颈内动脉注射硝普钠不会增加人体的脑血流量。

Intracarotid nitroprusside does not augment cerebral blood flow in human subjects.

作者信息

Joshi Shailendra, Young William L, Duong Huang, Aagaard Beverly A, Ostapkovich Noeleen D, Connolly E Sander, Pile-Spellman John

机构信息

Department of Anesthesiology, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA.

出版信息

Anesthesiology. 2002 Jan;96(1):60-6. doi: 10.1097/00000542-200201000-00016.

DOI:10.1097/00000542-200201000-00016

PMID:11753003

Abstract

BACKGROUND

The recent resurgence of interest in the cerebrovascular effects of nitroprusside can be attributed to the possibility of using nitric oxide donors in treating cerebrovascular insufficiency. However, limited human data suggest that intracarotid nitroprusside does not directly affect cerebrovascular resistance. In previous studies, physiologic or pharmacologic reactivity of the preparation was not tested at the time of nitroprusside challenge. The authors hypothesized that if nitric oxide is a potent modulator of human cerebral blood flow (CBF), then intracarotid infusion of nitroprusside will augment CBF.

METHODS

Cerebral blood flow was measured (intraarterial (133)Xe technique) in sedated human subjects undergoing cerebral angiography during sequential infusions of (1) intracarotid saline, (2) intravenous phenylephrine to induce systemic hypertension, (3) intravenous phenylephrine with intracarotid nitroprusside (0.5 microg x kg(-1) x min(-1)), and (4) intracarotid verapamil (0.013 mg x kg(-1) x min(-1)). Data (mean +/- SD) were analyzed by repeated-measures analysis of variance and post hoc Bonferroni-Dunn test.

RESULTS

Intravenous phenylephrine increased systemic mean arterial pressure (from 83 +/- 12 to 98 +/- 6 mmHg; n = 8; P < 0.001), and concurrent infusion of intravenous phenylephrine and intracarotid nitroprusside reversed this effect. However, compared with baseline, CBF did not change with intravenous phenylephrine or with concurrent infusions of intravenous phenylephrine and intracarotid nitroprusside. Intracarotid verapamil increased CBF (43 +/- 9 to 65 +/- 11 ml x 100 g(-1) x min(-1); P < 0.05).

CONCLUSIONS

The authors conclude that, in humans, intracarotid nitroprusside sufficient to decrease mean arterial pressure during recirculation, does not augment CBF. Failure of intracarotid nitroprusside to augment CBF despite demonstrable autoregulatory vasoconstriction and pharmacologic vasodilation questions the significance of nitric oxide-mediated vasodilation in human cerebral circulation.

摘要

背景

近期对硝普钠脑血管效应的兴趣再度兴起，这可能归因于使用一氧化氮供体治疗脑血管供血不足的可能性。然而，有限的人体数据表明，颈内动脉注射硝普钠并不会直接影响脑血管阻力。在以往的研究中，在硝普钠激发试验时并未测试制剂的生理或药理反应性。作者推测，如果一氧化氮是人类脑血流量（CBF）的有效调节因子，那么颈内动脉输注硝普钠将增加脑血流量。

方法

在接受脑血管造影的镇静人体受试者中，通过动脉内（133）Xe技术测量脑血流量，依次输注：（1）颈内动脉生理盐水，（2）静脉注射去氧肾上腺素以诱导全身性高血压，（3）静脉注射去氧肾上腺素并颈内动脉注射硝普钠（0.5μg·kg-1·min-1），以及（4）颈内动脉注射维拉帕米（0.013mg·kg-1·min-1）。数据（均值±标准差）通过重复测量方差分析和事后邦费罗尼-邓恩检验进行分析。

结果

静脉注射去氧肾上腺素可增加全身平均动脉压（从83±12mmHg升至98±6mmHg；n = 8；P < 0.001），同时静脉注射去氧肾上腺素和颈内动脉注射硝普钠可逆转这种效应。然而，与基线相比，静脉注射去氧肾上腺素或同时静脉注射去氧肾上腺素和颈内动脉注射硝普钠时，脑血流量并未改变。颈内动脉注射维拉帕米可增加脑血流量（从43±9ml·100g-1·min-1增至65±11ml·100g-1·min-1；P < 0.05）。