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The Influence of Nicardipine-, Nitroglycerin-, and Prostaglandin E1-Induced Hypotension on Cerebral Pressure Autoregulation in Adult Patients During Propofol-Fentanyl Anesthesia
28
Citations
20
References
2002
Year
Prostaglandin E1-induced HypotensionHypertensionAnesthetic MechanismBlood PressureCerebral Vascular RegulationCerebral Pressure AutoregulationIntracranial PressureBrain InjuryNeurologyContinuous InfusionPropofol-fentanyl AnesthesiaAnesthetic PharmacologyHealth SciencesVascular PharmacologyNeurological MonitoringNeuropharmacologyVascular BiologyCerebral Blood FlowPharmacologyNeurological AssessmentCardiovascular DiseaseNeurophysiologySlow Continuous InfusionAnesthesiaMedicineAnesthesiology
We investigated the influence of drug-induced hypotension at a mean arterial pressure (MAP) of 60–70 mm Hg on cerebral pressure autoregulation in 45 adult patients during propofol-fentanyl anesthesia. Time-averaged mean blood flow velocity in the right middle cerebral artery (Vmca) was continuously measured at a Paco2 of 39–40 mm Hg by using transcranial Doppler ultrasonography. Hypotension was induced and maintained with a continuous infusion of nicardipine, nitroglycerin, or prostaglandin E1. Cerebral autoregulation was tested by a slow continuous infusion of phenylephrine to induce an increase in MAP of 20–30 mm Hg. From the simultaneously recorded data of Vmca and MAP, cerebral vascular resistance (CVR) was calculated as MAP/Vmca. Furthermore, the index of autoregulation (IOR) was calculated as ΔCVR/ΔMAP, where ΔCVR = change in CVR and ΔMAP = change in MAP. The test was performed twice for each condition on each patient: baseline and hypotension. The IOR during baseline was similar among the groups. During nitroglycerin- and prostaglandin E1-induced hypotension, IOR was not different from baseline. In contrast, during nicardipine-induced hypotension, IOR significantly decreased compared with baseline (0.37 ± 0.08 versus 0.83 ± 0.07, P < 0.01). In conclusion, nicardipine, but not nitroglycerin or prostaglandin E1, significantly attenuates cerebral pressure autoregulation during propofol-fentanyl anesthesia.
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