Stowe D F, Bosnjak Z J, Marijic J, Kampine J P
Department of Anesthesiology, Medical College of Wisconsin, Milwaukee.
Anesthesiology. 1988 May;68(5):695-706. doi: 10.1097/00000542-198805000-00007.
Histamine is released during allergic reactions, and is known to produce cardiac dysrhythmias. The authors compared the cardiac effects of histamine and epinephrine during exposure to halothane in the isolated perfused guinea pig heart. Responses studied were spontaneous sinus rate, intra-atrial conduction time, atrial-septal conduction time (ASCT), intraventricular conduction time (IVCT), and left ventricular pressure (LVP). The incidence and type of dysrhythmias with histamine and halothane and with epinephrine and halothane were analyzed from electrograms. The authors found that halothane alone (0.7 to 2.1 vol%) causes dose-dependent depressions of sinus rate and LVP, prolongs ASCT and IVCT, and produces atrioventricular (AV) block with junctional bradycardia. Histamine alone (.01-10 microM) increases sinus rate and LVP but, like halothane, prolongs ASCT. Halothane antagonizes the inotropic and chronotropic effects of histamine, but enhances ASCT compared with histamine alone. Histamine with halothane greatly increases the incidence of junctional tachycardia with AV dissociation from 0% with histamine alone up to 48%. Epinephrine alone (0.1-5 microM), like histamine, increases sinus rate and LVP, but does not cause a relative increase in ASCT. Halothane antagonizes the inotropic and chronotropic effects of epinephrine, but increases the incidence of ventricular tachycardia from 6% to 28%, and the incidence of premature ventricular excitations from 0% to 40%, compared with epinephrine alone. The authors' in vitro findings show that histamine and halothane, like epinephrine and halothane, can cause dysrhythmias, but that the genesis and type of dysrhythmias induced by these agents are dissimilar. Consequently, the release of histamine with an anaphylactoid reaction during halothane anesthesia, and the treatment of the reaction with epinephrine, could result in dangerous ventricular tachydysrhythmias.
组胺在过敏反应期间释放,已知会导致心律失常。作者比较了组胺和肾上腺素在离体灌注豚鼠心脏中接触氟烷时对心脏的影响。研究的反应包括自发窦性心率、心房内传导时间、房间隔传导时间(ASCT)、心室内传导时间(IVCT)和左心室压力(LVP)。通过心电图分析了组胺与氟烷以及肾上腺素与氟烷联用导致的心律失常的发生率和类型。作者发现,单独使用氟烷(0.7至2.1体积%)会导致窦性心率和LVP呈剂量依赖性降低,延长ASCT和IVCT,并产生伴有交界性心动过缓的房室(AV)阻滞。单独使用组胺(0.01 - 10微摩尔)会增加窦性心率和LVP,但与氟烷一样,会延长ASCT。氟烷拮抗组胺的变力性和变时性作用,但与单独使用组胺相比,会增强ASCT。组胺与氟烷联用会使伴有AV分离的交界性心动过速的发生率从单独使用组胺时的0%大幅增加至48%。单独使用肾上腺素(0.1 - 5微摩尔)与组胺一样,会增加窦性心率和LVP,但不会导致ASCT相对增加。氟烷拮抗肾上腺素的变力性和变时性作用,但与单独使用肾上腺素相比,会使室性心动过速的发生率从6%增加至28%,室性早搏的发生率从0%增加至40%。作者的体外研究结果表明,组胺和氟烷与肾上腺素和氟烷一样,可导致心律失常,但这些药物诱发的心律失常的发生机制和类型不同。因此,在氟烷麻醉期间因类过敏反应释放组胺,并使用肾上腺素治疗该反应,可能会导致危险的室性快速性心律失常。