Abstract
We used an isolated perfused heart model to test the effects of acute hypoxia and adenosine (ADO) on the adult (A) and neonatal (N) (1-5 days) rabbit atrioventricular node (AVN). The AVN function was assessed by the AH interval at a constant atrial pacing cycle length (CL) just shorter than the intrinsic CL and by the longest pacing CL resulting in Wenckebach periodicity (WP), when the hearts were sequentially exposed to 0.01, 0.1 and 1 mM ADO, in both groups ADO caused a similar degree of dose-dependent increase in AH (93±53% in A, n=8; 58±24% in N, n=7, after 1 mM ADO) and WP (43±12% in A; 36±18% in N). When the hearts were exposed to 5 min of hypoxia (02 replaced with N2) there was a significant difference in the increase of WP between these 2 groups (128±44% in A; 34±13% in N, p <0.01). The change in WP in A caused by hypoxia was significantly greater (p<0.05) than that caused by 1 mM ADO, a dose that has been previously shown to cause complete AVN block in guinea pigs. In A when 1 mM aminophylline (AMO), a competitive antagonist to ADO, was added, it could attenuate the WP increment caused by 1mM ADO (32±13% by ADO; 19±8% by ADO+AMO, n=8, p <0.01), but it could not attenuate those caused by hypoxia (100±25% by hypoxia; 87±32% by hypoxia+AMO, p=0.38). We conclude that in the rabbit AVN: 1) The response to ADO is similar in A and N. 2) N is relatively resistant to acute hypoxia as compared to A. 3) The response to acute hypoxia in A could not be totally explained by the ADO release theory.
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Young, ML., Ramza, B. & Joyner, R. THE EFFECTS OF HYPOXIA AND ADENOSINE ON THE ELECTROPHYSIOLOGIC FUNCTION OF THE ADULT AND NEONATAL RABBIT ATRIOVENTRICULAR NODE. Pediatr Res 21 (Suppl 4), 196 (1987). https://doi.org/10.1203/00006450-198704010-00182
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DOI: https://doi.org/10.1203/00006450-198704010-00182