Effect of DHEA on the hemodynamic response to resuscitation in a porcine model of hemorrhagic shock.J Trauma. 2006 Dec; 61(6):1343-9.JT
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.
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).
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.
DHEA when added to standard fluid resuscitation showed no added benefit as resumed by the hemodynamic response.