[Effect of flumazenil on global cerebral blood flow and on intracranial pressure in the reperfusion phase following incomplete global cerebral ischemia].

Sedation with benzodiazepines in intensive care patients with head injuries has become part of a standard concept in controlling intracranial pressure (ICP) and metabolic demands of an injured brain. The specific benzodiazepine antagonist flumazenil, which is supposed to exert no direct effect on cerebral blood flow (CBF) in healthy volunteers, suggests that rapid reversal from midazolam sedation might be achieved without any deleterious side effects. It remains however ambiguous if the same holds true in subjects with head trauma. This study describes the effect of flumazenil on CBF, ICP and cerebral perfusion pressure (CPP) during the reperfusion period after incomplete global ischemia in 10 goats. After preparation progressively decreasing CBF in 7 goats was achieved by stepwise external occlusion of the a. max. interna. 90-120 min after reestablishment of CBF 15 mg midazolam i.v. were given followed by 0.5 mg flumazenil i.v. 5 min later. Within 60 sec after application of the antagonist an increase of CBF by 30-165% and of ICP by 25-310% was noted in 5 goats. Simultaneous changes in arterial pressure, CBF and ICP suggest a severe impact of the benzodiazepine antagonist after midazolam sedation on ICP and CBF during periods of impaired cerebral autoregulation. Until the cerebrovascular and cerebral metabolic effects of flumazenil have been elaborated in detail, it is recommended to titrate the effect of flumazenil over long intervals in head injured patients.