INHIBITION OF ADENOSINE-DEAMINASE AND ADMINISTRATION OF ADENOSINE INCREASE HYPOXIA-INDUCED VENTRICULAR ECTOPY

Eighteen anesthetized, instrumented beagles (both genders, 10.3 +/- 0. 5 kg) were used to investigate the effects of administered adenosine ( n=6), erythro-9-(2-hydroxy,3-nonyl)adenine (EHNA), a potent inhibitor of endogenous adenosine deaminase (n=6), and saline (n=6), on the inci dence of ventricular arrhythmias caused by systemic hypoxia (5% O-2, 9 5% N-2, PaO2 = 21 +/- 3 mmHg). After dogs were instrumented and monito red variables were in the steady-state, the above compounds were infus ed continuously into the cannulated left anterior descending (LAD) cor onary artery for three minutes before, and throughout a four-minute pe riod of hypoxia. After approximately 4 min of hypoxia the rates of ven tricular ectopy [(total beats-normal beats)/total beats x 100 = % ecto py] were 73 +/- 9%, 73 +/- 11%, and 35 +/- 8% for the three groups, re spectively. The percent ectopy of the adenosine and EHNA-treated dogs was significantly greater (p < 0.05) than that for the saline-treated controls. These findings suggest that adenosine contributes to the ven tricular arrhythmias of experimental systemic hypoxia.