Background: AMP is a potent arrhythmogenic agent which is used for diagnosis and treatment of supraventricular arrythmias with few known serious side effects. However, pulmonary dyscomfort has been described during the acute administration of AMP. We investigated the acute effects of AMP under complete hemodynamic and respiratory monitoring in an animal model.

Subjects: 7 piglets (15.6±3.5 kg) were sedated, intubated, ventilated, paralysed and instrumented to obtain hemodynamic measurements, i.e. heart rate (HF), central venous pressure (pRA), systemic arterial pressure (pAo), pulmonary artery pressure (pPA), and respiratory parameters.

Interventions: after baseline measurements, AMP and adenosine triphosphate (ATP) were given in increasing doses (0.05, 0.1 and 0.2 mg/kg, and 0.1, 0.2 and 0.4 mg, resp.). The application of each dose occured in bolus form (within 5 sec.)

Results: 5-10 sec following bolus administrations, the following hemodynamic changes occurred and reached their peak after 1-2 min:Table

Table 1
Full size table

Following the initial bradykardia during PHT, there was a period of tachykardia (HF maximaum 184±18) during which hemodynamic parameters returned to baseline. The doses of AMP and ATP did not correlate with maximum effect, but with lengh of duration.

Conclusions: The underlying substrate of the subjective finding of pulmonary dyscomfort during AMP-application could be acute and reversible PHT. Further, some of the side effects of AMP (systemic hypotension, arrhymogenic potential) could be caused by sudden volume overload of the right atrium and rebound catecholamine liberation following induced systemic hypotension. Finally, systemic hypotension could be partially caused by a sudden restricted cardiac output caused by acute increase of pulmonary vascular resistance.