Ketamine, not propofol, attenuates cerebrovascular response to carbon dioxide in humans with isoflurane anesthesia.
OBJECTIVE
To investigate the effects of ketamine and propofol on the cerebrovascular response to carbon dioxide (CO(2)) in humans during isoflurane anesthesia.


METHODS
Randomized clinical investigation.


METHODS
University hospital of a medical school.


METHODS
30 ASA physical status I and II adult, elective surgical patients.


METHODS
With each patient given air/oxygen/isoflurane anesthesia, the flow velocity in the middle cerebral artery (Vmca) and pulsatility index were measured using the transcranial Doppler method under hypocapnic [arterial CO(2)tension (PaCO(2)) 28-32 mmHg], normocapnic (PaCO(2) 38-42 mmHg), and hypercapnic conditions (PaCO(2) 48-52 mmHg). PaCO(2) was altered by supplementing the inspired gas with CO(2) without changing the respiratory conditions. Patients were then randomly assigned to receive either ketamine 1 mg. kg(-1) or propofol (2 mg. kg(-1)followed by an infusion of 6-10 mg. kg(-1). hr(-1)) (n = 15 for each drug), and the measurements were repeated.


RESULTS
Ketamine reduced both absolute and relative cerebrovascular reactivity to CO(2) significantly [2.9 +/- 0.8 (control) vs. 2.6 +/- 1.0 (ketamine) cm. sec(-1). mmHg(-1): p < 0.05; and 3.5 +/- 0.7 (control) vs. 2.8 +/- 0.9 (ketamine) %. mmHg(-1): p < 0.01, respectively]. However, ketamine did not reduce Vmca during hypercapnic conditions (117 +/- 29 cm. sec(-1)) compared with controls (120 +/- 28 cm. sec(-1)). Although propofol decreased Vmca during all conditions, it did not cause any change in either absolute or relative CO(2) reactivity [2.5 +/- 0.8 (control) vs. 2.5 +/- 1.0 (propofol) cm. sec(-1). mmHg(-1), and 3.3 +/- 1.3 (control) vs. 4.1 +/- 1.0 (propofol) %. mmHg(-1), respectively].


CONCLUSIONS
In humans given isoflurane anesthesia, a) ketamine reduced cerebrovascular response to CO(2), but cerebral blood flow (CBF) during hypercapnic conditions was comparable with controls, and b) although propofol decreases CBF, it maintains the cerebrovascular response to CO(2).
Nagase
K
K
Department of Anesthesiology & Critical Care Medicine, Gifu University School of Medicine, Gifu, Japan.
Iida
H
H
Ohata
H
H
Dohi
S
S
D000328:Adult; D000769:Anesthesia, Inhalation; D018685:Anesthetics, Inhalation; D018686:Anesthetics, Intravenous / 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*; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D007530:Isoflurane; D007649:Ketamine / Q000494:pharmacology*; D008297:Male; D020768:Middle Cerebral Artery / Q000502:physiology; D016202:N-Methylaspartate / Q000037:antagonists & inhibitors; D015742:Propofol / Q000494:pharmacology*
D018685:Anesthetics, Inhalation; D018686:Anesthetics, Intravenous; D002245:Carbon Dioxide; D016202:N-Methylaspartate; D007649:Ketamine; D007530:Isoflurane; D015742:Propofol