PROLONGED SEVERE HEMORRHAGIC-SHOCK AND RESUSCITATION IN RATS DOES NOTCAUSE SUBTLE BRAIN-DAMAGE

Objective: Some patients who survived severe hemorrhagic shock (HS) se em to exhibit persistent subtle neurobehavioral deficits, This finding is of concern if limited hypotensive fluid resuscitation is applied i n hypotensive victims with penetrating trauma. This study was designed to determine whether subtle brain damage would occur in rats after se vere prolonged HS, We hypothesized that rats surviving HS with mean ar terial pressure (MAP) controlled at 40 mm Hg for 60 minutes would reco ver with slight permanent brain damage in terms of cognitive function without morphologic loss of neurons and that rats surviving HS with MA P at 30 mm Hg for 45 minutes (60 minutes were not tolerated) would hav e grossly abnormal brain function and loss of neurons. Methods: Under light nitrous oxide-halothane anesthesia, spontaneously breathing rats underwent MAP-controlled HS (HS phase I), volume resuscitation to nor motension and invasive monitoring to 60 minutes (resuscitation phase I I), and observation to 10 days with detailed assessment of cognitive f unction (observation phase III). Five conscious rats served as normal controls. Three treatment groups were compared: group 1, shams (11 of 12 rats survived to 10 days); group 2, HS at MAP 40 mm Hg for 60 minut es (10 of 17 rats survived); group 3, HS at 30 mm Hg for 45 minutes (1 0 of 14 rats survived). Results: On post-HS day 10, all normal control s and all survivors of all three groups were functionally normal with overall performance category = 1 (normal) (overall performance categor y 1 = normal, 5 = death) and neurologic deficit scores less than or eq ual to 7% (neurologic deficit scores 0-10% = normal, 100% = brain deat h). Post-HS beam balance, beam walking, and Morris water maze test res ults in HS groups 2 and 3 showed latencies not significantly different from those in shams and normal controls, Light microscopic scoring of five selectively vulnerable brain regions and other regions in five c oronal sections revealed no ischemic (pyknotic, shrunken, eosinophilic ) neurons in any of the survivors to 10 days. There was no statistical difference between normal controls, sham animals, and both HS groups in the number of normal neurons counted in the hippocampal CA-1 region in the 10-day survivors. All nonsurvivors died with intestinal necros is, Conclusion: HS at MAP 40 mm Hg for 60 minutes or MAP 30 mm Hg for 45 minutes does not cause subtle functional or histologic brain damage in surviving rats. Controlling MAP at 30 mm Hg carries a risk of sudd en cardiac arrest. These data suggest that limited fluid resuscitation , to maintain MAP at about 40 mm Hg, as recommended for victims of pen etrating trauma with uncontrolled HS, is safe for the brain.