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Aim  To examine whether prolonged hemorrhagic shock ( HS ) at a mean arterial pressure ( MAP ) of 40 mmHg leads to brain damage.    Methods  Rats were anesthetized with sevoflurane. The  HS  model consisted of the following phases: I, pressure‐controlled  HS  at a  MAP  of 40 mmHg; II, fluid resuscitation to normalize blood pressure; III, observations with outcome evaluations in terms of survival, overall performance categories, and neurological deficit scores, as well as evaluation of apoptosis in the hippocampus at 96 h. Each group of six rats was randomized into 60 min (group 1) or 75 min (group 2) each of phases I and  II . Three sham rats were anesthetized for 150 min, and then awakened during phase  III .    Results  The three sham rats as well as five and two of the six rats in groups 1 and 2 ( P  < 0.05), respectively, survived for up to 96 h. All survivors were functionally normal with overall performance category = 1 and neurological deficit score = 0 at 96 h. Apoptotic neurons were not found in the hippocampus.    Conclusions  The higher mortality in group 2 suggested a more profound effect of  HS  compared with group 1. However, prolonged  HS  for 60 or 75 min did not cause functional damage or apoptosis in the hippocampus. These findings suggest that prolonged  HS  at a  MAP  of 40 mmHg, as a level at which cerebral blood flow seems preserved by autoregulatory mechanisms, does not lead to brain damage.

Prolonged severe hemorrhagic shock at a mean arterial pressure of 40 mmHg does not lead to brain damage in rats