Electrophysiologic alterations produced by hypoxia in the canine heart

The purpose of this study was to test whether hypoxia caused simultaneous stimulation of sympathetic and vagal cardiac nerves. To do this, we determined in chloralose-anesthetized, open-chest dogs, changes in sinus cycle length (SCL), atrioventricular nodal conduction time (AH interval), and effective refractory periods (ERP) of the right atrium (RA) and left ventricle (LV) during hypoxia induced by either hypoventilation or by breathing 10% oxygen in nitrogen. We found that hypoventilation decreased arterial pH (mean +/- SE: 7.365 +/- 0.011 versus 7.244 +/- 0.013, p less than 0.001) and Po2 (105.2 +/- 3.6 versus 50.5 +/- 2.0 mm Hg, p less than 0.001), and increased Pco2 (24.4 +/- 0.7 versus 41.9 +/- 1.1 mm Hg, p less than 0.001). SCL (373 +/- 19 versus 485 +/- 35 msec, p less than 0.001), AH interval (92 +/- 4 versus 111 +/- 6 msec, p less than 0.005), and LVERP (159.8 +/- 3.2 versus 162.0 +/- 3.3, p less than 0.05) lengthened, while RAERP shortened (137.7 +/- 2.6 versus 128.8 +/- 3.5, p less than 0.001). After bilateral vagotomy, these electrophysiologic changes were attenuated, and transection of ansae subclaviae following vagotomy did not affect hypoventilation-induced changes that were present after vagotomy alone. In contrast, breathing 10% oxygen decreased Po2 (104.2 +/- 3.3 versus 48.1 +/- 1.7, p less than 0.001) but did not change pH and Pco2. SCL lengthened slightly (444 +/- 15 versus 463 +/- 17, p less than 0.001), but other measured electrophysiologic parameters were not affected. The norepinephrine concentration in the coronary sinus blood increased by 109% to 121% during hypoxia induced by both methods. Hypoventilatory hypoxia blunted sympathetic-induced shortening of LVERP and potentiated vagally-induced SCL lengthening. Neither type of hypoxia affected induction of atrial and ventricular tachyarrhythmias by programmed electrical stimulation. We conclude that the electrophysiologic response during hypoventilatory hypoxia is due primarily to heightened vagal tone. Norepinephrine concentration in the coronary sinus blood more than doubled, but did not alter cardiac electrophysiologic properties, possibly because of simultaneous increase in vagal tone, or possibly due to the release of adenosine or other factors that impaired cardiac electrophysiologic response to elevated norepinephrine levels.