氟烷降低脑脊液的生成速率。血管加压素V1受体的可能作用。

Maktabi M A, Elbokl F F, Faraci F M, Todd M M

Department of Anesthesia, University of Iowa College of Medicine, Iowa City 52242-1079.

Anesthesiology. 1993 Jan;78(1):72-82. doi: 10.1097/00000542-199301000-00012.

BACKGROUND

Circulating vasoactive hormones (e.g., vasopressin) play an important role in the regulation of blood flow to the choroid plexus and the rate of cerebrospinal fluid (CSF) production. We tested the hypothesis that halothane decreases CSF production through a vasopressin-related mechanism and examined the related changes in blood flow to the choroid plexus.

METHODS

Using ventriculocisternal perfusion, CSF production was measured in chloralose anesthetized, normothermic rabbits whose lungs were mechanically ventilated. Rabbits received either 0.5 minimum alveolar concentration (MAC; end-tidal) of halothane (added to a preestablished chloralose anesthetic), 0.5 MAC of halothane in the presence of a vasopressin V1 antagonist (iv), or the V1 antagonist alone. In addition, we examined animals in which no intervention was made (time control) and animals subjected to a 25% decrease in mean blood pressure produced by hemorrhage, with and without the V1-antagonist. In a separate series of rabbits, regional and total blood flows to the brain and the choroid plexus were measured using radioactive microspheres. These studies were carried out under similar conditions, except that the effects of end-tidal 0.25, 0.5, and 1 MAC of halothane were examined in each rabbit (each added to a preestablished chloralose anesthetic).

RESULTS

Under control conditions, blood flow to the choroid plexus averaged 351 +/- 198 ml.min-1.100 g-1 (mean +/- SD) and CSF production averaged 10.1 +/- 1.9 microliters.min.-1. Halothane (0.25, 0.5, and 1 MAC) did not alter choroid plexus blood flow but decreased CSF production by 28 +/- 6% at 0.5 MAC (P < .05). In contrast, 1 MAC of halothane increased total blood flow to the brain by 20 +/- 25% (P < .05). The V1 antagonist, which did not affect production of CSF when given alone, prevented the decrease in CSF production in response to halothane. Hemorrhage decreased blood flow to the choroid plexus but not to the brain, and the V1 antagonist attenuated the decrease in the rate of CSF production by hemorrhage (34 +/- 11% vs. 48 +/- 18%, P < .05).

CONCLUSIONS

Halothane decreases CSF production with no net change in the blood flow to the choroid plexus. Decrease in CSF production appears to be mediated through a vasopressin-related mechanism and not to the blood pressure decrease seen during halothane anesthesia.

背景

循环血管活性激素（如血管加压素）在调节脉络丛血流和脑脊液（CSF）生成速率中起重要作用。我们检验了氟烷通过与血管加压素相关的机制降低脑脊液生成的假说，并研究了脉络丛血流的相关变化。

方法

采用脑室池灌注法，在氯醛糖麻醉、体温正常且机械通气的家兔中测量脑脊液生成。家兔接受以下处理：0.5最低肺泡浓度（MAC；呼气末）的氟烷（添加到预先设定的氯醛糖麻醉中）、在血管加压素V1拮抗剂存在下（静脉注射）的0.5 MAC氟烷，或单独使用V1拮抗剂。此外，我们还研究了未进行干预的动物（时间对照）以及通过出血使平均血压降低25%的动物，分别给予或不给予V1拮抗剂。在另一组家兔中，使用放射性微球测量脑和脉络丛的局部及总血流量。这些研究在相似条件下进行，不同之处在于每只家兔分别接受呼气末0.25、0.5和1 MAC氟烷的影响（每种均添加到预先设定的氯醛糖麻醉中）。

结果

在对照条件下，脉络丛血流平均为351±198 ml·min⁻¹·100 g⁻¹（均值±标准差），脑脊液生成平均为10.1±1.9微升·min⁻¹。氟烷（0.25、0.5和1 MAC）未改变脉络丛血流，但在0.5 MAC时使脑脊液生成减少28±6%（P<.05）。相比之下，1 MAC氟烷使脑的总血流量增加20±25%（P<.05）。单独给予时不影响脑脊液生成的V1拮抗剂可防止氟烷引起的脑脊液生成减少。出血使脉络丛血流减少，但不影响脑血流，V1拮抗剂减弱了出血引起的脑脊液生成速率降低（34±11%对48±18%，P<.05）。