Excess tachycardia: heart rate after antimuscarinic agents in conscious dogs

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Abstract
In conscious dogs the heart rate after atropine is higher than after bilateral vagotomy [excess tachycardia (ET)]. In 6 dogs the cervical vagosympathetic trunks were exteriorized in skin tubes and arterial and venous catheters were chronically implanted. Atropine sulfate (0.1 mg/kg i.v.) injected during cold blockade of the vagi increased the heart rate by only 6 .+-. 4 (SE) beats/min (NS) but rewarming the vagi in 5 of the 6 dogs after atropine resulted in an additional heart rate increase (ET) of 26 .+-. 6 beats/min (P < 0.005). The ET (41 .+-. 11 beats/min) tended to be larger when the animals were pretreated with 1 mg/kg propranolol (P = 0.09). Similar results were obtained when atropine methylbromide, a charged derivative of atropine sulfate, or glycopyrrolate, a synthetic antimuscarinic agent, was substituted for atropine sulfate (ET: 51 .+-. 6 and 51 .+-. 16 beats/min, respectively). Raising the arterial blood pressure with phenylephrine increased the heart rate further; lowering the blood pressure with Na nitroprusside attenuated or abolished the ET. ET is produced by antimuscarinic agents in general and is not mediated by the .beta.-adrenergic system. It is present only when the cervical vagi are intact, probably because it is mediated by cholinergic vagal efferent fibers via a mechanism that has not yet been recognized in cardiac rate control.