Effect of DHEA on the hemodynamic response to resuscitation in a porcine model of hemorrhagic shock

BACKGROUND: Hemorrhagic shock is a major cause of death from trauma. Pharmacologic treatment has not been satisfactory. The objective of this study was to use a porcine model of hemorrhagic shock and resuscitation to access the hemodynamic effects of dehydroepiandrosterone (DHEA), an adrenal steroid hormone reported to improve cardiac function in patients. METHODS: Hemorrhagic shock was produced in 20- to 30-kg male Yorkshire pigs anesthetized with 2% isoflurane by withdrawing blood through a carotid cannula to a mean arterial pressure (MAP) of 40 to 45 mm Hg and maintaining that level for 60 minutes by further removals of blood. Resuscitation was with 21 mL/kg Ringer's lactate (LR), with (n = 6) or without (n = 6) DHEA (4 mg/kg) dissolved in propylene glycol. The animals were killed after 7 days. Continuous cardiac output (CCO) was recorded using a modified Swan-Ganz catheter system. MAP, heart rate (HR), central venous pressure (CVP), and pulmonary arterial pressure (PAP) were measured every 5 minutes until 60 minutes postresuscitation. From MAP, CCO, HR, and CVP, we calculated total peripheral resistance (TPR), stroke volume (SV), and left ventricular stroke work (SW). RESULTS: The MAP, CCO, SV, and SW decreased significantly during hemorrhagic shock, and then gradually increased to baseline levels during and 1 hour after resuscitation. The TPR was increased during hemorrhagic shock, and then gradually decreased to baseline levels during and after resuscitation. DHEA administration was associated with no significant improvement. CONCLUSION: DHEA when added to standard fluid resuscitation showed no added benefit as resumed by the hemodynamic response.