Gaide M S, Altman C B, Cameron J S, Kaiser C J, Myerburg R J, Bassett A L
Agents Actions. 1984 Dec;15(5-6):488-93. doi: 10.1007/BF01966761.
Histamine (10(-3) M) increased the spontaneous rate similarly in isolated preparations of normal left ventricular tissue from control, i.e. normal and sham-operated, dogs (control preparations) and in preparations consisting of normal and contiguous infarcted left ventricular tissue from dogs with subacute, i.e. 24 hours after left coronary artery ligation, myocardial infarction (infarcted preparations). Histamine (10(-3) M) markedly enhanced the irregular rhythm of infarcted preparations. The H1-receptor antagonist, chlorpheniramine (10(-4) M), and the H2-receptor antagonist, cimetidine (10(-3) M), antagonized the effects of histamine (10(-3) M) on the spontaneous rate of both control and infarcted preparations. The H1-receptor agonist, 2-pyridyl ethylamine (PEA, 10(-4) M), increased the spontaneous rate of control and infarcted preparations; these effects were antagonized by chlorpheniramine (10(-4) M). The H2-receptor agonist, dimaprit, had no effect. Similar to histamine (10(-3) M), PEA (10(-4) M) enhanced the irregular rhythm of infarcted preparations; dimaprit had no effect. High local concentrations of histamine may occur in poorly perfused ischemic tissue. The enhancement of irregular rhythm produced by histamine, and the specific H1-receptor agonist, PEA, leads us to suggest its involvement in arrhythmias associated with subacute myocardial infarction.
组胺（10⁻³ M）使来自对照组（即正常和假手术）犬的正常左心室组织分离制剂（对照制剂）以及由亚急性（即左冠状动脉结扎24小时后）心肌梗死犬的正常和相邻梗死左心室组织组成的制剂的自发率同样增加。组胺（10⁻³ M）显著增强梗死制剂的不规则节律。H1受体拮抗剂氯苯那敏（10⁻⁴ M）和H2受体拮抗剂西咪替丁（10⁻³ M）拮抗组胺（10⁻³ M）对对照制剂和梗死制剂自发率的影响。H1受体激动剂2-吡啶乙胺（PEA，10⁻⁴ M）增加对照制剂和梗死制剂的自发率；这些作用被氯苯那敏（10⁻⁴ M）拮抗。H2受体激动剂二甲双胍没有作用。与组胺（10⁻³ M）相似，PEA（10⁻⁴ M）增强梗死制剂的不规则节律；二甲双胍没有作用。在灌注不良的缺血组织中可能会出现高局部浓度的组胺。组胺和特异性H1受体激动剂PEA产生的不规则节律增强使我们认为其与亚急性心肌梗死相关的心律失常有关。
