CORONARY SPASM INDUCED WITH PARASYMAPTHETIC ACTIVATION IN THE PATIENTS WITH ISCHEMIC HEART DISEASE
CORONARY SPASM INDUCED WITH PARASYMAPTHETIC ACTIVATION IN THE PATIENTS WITH ISCHEMIC HEART DISEASE
批准号:
11671530
负责人:
WATANABE Seiji
金额:
$1.73万
依托单位:
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
项目状态:
已结题
起止时间:
1999 至 2000
中文摘要
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英文摘要
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
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