063) 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 (p = 0.0002).

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.

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