Effects of hypoxia on adult and neonatal pacemaker rates

Fetal bradycardia during parturition may result both from autonomic reflex effects and from the direct effect of hypoxia on the myocardium. To compare the relative sensitivities of neonatal and adult sinoatrial nodes to hypoxia, action potentials were recorded simultaneously from isolated neonatal and adult sinoatrial nodal tissues of the guinea pig with intracellular microelectrodes. Action potential rates were measured during normoxia and hypoxia, with and without acidosis, glucose, and epinephrine. Control (PO2 greater than 450 torr) intrinsic pacemaker activity was higher in the neonate than in the adult (296 versus 222 beats per minute). Epinephrine maximally increased rates to similar levels in the two age groups. Hypoxia (PO2 equals 33 torr) markedly lowered adult (44%) and neonatal (35%) rates, but the fall in rates was similar. The addition of acidosis or the removal of glucose during hypoxia produced a greater fall of pacemaker rates in the neonates compared with the adults. The addition of epinephrine during hypoxia caused adult rates to increase to control normoxic levels, but neonatal rates remained significantly depressed below control levels. The results suggest that the neonatal pacemaker node is no better protected against bradycardia during hypoxia alone than is the adult node, but that the neonatal node is more susceptible to bradycardia induced by hypoxia with acidosis or removal of glucose. The hypoxic neonatal node, moreover, responds with a lesser increase in pacemaker rate during epinephrine stimulation than does the adult node.