Hemorrhage and intracranial hypertension in combination increase cerebral production of thromboxane A₂

Background and Methods: To determine the effects of reduced cerebral perfusion pressures produced by hemorrhage alone or in combination with intracranial hypertension on thromboxane A₂ (TxA₂) production, we undertook a randomized study in 38 anesthetized, mongrel dogs. Animals were subjected to 30 mins of hemorrhagic shock with normal (group 1) or increased (group 2) intracranial pressure (ICP). Group 1 animals (n = 22) were hemorrhaged to reduce cerebral perfusion pressure to 40 mm Hg for 30 mins. In group 2 (n = 16), cerebral perfusion pressure was reduced by the combination of less severe hypotension and intracranial hypertension (20 mm Hg). Cerebral and systemic hemodynamic measurements were recorded, including cerebral blood flow (sagittal sinus outflow method); ICP; cerebral perfusion pressure; and arterial and cerebral venous concentrations of TxB₂ (double-antibody radioimmunoassay technique), the major metabolite of TxA₂. Data were obtained at baseline and at the beginning and end of the 30-min shock period. Results: Hemorrhagic shock significantly (p < .05) decreased cerebral blood flow in both groups. At the beginning of the shock period, cerebral blood flow was higher in group 1 than in group 2 (p < .05) and venous-arterial differences in TxB₂ increased significantly (p < .05) in group 2, but not in group 1. At the end of the 30-min shock period, venous-arterial levels of TxB₂ remained significantly (p < .05) higher in group 2. Conclusions: Increased cerebral production of TxA₂ during hypotension accompanied by intracranial hypertension may contribute to the severity of neural damage produced by the combination of head trauma and shock.