CORONARY SPASM INDUCED WITH PARASYMAPTHETIC ACTIVATION IN THE PATIENTS WITH ISCHEMIC HEART DISEASE

缺血性心脏病患者副交感激活引起的冠状动脉痉挛

• 批准号: 11671530
• 负责人: WATANABE Seiji
• 金额: $ 1.73万
• 依托单位: KURUME UNIVERSITY
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1999
• 资助国家: 日本
• 起止时间: 1999 至 2000
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-11671530/
• 关键词: CORONARY SPASM; MYOCARDIAL ISCHEMIA; PARASYMAPATHEIC NERVE; CHOLINESTERASE INHIBITOR; コリンエステラーゼ阻害薬; 冠循環; エンドセリン; 血管内皮機能

To investigate the effects of edrophonium (Edr), which could produce the parasympathetic activation, on electrocardiogram (ECG) and hemodynamics, we studied 32 patients receiving elective coronary artery surgery. The patients were randomly divided into two groups ; control (C) group with only saline injection (n=14) and Edr (E) group with Edr followed by the saline injection (n=18). A bolus dose of Edr (0.25 mg・kg^<-1>) was injected through a central venous catheter during harvesting of the left internal thoracic artery . Edr induced mild sinus bradycardia in all patients. The RR interval prolonged after Edr (p<0.01 vs. C group) and the peak prolongation appeared at 2-4 min (p<0.01 vs. baseline). The maximum reduction of heart rate (HR) after Edr was amplified proportionally with increasing baseline HR (r=-0.74, p<0.001). The relationship between the baseline HR and the maximum reduction of HR was apparently different between the two groups (p<0.01). The PQ duration on ECG was elongate … More d in 1 to 3 min after Edr (p<0.01 ) while QRS duration did not. The PQ duration quickly restored to the baseline value at 4 min after Edr, while the RR prolongation persisted for 20 min. There was no newly developed deviation of ST segments on the both leads ll and V_5 for 20 min-observation. Although mixed venous hemoglobin oxygen saturation (SvO_2) decreased for 15 min after Edr (p=0.01 vs. C group), none of the systemic and pulmonary arterial pressures, and central venous pressure changed during this period. A bolus injection of Edr showed a frequency -dependent, temporal depression on HR with little deterioration of hemodynamics except SvO_2. Edr could be expected to induce clinically tol erable sinus bradycardia without any severe A-V conduction block in patients with ischemic heart disease. We found no evidence of newly myocardial ischemia, which could be produced by the parasympathetic activation. Only the parasympathetic activation rarely produces the coronary spasm even in the patients with ischemic heart disease. Less

为探讨能引起副交感神经兴奋的依地芬铵（Edr）对32例择期冠状动脉手术患者心电图（ECG）和血流动力学的影响。将患者随机分为对照组（C组，n=14）和Edr组（E组，n=18），对照组仅注射生理盐水，Edr组先注射Edr，再注射生理盐水。在<-1>获取左胸廓内动脉时，通过中心静脉导管注射Edr（0.25 mg·kg-1）。Edr诱发轻度窦性心动过缓。EDR后RR间期延长（与对照组相比P&lt;0.01），延长高峰出现在2-4 min（与对照组相比P&lt;0.01）。Edr后心率（HR）的最大降低与基线HR的增加成比例放大（r=-0.74，p&lt;0.001）。两组HR最大下降幅度与基线HR的关系有显著性差异（p&lt;0.01）。心电图PQ持续时间延长 ...更多信息 EDR后1 ~ 3 min内QRS波时限明显延长（P&lt;0.01），而EDR后1 ~ 3 min内QRS波时限无明显变化。EDR后4 min PQ间期迅速恢复至基线值，RR延长持续20 min，观察20 min，II、V_5导联ST段均无新的偏移。尽管Edr后15分钟混合静脉血红蛋白氧饱和度（SvO_2）降低（p=0.01 vs. C组），但在此期间，体循环和肺动脉压以及中心静脉压均无变化。大剂量注射Edr对HR表现出频率依赖性的暂时性抑制，除SvO_2外，血流动力学几乎没有恶化。EDR可诱导缺血性心脏病患者出现临床可耐受的窦性心动过缓，且无严重房室传导阻滞。我们没有发现新的心肌缺血的证据，这可能是由副交感神经激活。即使在缺血性心脏病患者中，只有副交感神经激活很少引起冠状动脉痉挛。少