1. Four groups of mice were subjected to controlled fatal head trauma and then evaluated for the presence of ascites (neurogenic hyperacute ascites, NHA). The animals died virtually instantaneously and without evidence of maintained pain or suffering. The volume of ascites was determined in one group of animals. Two of the traumatized groups were pretreated, one with the β-blocker propranolol and the other with the α-blocker phentolamine. A fifth, non-traumatized, group which was killed with ether inhalation served as a control group. Two more groups of non-traumatized mice were administered either the α-adrenergic agonist methoxamine hydrochloride or the β-agonist isoethrane mesylate before killing by ether inhalation, and then evaluated for ascites.
2. Transudative ascitic fluid was found in 87–100% of untreated traumatized mice and in no control animals. Pretreatment with phentolamine had no effect on the prevalence of ascites. Pretreatment with propranolol produced a significant decrease in the prevalence of ascites compared with trauma alone (P < 0.001). Isoethrane (β-agonist) administration caused ascites in 100% of the treated animals. Methoxamine (α-agonist) administration did not cause ascites.
3. A previously undescribed consequence of acute brain trauma is described (NHA) which appears to be mediated by β-sympathetic activity of central origin. NHA is inhibited by β-blockade and can be simulated with β-agonist administration.