Testosterone: the crucial hormone responsible for depressing myocardial function in males after trauma-hemorrhage

To determine whether testosterone depletion in males before trauma-hemorrhage has any salutary effects on cardiac performance after hemorrhage and resuscitation.

Studies indicate that castration of male mice before trauma-hemorrhage prevents the immunodepression seen after hemorrhage and resuscitation. However, the effect of precastration on cardiac performance under such conditions remains unknown.

Male rats were castrated or sham-castrated 14 days before the experiment. After laparotomy (i.e., induction of trauma), the rats were bled to and maintained at a mean arterial pressure of 40 mm Hg until 40% of the maximal shed volume was returned in the form of Ringer's lactate solution. The animals were then resuscitated with four times the shed blood volume with Ringer's lactate solution over 60 minutes. Heart performance was measured using a left ventricular catheter connected to an in vivo heart performance analyzer. Indices of left ventricular performance (i.e., maximal rate of the pressure increase [+dP/dt(max)] and decrease [-dP/dt(max)) were measured up to 4 hours after trauma, hemorrhagic shock, and resuscitation.

In sham-castrated animals, trauma-hemorrhage and resuscitation decreased the in vivo heart performance as evidenced by the reduced values of +dP/dt(max) and -dP/dt(max). Precastrated animals, however, showed significantly higher values of +dP/dt(max) and -dP/dt(max) than sham-castrated animals after trauma-hemorrhage and resuscitation.

Testosterone antagonism in males might be an effective approach for maintaining myocardial function after adverse circulatory conditions. Although testosterone depletion in male trauma victims is neither practical nor advocated, testosterone receptor blockade after trauma may represent a novel and useful adjunct for maintaining normal myocardial performance under those conditions.