Shen W K, Hammill S C, Munger T M, Stanton M S, Packer D L, Osborn M J, Wood D L, Bailey K R, Low P A, Gersh B J
Division of Cardiovascular Diseases and Internal Medicine, Section of Biostatistics and Peripheral Neuropathy Research Laboratory, Mayo Clinic, Rochester, Minnesota 55905, USA.
J Am Coll Cardiol. 1996 Jul;28(1):146-54. doi: 10.1016/0735-1097(96)00100-3.
This study examined the hypothesis that adenosine could provoke a vasovagal response in susceptible patients. Mechanisms of the vasovagal response were further explored by studying the adenosine-mediated reactions.
Increased sympathetic activity is frequently observed before vasovagal syncope. Recent studies have demonstrated that adenosine, in addition to its direct bradycardiac and vasodilatory effects, can increase sympathetic discharge by activating cardiovascular afferent nerves.
The effects of adenosine and head-up tilt-table testing with or without isoproterenol were prospectively evaluated in 85 patients examined for syncope after negative results of electrophysiologic testing (51 men and 34 women, mean [+/- SD] age 61 +/- 17 years). Adenosine bolus injections of 6 mg and 12 mg were sequentially administered to patients in the upright position. The same protocol was implemented in 14 normal control subjects (7 men and 7 women, mean [+/- SD] age 38 +/- 10 years).
Transient hypertension or tachycardia was observed in 57 (67%) and 20 (24%) patients after administration of 6 mg and 12 mg of adenosine, respectively, during the immediate phase (first 15 s), suggesting direct sympathetic activation. Hypotension and reflex tachycardia were observed in all patients during the delayed phase (15 to 60 s after adenosine injection), suggesting baroreceptor unloading. A vasovagal response was induced in 22 (26%) and 29 (34%) patients after adenosine administration and during tilt-table testing. Inducibility of a vasovagal response by these two methods was comparable (p = 0.12). Of the control subjects, one (7%) had a vasovagal response after adenosine administration and one (7%) had a positive response during tilt-table testing.
These observations support the idea that adenosine is an endogenous modulator of the cardiac excitatory afferent nerves. Sympathetic activation by adenosine can be direct (i.e., cardiac excitatory afferent nerves) and indirect (i.e., vasodilation and reflex sympathetic activation). Adenosine could be an important modulator in triggering a vasovagal response in susceptible patients during examination for syncope.
本研究检验了腺苷可在易感患者中引发血管迷走反应这一假说。通过研究腺苷介导的反应进一步探索血管迷走反应的机制。
血管迷走性晕厥发作前常观察到交感神经活动增强。近期研究表明,腺苷除了具有直接的减慢心率和血管舒张作用外,还可通过激活心血管传入神经增加交感神经放电。
对85例电生理检查结果为阴性的晕厥患者(51例男性和34例女性,平均年龄[±标准差]61±17岁)前瞻性评估腺苷以及联合或不联合异丙肾上腺素进行头高位倾斜试验的效果。对处于直立位的患者依次静脉推注6mg和12mg腺苷。14名正常对照者(7例男性和7例女性,平均年龄[±标准差]38±10岁)采用相同方案。
分别在推注6mg和12mg腺苷后的即刻期(最初15秒),57例(67%)和20例(24%)患者出现短暂高血压或心动过速,提示直接交感神经激活。在延迟期(腺苷注射后15至60秒)所有患者均出现低血压和反射性心动过速,提示压力感受器负荷减轻。腺苷给药后及倾斜试验期间,分别有22例(26%)和29例(34%)患者诱发血管迷走反应。这两种方法诱发血管迷走反应的可能性相当(p = 0.12)。在对照者中,1例(7%)在腺苷给药后出现血管迷走反应,1例(7%)在倾斜试验期间出现阳性反应。
这些观察结果支持腺苷是心脏兴奋性传入神经的内源性调节因子这一观点。腺苷对交感神经的激活作用可以是直接的(即通过心脏兴奋性传入神经)和间接的(即通过血管舒张和反射性交感神经激活)。在晕厥检查期间,腺苷可能是触发易感患者血管迷走反应的重要调节因子。