Nagase K, Iida H, Ohata H, Dohi S
Department of Anesthesiology & Critical Care Medicine, Gifu University School of Medicine, Gifu, Japan.
J Clin Anesth. 2001 Dec;13(8):551-5. doi: 10.1016/s0952-8180(01)00328-2.
To investigate the effects of ketamine and propofol on the cerebrovascular response to carbon dioxide (CO(2)) in humans during isoflurane anesthesia.
Randomized clinical investigation.
University hospital of a medical school.
30 ASA physical status I and II adult, elective surgical patients.
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.
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].
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).
探讨氯胺酮和丙泊酚对异氟烷麻醉期间人体脑血管对二氧化碳（CO₂）反应的影响。
随机临床研究。
一所医学院的大学医院。
30例美国麻醉医师协会（ASA）身体状况为Ⅰ级和Ⅱ级的择期手术成年患者。
每位患者接受空气/氧气/异氟烷麻醉，在低碳酸血症（动脉血二氧化碳分压（PaCO₂）28 - 32 mmHg）、正常碳酸血症（PaCO₂ 38 - 42 mmHg）和高碳酸血症条件（PaCO₂ 48 - 52 mmHg）下，使用经颅多普勒方法测量大脑中动脉血流速度（Vmca）和搏动指数。通过在不改变呼吸条件的情况下向吸入气体中补充CO₂来改变PaCO₂。然后将患者随机分为两组，分别接受氯胺酮1 mg·kg⁻¹或丙泊酚（2 mg·kg⁻¹，随后以6 - 10 mg·kg⁻¹·h⁻¹的速度输注）（每种药物各15例），并重复测量。
氯胺酮显著降低了对CO₂的绝对和相对脑血管反应性[（对照）2.9 ± 0.8 vs.（氯胺酮）2.6 ± 1.0 cm·sec⁻¹·mmHg⁻¹：p < 0.05；以及（对照）3.5 ± 0.7 vs.（氯胺酮）2.8 ± 0.9 %·mmHg⁻¹：p < 0.01]。然而，与对照组（120 ± 28 cm·sec⁻¹）相比，氯胺酮在高碳酸血症条件下并未降低Vmca（117 ± 29 cm·sec⁻¹）。虽然丙泊酚在所有条件下均降低了Vmca，但它并未引起绝对或相对CO₂反应性的任何变化[（对照）2.5 ± 0.8 vs.（丙泊酚）2.5 ± 1.0 cm·sec⁻¹·mmHg⁻¹，以及（对照）3.3 ± 1.3 vs.（丙泊酚）4.1 ± 1.0 %·mmHg⁻¹]。
在接受异氟烷麻醉的人体中，a）氯胺酮降低了脑血管对CO₂的反应，但高碳酸血症条件下的脑血流量（CBF）与对照组相当；b）虽然丙泊酚降低了CBF，但它维持了脑血管对CO₂的反应。
