Park Kyung W, Dai Hai B, Metais Caroline, Comunale Mark E, Sellke Frank W
Department of Anesthesia and Critical Care, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusettes 02215, USA.
Can J Anaesth. 2002 Apr;49(4):427-33. doi: 10.1007/BF03017335.
Since isoflurane is known to attenuate endothelium-dependent dilation (EDD) in normal cerebral arterioles, we examined whether the anesthetic has a similar effect and further impairs EDD in vessels exposed to SAH.
Autologous blood was introduced in the subarachnoid space and the parietal lobe harvested. Control animals were sacrificed without introduction of blood. The response of microvessles to the endothelium-dependent dilator adenosine diphosphate (ADP) 10(-9)-10(-4) M, the endothelium-independent dilator nitroprusside 10(-9)-10(-4) M, and ET-1 10(-13)-10(-8) M was measured by videomicroscopy in the presence of 0-2 minimum alveolar concentration (MAC) of isoflurane.
Isoflurane attenuated EDD to ADP in control vessels [66 +/- 5% (control) vs 27 +/- 11% (2 MAC) dilation to ADP 10(-4) M, P < 0.05]. Although SAH was associated with reduced dilation to ADP, exposure to isoflurane did not further impair dilation to ADP after SAH [26 +/- 3% (SAH) vs 21 +/- 5% (SAH/2 MAC) dilation to ADP 10(-4) M, P = NS]. Dilation to nitroprusside was not affected by isoflurane or SAH. Constriction to ET-1 was reduced by 2 MAC of isoflurane [21 +/- 1% (control) vs 13 +/- 5% (2 MAC) constriction to ET-1 10(-8) M, P < 0.05], but not by 1 MAC of isoflurane in control vessels. Constriction to ET-1 was greatly attenuated by 1 or 2 MAC of isoflurane after SAH [32 +/- 5% (SAH) vs 18 +/- 4% (SAH/2 MAC) constriction to ET-1 10(-8) M, P < 0.05].
In rats, isoflurane does not further impair EDD after SAH and modulates the constrictive response to ET-1. Such an effect of isoflurane would not predispose the SAH-exposed vessels to vasospasm.
由于已知异氟烷可减弱正常脑动脉中内皮依赖性舒张（EDD），我们研究了这种麻醉剂是否具有类似作用，并进一步损害蛛网膜下腔出血（SAH）后血管的EDD。
将自体血注入蛛网膜下腔并采集顶叶。对照组动物在未注入血液的情况下处死。在0 - 2最低肺泡浓度（MAC）的异氟烷存在下，通过视频显微镜测量微血管对内皮依赖性舒张剂二磷酸腺苷（ADP）10（-9）- 10（-4）M、内皮非依赖性舒张剂硝普钠10（-9）- 10（-4）M以及内皮素-1 10（-13）- 10（-8）M的反应。
异氟烷减弱了对照组血管对ADP的EDD [对ADP 10（-4）M的舒张反应，对照组为66 ± 5%，2 MAC时为27 ± 11%，P < 0.05]。虽然SAH与对ADP的舒张反应降低有关，但SAH后暴露于异氟烷并未进一步损害对ADP的舒张反应[对ADP 10（-4）M的舒张反应，SAH组为26 ± 3%，SAH/2 MAC组为21 ± 5%，P = 无显著差异]。对硝普钠的舒张反应不受异氟烷或SAH的影响。2 MAC的异氟烷可降低对内皮素-1的收缩反应[对内皮素-1 10（-8）M的收缩反应，对照组为21 ± 1%，2 MAC时为13 ± 5%，P < 0.05]，但1 MAC的异氟烷对对照组血管无此作用。SAH后，1或2 MAC的异氟烷可显著减弱对内皮素-1的收缩反应[对内皮素-1 10（-8）M的收缩反应，SAH组为32 ± 5%，SAH/2 MAC组为18 ± 4%，P < 0.05]。
在大鼠中，异氟烷在SAH后不会进一步损害EDD，并调节对内皮素-1的收缩反应。异氟烷的这种作用不会使暴露于SAH的血管易发生血管痉挛。
