Effects of nicardipine-, nitroglycerin-, and prostaglandin E1-induced hypotension on human cerebrovascular carbon dioxide reactivity during propofol-fentanyl anesthesia.
OBJECTIVE
To investigate the effects of nicardipine-, nitroglycerin-, and prostaglandine E1-induced hypotension on cerebrovascular carbon dioxide (CO2) reactivity over a wide range of arterial CO2 tension (PaCO2) (PaCO2; range 25 to 50 mmHg).


METHODS
Prospective, randomized study.


METHODS
Operating room of a university-affiliated hospital.


METHODS
36 ASA physical status I and II patients without cerebrovascular disease, hypertension, or diabetes mellitus, undergoing an elective abdominal surgery.


METHODS
Patients were randomly allocated to one of three groups (nicardipine-, nitroglycerin-, or prostaglandin E1-induced hypotension group; 12 in each group). Anesthesia was induced and maintained with a bolus dose, followed by a continuous infusion of propofol (6.7 +/- 1.5 mg/kg/hr) and fentanyl (1.68 +/- 0.4 micrograms/kg/hr). Deliberate hypotension of mean arterial pressure 55 to 60 mmHg was induced and maintained with a bolus dose, followed by a continuous infusion of nicardipine (6.80 +/- 0.75 micrograms/kg/min), nitroglycerin (3.20 +/- 1.10 micrograms/kg/min), or prostaglandin E1 (0.103 +/- 0.052 microgram/kg/min).


RESULTS
Time-averaged mean red blood cell velocity in the right middle cerebral artery (Vmca) at PaCO2 ranging from 25 to 50 mmHg was measured with transcranial Doppler ultrasonography. A minimum of six simultaneous measurements of Vmca and PaCO2 were obtained during baseline and deliberate hypotension in each patient. Absolute slope between Vmca and PaCO2 during baseline and deliberate hypotension was determined individually by linear regression analysis. Absolute slope was treated as the variable, because it yielded a significant close correlation coefficient (r > 0.95; p < 0.05). Comparisons between baseline and deliberate hypotension were made by analysis of variance for repeated measures. Mean absolute slope was significantly reduced from 1.88 +/- 0.57 cm/sec/mmHg (mean +/- SD) to 1.21 +/- 0.46 in the nicardipine group (p < 0.05), from 1.75 +/- 0.69 to 1.35 +/- 0.47 in the nitroglycerin group (p < 0.05), and from 1.95 +/- 0.89 to 1.33 +/- 0.70 (p < 0.05) in the prostaglandin E1 group, respectively.


CONCLUSIONS
Nicardipine-, nitroglycerin-, and prostaglandin E1-induced hypotension attenuate the human cerebrovascular CO2 reactivity during propofol-fentanyl anesthesia.
Endoh
H
H
Department of Anesthesiology, Niigata University School of Medicine, Japan. endoh@med.niigata-u.ac.jp
Honda
T
T
Komura
N
N
Shibue
C
C
Watanabe
I
I
Shimoji
K
K
D000328:Adult; D000527:Alprostadil / Q000494:pharmacology*; D000704:Analysis of Variance; D018686:Anesthetics, Intravenous / Q000008:administration & dosage*; D000959:Antihypertensive Agents / Q000494:pharmacology*; D001783:Blood Flow Velocity / Q000187:drug effects; D001794:Blood Pressure / Q000187:drug effects; D002245:Carbon Dioxide / Q000097:blood*; D002560:Cerebrovascular Circulation / Q000187:drug effects / Q000502:physiology*; D004912:Erythrocytes / Q000187:drug effects; D005260:Female; D005283:Fentanyl / Q000008:administration & dosage*; D006801:Humans; D007022:Hypotension / Q000139:chemically induced / Q000503:physiopathology*; D016014:Linear Models; D008297:Male; D020768:Middle Cerebral Artery / Q000187:drug effects; D009529:Nicardipine / Q000494:pharmacology*; D005996:Nitroglycerin / Q000494:pharmacology*; D015742:Propofol / Q000008:administration & dosage*; D011446:Prospective Studies; D017585:Ultrasonography, Doppler, Transcranial; D014665:Vasodilator Agents / Q000494:pharmacology*
D018686:Anesthetics, Intravenous; D000959:Antihypertensive Agents; D014665:Vasodilator Agents; D002245:Carbon Dioxide; D009529:Nicardipine; D000527:Alprostadil; D005996:Nitroglycerin; D005283:Fentanyl; D015742:Propofol