Abstract

Brain death (BD) induces hemodynamic instability with microcirculation hypoperfusion leading to increased heart tissue inflammation and dysfunction. This study investigates the effects of 7.5% hypertonic saline solution administration on the course of myocardial and left ventricular (LV) function changes observed after BD induction in rats. Male Wistar rats were anesthetized and mechanically ventilated. BD was induced by inflation of a balloon catheter placed into intracranial cavity. Rats were randomly divided into three groups: NS - rats maintained with normal saline immediately after BD induction (0.9% NaCl, 4 mL/Kg); HS - rats treated with hypertonic saline (7.5% NaCl, 4 mL/Kg) immediately after BD; HS60 - rats treated with hypertonic saline (7.5% NaCl, 4 mL/Kg) 60 minutes after BD. LV function was evaluated by conductance microcatheter technique for 6 hours after induction of BD. Immunohistochemistry was performed to investigate endothelial intercellular adhesion molecules and apoptotic proteins expressions in LV samples collected after animal’s euthanasia. All groups presented similar hypertensive peak followed by hypotension after BD induction. Six hours after induction of BD, preload recruitable stroke work and dp/dt(max) were significantly reduced in comparison to baseline in NS group, whereas these parameters were preserved at similar baseline levels in both HS and HS60 groups. LV ejection fraction was also reduced in NS group (70% of baseline) at 6 hours, but in contrast it was preserved in HS60 group, which presented significantly elevated values in comparison to NS group (72 ± 6 vs. 41 ± 6, p<0.001). Tau was significantly elevated versus baseline 6 hours after induction of BD especially in NS and HS60 groups. Both treatments, HS and HS60, reduced the expression of vascular cell adhesion molecules (VCAM-1) and increased the levels of BCL-2 anti-apoptotic proteins, when compared to NS group. Data presented suggest that treatment of BD rats with hypertonic saline solution improves LV function and reduces myocardial injury, even when performed in the course of BD progression.

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