Excess tachycardia: heart rate after antimuscarinic agents in conscious dogs.

In conscious dogs the heart rate after atropine is higher than after bilateral vagotomy; we have termed the additional heart rate with atropine "excess tachycardia" (ET). In six dogs the cervical vagosympathetic trunks were exteriorized in skin tubes, and arterial and venous catheters were chronically implanted. Atropine sulfate (0.1 mg/kg iv) injected during cold blockade of the vagi increased the heart rate by only 6 +/- 4 (SE) beats/min (NS) but rewarming the vagi in five of the six dogs after atropine resulted in an additional heart rate increase (ET) of 26 +/- 6 beats/min (P less than 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 sodium nitroprusside attenuated or abolished the ET. Our results show that ET is produced by antimuscarinic agents in general and is not mediated by the beta-adrenergic system. Furthermore, ET is present only when the cervical vagi are intact, probably because ET is mediated by cholinergic vagal efferent fibers via a mechanism that has not yet been recognized in cardiac rate control.