Amplification by hyperoxia of coronary vasodilation induced by propofol.

UNLABELLED: We tested the hypothesis that in vitro coronary and myocardial effects of propofol (10-300 microM) should be significantly modified in an isolated and erythrocyte-perfused rabbit heart model in the absence (PaO(2) = 137 +/- 16 mm Hg, n = 12) or in the presence (PaO(2) = 541 +/- 138 mm Hg, n = 12) of hyperoxia. The induction of hyperoxia provoked a significant coronary vasoconstriction (-13% +/- 7%). Propofol induced increased coronary vasodilation in the presence of hyperoxia. Because high oxygen tension has been reported to induce a coronary vasoconstriction mediated by the closure of adenosine triphosphate-sensitive potassium channels, we studied the effects of propofol in 2 additional groups of hearts (n = 6 in each group) pretreated by glibenclamide (0.6 microM) and cromakalim (0.5 microM) in the absence and presence of hyperoxia, respectively. The pretreatment by glibenclamide induced a coronary vasoconstriction (-16% +/- 7%) which did not affect propofol coronary vasodilation. The pretreatment by cromakalim abolished the amplification of propofol coronary vasodilation in the presence of hyperoxia. Propofol induced a significant decrease in myocardial performance for a concentration >100 micro M both in the absence and presence of hyperoxia. We conclude that propofol coronary vasodilation is amplified in the presence of hyperoxia. This phenomenon is not explained by the previous coronary vasoconstriction induced by glibenclamide. However, the pretreatment of hearts by cromakalim abolished the amplification of propofol coronary vasodilation in the presence of hyperoxia. The myocardial effects of propofol were not affected by the presence of hyperoxia. IMPLICATIONS: Propofol induced a coronary vasodilation that was amplified in the presence of hyperoxia. This phenomenon does not seem to be related to previous coronary vasoconstriction. The myocardial effects of propofol were not significantly modified in the presence of hyperoxia.

Detection of brain death onset using the bispectral index in severely comatose patients.

OBJECTIVES: To evaluate the accuracy of bispectral index (BIS) monitoring for the diagnosis of brain death in severely comatose patients. DESIGN: A prospective study in an intensive care unit of a university hospital. POPULATION: Fifty-six severely comatose patients (Glasgow Coma Score < or = 5) admitted to the ICU mainly because of intracerebral hemorrhage, head injury, or postanoxic coma. METHODS: BIS was recorded continuously during the hospitalization in the ICU. Where necessary, clinical brain death was confirmed by EEG or cerebral angiography. MEASUREMENTS AND RESULTS: Twelve patients were already clinically brain dead at the time of admission, and their individual BIS values were 0. In each of these 12 patients brain death was thereafter confirmed by EEG or cerebral angiography. Forty-four patients were not clinically brain-dead at the time of admission, and their individual BIS values were between 20 and 79. Twenty-seven of these patients became brain-dead, and their individual BIS values dropped to 0 in a few hours to a few days. In these 27 patients EEG or cerebral angiography was performed after the BIS value decreased to 0 and confirmed brain death in all cases. Seventeen patients who did not become brain dead during their hospitalization in the ICU had persistent electrocerebral activity on EEG, and their average BIS values remained above 35. CONCLUSION: BIS can be used in severely comatose patients as an assessment of brain death onset, enabling appropriate scheduling of either EEG or cerebral angiography to confirm brain death.