Radiographically determined injuries to the lung parenchyma have a closer association with adverse outcome than chest-wall injuries but are often not diagnosed until 24 hours after injury. Therefore, clinical decision making, such as about the choice of surgery for long bone fractures, may be flawed if this information is used alone. A new thoracic trauma severity score may serve as an additional tool to improve the accuracy of the prediction of thoracic trauma-related complications.

Although studies have shown that testosterone receptor blockade with flutamide after hemorrhage restores the depressed immune function, it remains unknown whether administration of flutamide following trauma and hemorrhage and resuscitation has any salutary effects on the depressed cardiovascular and hepatocellular functions. To study this, male rats underwent a laparotomy (representing trauma) and were then bled and maintained at a mean arterial pressure (MAP) of 40 mmHg until the animals could not maintain this pressure. Ringer lactate was given to maintain a MAP of 40 mmHg until 40% of the maximal shed blood volume was returned in the form of Ringer lactate. The rats were then resuscitated with four times the shed blood volume in the form of Ringer lactate over 60 min. Flutamide (25 mg/kg) or an equal volume of the vehicle propanediol was injected subcutaneously 15 min before the end of resuscitation. Various in vivo heart performance parameters (e.g., maximal rate of the pressure increase or decrease), cardiac output, and hepatocellular function (i.e., the maximum velocity and the overall efficiency of indocyanine green clearance) were determined at 20 h after resuscitation. Additionally, hepatic microvascular blood flow (HMBF) was determined using a laser Doppler flowmeter. The results indicate that left ventricular performance, cardiac output, HMBF, and hepatocellular function decreased significantly at 20 h after the completion of trauma, hemorrhage, and resuscitation. Administration of the testosterone receptor blocker flutamide, however, significantly improved cardiac performance, HMBF, and hepatocellular function. Thus flutamide appears to be a novel and useful adjunct for improving cardiovascular and hepatocellular functions in males following trauma and hemorrhagic shock.

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ObjectiveTo determine whether testosterone depletion in males before trauma-hemorrhage has any salutary effects on cardiac performance after hemorrhage and resuscitation. Summary Background DataStudies indicate that castration of male mice before traumahemorrhage prevents the immunodepression seen after hemorrhage and resuscitation. However, the effect of precastration on cardiac performance under such conditions remains unknown. MethodsMale 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,,j and decrease [-dP/dtmaJ) were measured up to 4 hours after trauma, hemorrhagic shock, and resuscitation. ResultsIn sham-castrated animals, trauma-hemorrhage and resuscitation decreased the in vivo heart performance as evidenced by the reduced values of +dP/dtma,, and -dP/dtm,. Precastrated animals, however, showed significantly higher values of +dP/dtmax and -dP/dtmax than sham-castrated animals after trauma-hemorrhage and resuscitation. ConclusionsTestosterone 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. Despite aggressive fluid resuscitation, severe trauma is often associated with cardiovascular instability, severe in-