Journal of Nippon Medical School: Vol.66 No.2 page.119

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ArticleTitle Possible contribution of α -adrenergic abnormalities to cerebral ischemia in the patients with sinus bradycardia Analysis by pharmacologic autonomic nervous test

AuthorList Atsunobu Nomura, Hirokazu Saitoh, Hirotsugu Atarashi, Hirokazu Hayakawa

Affiliation The First Department of Internal Medicine, Nippon Medical School

Language JA

Volume 66

Issue 2

Year 1999

Page 119-126

Received October 29, 1998

Accepted January, 11, 1999

Keywords sinus bradycardia, syncope, alpha- adrenergic receptor, vasoconstriction

Abstract Background : Syncope of patients with bradyarrhythmia is perceived as severe sign of low cardiac output caused by bradycardia and as a major criteria for pacemaker implantation (PMI). However, it has been reported that PMI can not always prevent syncope ; it has been suggested that not bradycardia but an abnormality of the autonomic nervous system blays a part in syncope.
Purpose : To investigate the relation between autonomic nervous dysfunction and syncope in cases of sinus bradycardia (SB). Subjects : Thirty- nine patients with SB were divided into two groups according to the presence (group S, n=16, 46.9 ± 20.0 years) or absence (group N, n=23, 40.4 ± 17.6 years) of syncope or presyncope.
Methods : Corrected sinus node recovery time (CSNRT) was measured by electrophysi-ologic study. Pharmacologic autonomic nervous tests were performed as follows in a quiet room. Increased HR by application of 0.04 mg/kg atropine (para- tone), and by 0.004 g/kg/min isopro-terenol divided by 0.004 (β-sens) were evaluated. β-tone was obtained by subtracting HR after application of propranolol (0.2 mg/kg) from that of atropine. Basal β-sympathetic activity was evaluated by β-sec that was obtained by β-tone/β-sens. Increased SBP by application of 0.4 g/kg/min phenylephrine divided by 0.4 (α -sens) was evaluated. α-tone was obtained by subtracting minimum SBP after 0.2 mg/kg phentolamine from SBP after application of propranolol . Basal α sympathetic activity was evaluated by α-sec, that was obtained by α-tone/α-sens.
Result : There were no significant differences in basal clinical characteristics (age, sex, cardiac function) between the groups. The parameters of the functions of parasympathetic and β -sympathetic receptors (para- tone, β-sens, β-tone, β-sec) showed no significant differences between the groups. α-sens was attenuated (P<0.01) and α-sec was augmented (P<0.0001) significantly in group S.
Conclusion : It was suggested that syncope or presyncope in SB patients could be attributedto failure of vasoconstriction mediated by α-sympathetic receptor but to severity of sinus node dysfunction .

Correspondence to Atsunobu Nomura, The First Department of Internal Medicine, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8603, Japan

ArticleTitle	Possible contribution of α -adrenergic abnormalities to cerebral ischemia in the patients with sinus bradycardia Analysis by pharmacologic autonomic nervous test
AuthorList	Atsunobu Nomura, Hirokazu Saitoh, Hirotsugu Atarashi, Hirokazu Hayakawa
Affiliation	The First Department of Internal Medicine, Nippon Medical School
Language	JA
Volume	66
Issue	2
Year	1999
Page	119-126
Received	October 29, 1998
Accepted	January, 11, 1999
Keywords	sinus bradycardia, syncope, alpha- adrenergic receptor, vasoconstriction
Abstract	Background : Syncope of patients with bradyarrhythmia is perceived as severe sign of low cardiac output caused by bradycardia and as a major criteria for pacemaker implantation (PMI). However, it has been reported that PMI can not always prevent syncope ; it has been suggested that not bradycardia but an abnormality of the autonomic nervous system blays a part in syncope. Purpose : To investigate the relation between autonomic nervous dysfunction and syncope in cases of sinus bradycardia (SB). Subjects : Thirty- nine patients with SB were divided into two groups according to the presence (group S, n=16, 46.9 ± 20.0 years) or absence (group N, n=23, 40.4 ± 17.6 years) of syncope or presyncope. Methods : Corrected sinus node recovery time (CSNRT) was measured by electrophysi-ologic study. Pharmacologic autonomic nervous tests were performed as follows in a quiet room. Increased HR by application of 0.04 mg/kg atropine (para- tone), and by 0.004 g/kg/min isopro-terenol divided by 0.004 (β-sens) were evaluated. β-tone was obtained by subtracting HR after application of propranolol (0.2 mg/kg) from that of atropine. Basal β-sympathetic activity was evaluated by β-sec that was obtained by β-tone/β-sens. Increased SBP by application of 0.4 g/kg/min phenylephrine divided by 0.4 (α -sens) was evaluated. α-tone was obtained by subtracting minimum SBP after 0.2 mg/kg phentolamine from SBP after application of propranolol . Basal α sympathetic activity was evaluated by α-sec, that was obtained by α-tone/α-sens. Result : There were no significant differences in basal clinical characteristics (age, sex, cardiac function) between the groups. The parameters of the functions of parasympathetic and β -sympathetic receptors (para- tone, β-sens, β-tone, β-sec) showed no significant differences between the groups. α-sens was attenuated (P<0.01) and α-sec was augmented (P<0.0001) significantly in group S. Conclusion : It was suggested that syncope or presyncope in SB patients could be attributedto failure of vasoconstriction mediated by α-sympathetic receptor but to severity of sinus node dysfunction .
Correspondence to	Atsunobu Nomura, The First Department of Internal Medicine, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8603, Japan