Abstract
Since hypoxia inhibits conduction & automaticity predominantly in tissues dependent on the slow (Ca-channel) current, sinus node (SN) function should be selectively depressed. The effects of acute, severe hypoxia (H) on SN refractoriness and sinoatrial conduction time (SACT) were studied using rabbit SN-right atrial preparations and standard micro-electrode techniques. True SN pacemaker cells were identified by intracellular action potentials having low amplitude (65±7mV) and Vmax (3.3±1.0 V/s), and rapid rates of spontaneous diastolic depolarization (51±15 mV/s). Spontaneous sinus cycle length (CL) (control = 460±58ms) increased by 36% with H. Retrograde SACT, measured from the crista terminalis to a true SN pacemaker cell, was rate dependent; increasing at shorter paced CL. SACT increased at all paced CL with H. At a CL of 400ms, SACT increased from 41±12 to 101±19ms (+146%). The minimum paced CL with 1:1 atrio-SN conduction (CLm) increased from 203±34 to 308±41ms (+52%) with H. SACT at CLm increased from 65±19 to 134±30ms (+105%). SN effective refractory period (ERP)(at a paced CL of 400ms) increased from 158±37 to 261±45ms (+66%). All changes in SN function related to H were significant (at least p<0.05). SN pacing from the crista terminalis was never limited by atrial muscle conduction (fast, Na-channel dependent) or refractoriness. Atrial ERP changed from 86±14 to 96±20ms (NS) with H. In summary, acute H adversely affects SN automaticity, conduction and refractoriness; presumably related to alterations in the Ca current. These changes may be responsible for many of the bradyarrhythmias seen clinically during severe H.
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Yabek, S. CHARACTERIZATION OF SINUS NODE REFRACTORINESS AND SINOATRIAL CONDUCTION DURING ACUTE HYPOXIA. Pediatr Res 21 (Suppl 4), 196 (1987). https://doi.org/10.1203/00006450-198704010-00181
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DOI: https://doi.org/10.1203/00006450-198704010-00181