@article{oai:niigata-u.repo.nii.ac.jp:00006364,
 author = {Endoh, Hiroshi and Honda, Tadayuki and Komura, Noboru and Shibue, Chieko},
 issue = {4},
 journal = {Acta medica et biologica, Acta medica et biologica},
 month = {Dec},
 note = {The purpose of the present study was to evaluate the effects of nicardipine (NIC), nitroglycerin (NTG), and prostaglandin E_1 (PGE_1) on cerebrovascular CO_2 reactivity during propofol-fentanyl anesthesia in humans. Cerebrovascular CO_2 reactivity was evaluated with transcranial Doppler sonography (TCD) in 30 patients. The patients were randomly allocated to NIC, NTG or PGE_1 groups. Anesthesia was induced and maintained with a bolus, followed by a continuous infusion of propofol (6.73±0.45 mg/kg/hr) and fentanyl (1.72±0.54 ,μg/kg/hr). Time-mean blood flow velocity in the right middle cerebral artery (Vmca) was measured with TCD at an end-tidal CO_2 tension (P_<ET>C0_2 ) of 50, 45, 40, 35, 30, and 25 mmHg during normotension and hypotension. Induced hypotension of mean arterial pressure 55-60 mmHg was maintained with a continuous infusion of NIC (6.99±0.73 ,μg/kg/min), NTG (2.98±1.10 ,μg/kg/min) or PGE_1 (0.103±0.052 μg/kg/ min). The CO_2 reactivity of Vmca was determined by linear or exponential regression analysis and was compared between normotension and induced hypotension with repeated measures ANOVA. There was a significant close linear and exponential regression between Vmca and P_<ET>CO_2 during normotension and hypotension in each subject (r >0.95, p <0.05). Absolute slopes and exponents were significantly attenuated during drug-induced hypotension, when compared with normotension (p <0.05). These results strongly suggest that the cerebrovascular CO_2 reactivity is preserved. However, the cerebrovascular sensitivity to CO_2 is attenuated during NIC, NTG, and PGE_1-induced hypotension.},
 pages = {133--138},
 title = {Effects of Induced Hypotension on Cerebral Vasomotor Response to Carbon Dioxide in Humans},
 volume = {46},
 year = {1998}
}