TY - JOUR
T1 - Inhibitory action of propranolol and its stereoisomers on epinephrine-induced changes in electrocardiogram
AU - Hayase, Shoji
AU - Ito, Hiroyasu
AU - Kondo, Yasushi
AU - Imao, Taiichiro
AU - Yoshimura, Tsuyoshi
AU - Watanabe, Ikuo
AU - Hirakawa, Senri
PY - 1972
Y1 - 1972
N2 - Isoproterenol, epinephrine, and norepinephrine, intracoronarily injected with the coronary artery catheterization, produced a marked “ischemic” change in ECG, while phenylephrine failed to do so. This change was inhibited by the pretreatment with propranolol, but not by that with phenoxybenzamine. No marked change was produced in the coronary blood flow by these catecholamines, but a change occurred in blood pressure pulse pattern recordable from the carotid artery in association with ECG changes. When the magnitude of the “ischemic” change in ECG produced by graded-dose administration of epinephrine was quantitated in terms of ST·T-Area, it was found that the change in ST·T-Area depended on the dose of epinephrine used; norepinephrine produced changes in ECG with nearly equal potency to epinephrine. ECG changes caused by epinephrine in dose of 1 μg was completely inhibited by the pretreatment with about 125 μg of DL-propranolol, L-propranolol or ICI 50172, but 400 μg of D-propranolol was required to produce the same blocking effect. On the other hand, procaine had no such inhibitory effect. From these results it is suggested that the epinephrine-induced ECG changes of “ischemic” type appear to represent a beta-adrenergic response. When the ST and T changes were quantitated in terms of ST·T-Area, propranolol exerted a blocking action on such epinephrine-induced ECG changes, and D-propranolol was one third as potent in this respect as L-propranolol.
AB - Isoproterenol, epinephrine, and norepinephrine, intracoronarily injected with the coronary artery catheterization, produced a marked “ischemic” change in ECG, while phenylephrine failed to do so. This change was inhibited by the pretreatment with propranolol, but not by that with phenoxybenzamine. No marked change was produced in the coronary blood flow by these catecholamines, but a change occurred in blood pressure pulse pattern recordable from the carotid artery in association with ECG changes. When the magnitude of the “ischemic” change in ECG produced by graded-dose administration of epinephrine was quantitated in terms of ST·T-Area, it was found that the change in ST·T-Area depended on the dose of epinephrine used; norepinephrine produced changes in ECG with nearly equal potency to epinephrine. ECG changes caused by epinephrine in dose of 1 μg was completely inhibited by the pretreatment with about 125 μg of DL-propranolol, L-propranolol or ICI 50172, but 400 μg of D-propranolol was required to produce the same blocking effect. On the other hand, procaine had no such inhibitory effect. From these results it is suggested that the epinephrine-induced ECG changes of “ischemic” type appear to represent a beta-adrenergic response. When the ST and T changes were quantitated in terms of ST·T-Area, propranolol exerted a blocking action on such epinephrine-induced ECG changes, and D-propranolol was one third as potent in this respect as L-propranolol.
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U2 - 10.1253/jcj.36.1065
DO - 10.1253/jcj.36.1065
M3 - Article
C2 - 4678755
AN - SCOPUS:0015410848
SN - 0047-1828
VL - 36
SP - 1065
EP - 1088
JO - JAPANESE CIRCULATION JOURNAL
JF - JAPANESE CIRCULATION JOURNAL
IS - 10
ER -