摘要
目的为在气管插管时减轻心血管应激反应和维持血流动力学稳定,选出尼卡地平的理想剂量。方法45例(ASA-Ⅰ、Ⅱ)乳腺肿瘤切除病人随机分为 3组,每组 15例。在喉镜窥视前 3min,分别静注生理盐水 10ml(组Ⅰ)或厄卡地平15μg·kg-1(组Ⅱ)或30μg·kg-1(组Ⅲ),麻醉诱导药为:芬太尼2.0μg·kg-1、异丙酚1.5mg·kg-1(不少于30s)。气管插管一次完成。记录麻醉前(T0),静注尼卡地平或生理盐水后2min,静注琥珀胆碱前(T1)、插管后即刻(T2)、插管后3min(T3)、5min(T4)、10min(T5)所测定的平均动脉压(MAP)和心率(HR)。结果①组Ⅱ和组Ⅲ的MAP在静注尼卡地平后T1比麻醉前T0均有明显下降(P<0.05;P<0.01),其中,组Ⅲ的MAP比组Ⅱ下降明显(P<0.05)。此期,组Ⅱ和组Ⅲ的HR均有显著增加(P<0.05;P<0.01),其中,组Ⅲ的HR比组Ⅱ增加更显著(P<0.01)。②组Ⅱ和组Ⅲ的MAP在插管后T2与麻醉前T0比较,无显著差异。组Ⅰ的MAP升高显著(P<0.01)。其中,组Ⅱ和组Ⅲ与组Ⅰ比较差异显著(P<0.01)。结论静注尼卡地平15μ?
Objective To determine the optical dose of nicardipine(N) for the hemodynamic stability and less cardiovascular stress response during the pre - postintubation period. Methods Forty-five patients(ASA - Ⅰ, Ⅱ) undergoing excision of bed tumor were randomly divided into three group: group Ⅰ (normal saline), group Ⅱ (N15μg/kg), group Ⅲ (N30μg/kg). The medicine was given intravenously(iv) 3 minutes before laryngoscopy, then the inducement with 1. 5mg/kg propofol iv and 2. 0μg/kg fentanyl was administered. And systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (Map), heart rate (HR) and the-pressure product (RPP) were recorded respectively from 10 min before tracheal intubation to 10 min after tracheal intubation. Results ①The MAP of group Ⅱ and group Ⅲ before laryngoscopy decreased significantly than preinducement (P < 0.05, P < 0.01 ). The decrease of the blood pressure in group Ⅲ was more significantly than group Ⅱ. ②The increase of the MAP in both group Ⅱ and group Ⅲ after intubation was not significantly than preinducement. The increase of the MAP in control group was more significantly than both group Ⅱ and group Ⅲ (P < 0.01). Conclusion The calcium-channel blocker, nicardipine (15μg/kg intravenously 3 min before tracheal intubation) can decrease the response of tracheal intubation and prevent from low blood pressure.
出处
《哈尔滨医科大学学报》
CAS
2000年第4期283-285,共3页
Journal of Harbin Medical University
关键词
气管插管
尼卡地平
围麻醉期
血流动力学
tracheal intubation
nicardipine
cardiovascular stress response
hemodynamic stability