Abstract

The heart rate and arrhythmogenic effects of acute hypoxia (H) are incompletely understood. Some studies have suggested a differential effect of H dependent upon the extent to which Ca and Na participate in the action potential (AP). We studied the effects of acute, severe H on SN and atrial parameters using rabbit preparations and standard microelectrode techniques. AP from true SN pacemaker cells (dependent on the slow inward Ca current (isi)) were most effected by H. There were significant (p·0.05) decreases in spontaneous rate, AP amplitude (APA), maximum dia stolic potential (MDP) and slope of phase 4 depolarization. Corrected SNRT and SACT were markedly increased. H produced SN entrance block, pacemaker shifts and ectopic activity in many preparations. AP from subsidiary SN cells (a two component AP dependent on Na and Ca) were less effected by H. There were only moderate decreases in APA and MDP. AP from atrial muscle are very dependent on the fast Na current for depolarization. H produced no changes in APA, MDP or Vmax. AP duration (at 50 and 90% repolarization) and atrial effective refractory period were significantly shortened by H. The decrease in AP duration (due to shortening of the plateau) may be related to H induced decreases in the Ca isi. In summary, many of the arrhythmias resulting from clinical H can be explained by the observed changes in cellular electrophysiology. There appears to be a high sensitivity of Ca dependent channels (and AP) to the effects of H.

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