Effect of midazolam infusion and flumazenil administration on epinephrine arrhythmogenicity in dogs anesthetized with halothane.
Effect of midazolam infusion and flumazenil administration on epinephrine arrhythmogenicity in dogs anesthetized with halothane.
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咪达唑仑输注和氟马西尼给药对氟烷麻醉犬肾上腺素致心律失常的影响。
DOI：
10.1097/00000542-199301000-00021
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发表时间：
1993
期刊：
影响因子：
8.8
通讯作者：
Kumar,MS
中科院分区：
文献类型：
--
作者：
Court,MH;Dodman,NH;Greenblatt,DJ;Agarwal,RK;Kumar,MS
背景咪达唑仑越来越多地被用于心血管疾病患者。虽然临床剂量的咪达唑仑对心脏功能的影响最小，咪达唑仑（和其他苯二氮卓类镇静剂）对心脏mammogenesis的影响尚未得到充分阐明。MethodsIn这项研究中，我们研究了咪达唑仑的效果，与氟马西尼，对mammogenic血清浓度的肾上腺素（ACE）在六氟烷麻醉犬。咪达唑仑以负荷剂量（1.5 mg/kg，5 min内给药）给药，然后以两种速率（10和40 μ g）输注4.5 h。kg-1 × min-1），以达到并维持预定的临床和临床上血浆咪达唑仑浓度。在咪达唑仑输注前、咪达唑仑输注2小时后和咪达唑仑输注3.5小时后测定肾上腺素的促肾上腺素血清浓度，并在6只狗中的4只中进行1 mg氟马西尼/kg静脉注射盐水对照研究。基本上跨越了人类的临床有效范围。在高剂量输注研究中，血浆咪达唑仑浓度高达4倍，范围为1168 - 3563 ng/ml。低剂量咪达唑仑和生理盐水输注后，肾上腺素值的促肾上腺素血清浓度不变。在高剂量研究中，ACE从基线值68+/-13（SEM）ng/ml增加到112+/-25 ng/ml（P=. 03)在咪达唑仑输注后，氟马西尼给药后降至79+/-13 ng/ml。然而，血浆咪达唑仑浓度与对照ACE标准化的ACE值（ACE比值）相关性较差。低剂量（-14%）和高剂量（-19%）咪达唑仑输注后，舒张动脉压显著降低。这种血压下降不受氟马西尼给药的影响。其他血流动力学参数不受药物treatment.ConclusionsThis研究表明，咪达唑仑输注的结果要么没有效果（临床血浆咪达唑仑浓度）或氟马西尼可逆抑制（超临床浓度）氟烷肾上腺素hermogenesis。
BackgroundMidazolam is being selected increasingly for use in patients with cardiovascular compromise. Although clinical doses of midazolam have minimal effects on cardiac function, the influence of midazolam (and other benzodiazepine sedatives) on cardiac arrhythmogenesis has yet to be elucidated fully.MethodsIn this study, we investigated the effect of midazolam, with and without flumazenil, on the arrhythmogenic serum concentration of epinephrine (ACE) in six halothane-anesthetized dogs. Midazolam was administered as a loading dose (1.5 mg/kg over 5 min) followed by a 4.5-h infusion at two rates (10 and 40 micrograms. kg-1 x min-1) to achieve and maintain predetermined clinical and supraclinical plasma midazolam concentrations. The arrhythmogenic serum concentration of epinephrine determinations were made prior to midazolam infusion, following 2 h of midazolam infusion and following 3.5 h of midazolam infusion and 1 mg flumazenil/kg iv Saline control studies were also performed in four of the six dogs.ResultsPlasma midazolam concentrations ranged from 363 to 855 ng/ml in the low-dose infusion study, essentially spanning the clinically effective range for humans. In the high-dose infusion study, plasma midazolam concentrations were up to four times greater, ranging from 1168 to 3563 ng/ml. The arrhythmogenic serum concentration of epinephrine values were unchanged following low-dose midazolam infusion and saline. In the high-dose study, ACE increased from baseline values of 68+/-13 (SEM) ng/ml to 112+/-25 ng/ml (P=. 03) following midazolam infusion and decreased to 79+/-13 ng/ml with flumazenil administration. Plasma midazolam concentrations, however, were poorly correlated with ACE values normalized for control ACE (ACE ratio). Diastolic arterial pressure was significantly depressed following both low-dose (-14%) and high-dose (-19%) midazolam infusion. This decrease in blood pressure was unaffected by flumazenil administration. Other hemodynamic parameters were unaffected by drug treatment.ConclusionsThis study has demonstrated that midazolam infusion results in either no effect (with clinical plasma midazolam concentrations) or flumazenil-reversible suppression (with supraclinical concentrations) of halothane-epinephrine arrhythmogenesis.
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