Abe H, Kobayashi H, Nakashima Y, Izumi F, Kuroiwa A
Second Department of Internal Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
Pacing Clin Electrophysiol. 1995 Jul;18(7):1419-26. doi: 10.1111/j.1540-8159.1995.tb02604.x.
To examine hemodynamic, plasma catecholamines, and cyclic AMP changes during tilt in patients with neurocardiogenic (vasodepressor) syncope, six patients underwent 80 degrees head-up tilt test for 10 minutes with isoproterenol infusion (1-3 micrograms/min). Venous blood was sampled in the supine position, at 3 minutes of tilt, and at the onset of vasodepressor reaction during tilt. All patients had previous tilt studies in which vasodepressor syncope had been induced reproducibly (mean 3.3 episodes in each patient). Syncope was induced at 6.1 +/- 0.4 minutes of tilt with an infusion of isoproterenol (mean 1.7 +/- 0.3 micrograms/min). Although arterial pressure and heart rate did not change significantly between in the supine position and at 3 minutes of tilt, plasma norepinephrine increased significantly at 3 minutes of tilt (0.44 +/- 0.10 ng/mL; P < 0.05) and at the onset of vasodepressor reaction (0.49 +/- 0.12 ng/mL; P < 0.01) compared to the supine position with isoproterenol (0.34 +/- 0.10 ng/mL). Also, cyclic AMP (cAMP) increased significantly at 3 minutes of tilt (25.3 +/- 2.0 pmol/mL; P < 0.005) and at the onset of vasodepressor reaction (29.6 +/- 1.7 pmol/mL; P < 0.005) compared to the supine position with isoproterenol (20.4 +/- 1.9 pmol/mL). After administration of selective beta 1-blocker, metoprolol (40 mg/day), plasma norepinephrine, and cAMP during tilt did not change significantly compared to baseline tilt. However, metoprolol prevented the syncope in 3 of 6 patients. After administration of beta 1-, beta 2-blocker, propranolol (30 mg/day), cAMP at 3 minutes of tilt decreased significantly compared to the baseline tilt (16.9 +/- 1.4 pmol/mL vs 25.3 +/- 2.0 pmol/mL; P < 0.05) and propranolol prevented the syncope in all six patients. We concluded that the increase of cAMP may play an important role for the induction of vasodepressor reaction in patients with neurocardiogenic (vasodepressor) syncope. The concentration of cAMP showed more sensitive response to vasodepressor reaction than that of norepinephrine.
为研究神经心源性（血管减压性）晕厥患者在倾斜试验过程中的血流动力学、血浆儿茶酚胺及环磷酸腺苷（cAMP）的变化，6例患者在静脉输注异丙肾上腺素（1 - 3微克/分钟）的情况下进行了80度头高位倾斜试验10分钟。于仰卧位、倾斜3分钟时以及倾斜过程中血管减压反应发作时采集静脉血样。所有患者此前均进行过倾斜试验，且均能重复诱发出血管减压性晕厥（每位患者平均发作3.3次）。在输注异丙肾上腺素（平均1.7±0.3微克/分钟）的情况下，倾斜6.1±0.4分钟时诱发出晕厥。尽管仰卧位与倾斜3分钟时动脉压和心率无显著变化，但与仰卧位输注异丙肾上腺素时（0.34±0.10纳克/毫升）相比，倾斜3分钟时（0.44±0.10纳克/毫升；P<0.05）及血管减压反应发作时（0.49±0.12纳克/毫升；P<0.01）血浆去甲肾上腺素显著升高。此外，与仰卧位输注异丙肾上腺素时（20.4±1.9皮摩尔/毫升）相比，倾斜3分钟时（25.3±2.0皮摩尔/毫升；P<0.005）及血管减压反应发作时（29.6±1.7皮摩尔/毫升；P<0.005）cAMP显著升高。给予选择性β1受体阻滞剂美托洛尔（40毫克/天）后，倾斜过程中血浆去甲肾上腺素及cAMP与基线倾斜试验相比无显著变化。然而，美托洛尔预防了6例患者中3例的晕厥发作。给予β1、β2受体阻滞剂普萘洛尔（30毫克/天）后，与基线倾斜试验相比，倾斜3分钟时cAMP显著降低（16.9±1.4皮摩尔/毫升对25.3±2.0皮摩尔/毫升；P<0.05），且普萘洛尔预防了所有6例患者的晕厥发作。我们得出结论，cAMP升高可能在神经心源性（血管减压性）晕厥患者血管减压反应的诱发中起重要作用。cAMP浓度对血管减压反应的反应比去甲肾上腺素更为敏感。
