Traumatic brain injury attenuates the effectiveness of lactated Ringer's solution resuscitation of hemorrhagic shock in rats.

Traumatic brain injury suppresses spontaneous cardiovascular compensation for hemorrhage, prompting us to examine the possibility that trauma to the brain modifies hemodynamic response to therapy in hemorrhage. Thirty rats that were anesthetized were randomly assigned to four groups--hemorrhagic shock (H), hemorrhagic shock after brain trauma (TH), hemorrhagic shock treated with lactated Ringer's (LR) solution (HR), and hemorrhagic shock after brain trauma treated with LR (THR). After hemorrhage, group TH had significantly lower mean arterial pressure (MAP), cardiac index (CI) and stroke volume index (SVI) than group H. Throughout the postresuscitative period, group HR had significantly higher MAP, CI, SVI and central venous pressure than group H. At 50 and 70 minutes after the start of hemorrhage, group THR showed significantly lower MAP, CI and SVI than group HR. This difference in hemodynamics is not because of transcapillary refill effect, because brain trauma did not cause changes in hematocrit and plasma protein levels. As heart rate, preload and afterload were not significantly different between groups THR and HR, the attenuation of fluid resuscitation can be attributed mainly to a depressed cardiac function. Furthermore, neither brain trauma nor fluid replacement altered the content of water in the brain in hemorrhaged rats. These data indicate that brain trauma not only suppresses spontaneous hemodynamic recovery from hemorrhage, but also impedes the efficacy of LR resuscitation. The results of the current study suggested that a more aggressive fluid replacement may be needed to treat hemorrhagic shock in individuals with brain injury.