Suppression by traumatic brain injury of spontaneous hemodynamic recovery from hemorrhagic shock in rats

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Abstract
✓ The effects of brain trauma on cardiovascular and endocrine responses to hemorrhage were investigated. Forty anesthetized rats were randomly assigned to one of four groups of 10 rats each: a control group (Group C); a group with induction of hemorrhage at 16.2 ml/kg/10 min (Group H); a group with fluid-percussion brain injury at a peak pressure of 1.7 atm and an impulse duration of 25 msec (Group T); and a group receiving hemorrhagic shock following brain trauma (Group TH). Group C and T rats showed no significant alterations in cardiovascular function. At the end of hemorrhage there were no significant differences between Groups TH and H in the nadirs of mean arterial blood pressure (MABP) (mean values ± standard error of the mean: 42 ± 2 vs. 40 ± 4 mm Hg) and stroke volume index (SVI) (0.61 ± 0.11 vs. 0.66 ± 0.10 ml/bt/kg); however, 1 hour post-hemorrhage recovery was blunted in Group TH compared to Group H (MABP 56 ± 4 vs. 65 ± 3 mm Hg; cardiac index 182 ± 15 vs. 220 ± 15 ml/min/kg; and SVI 0.71 ± 0.06 vs. 0.81 ± 0.06 ml/bt/kg). Since the two groups showed no significant differences in heart rate, preload (central venous pressure), and afterload (systemic vascular resistance), the reduced cardiac index recovery in Group TH is believed due to the attenuation of cardiac contractile performance. The Group TH preparation potentiated hormonal responses to hemorrhage with significantly higher epinephrine and aldosterone levels than in Group H. Brain trauma enhanced the norepinephrine response to hemorrhage, even at an injury level that by itself did not result in an increase in this hormone. Group TH rats also had significantly lower blood pH and HCO3 levels. The data suggest that brain trauma suppresses MABP and cardiac index recovery after hemorrhage mainly by inhibiting cardiac contractile performance, probably due to high catecholamine levels and severe metabolic acidosis.