Cardiac Responses to Sympathetic and Vagal Stimulation in the Newborn Lamb During Acidosis and Hypoxia

Abstract

Heart rate (HR) and left ventricular co ntractility (VC) responses to sympathetic and vagal nerve stimulation were assessed in 15 lambs from < 1 to 3 days of during lactic acidemia, hypercapnia and hypoxemia. These were compared with responses under control conditions. In all experiments supramaximal electrical stimulation of the left inferior cardiac sympathetic nerve produced large increases of VC as measured by the dP/dt max from a given end-diastolic pressure (LVEDP) when HR, mean aortic pressure and cardiac output (Medicon) were held constant. With a pH of 7.39 the dp/dt max increased from 3,000 (±155 SE) to 4,244 (±147 SE) mm Hg/sec during stimulation, while the LVEDP fell from 7.3 (±0.73 SE) to 5.8 (±0.79). During acidemia the increase (1,310±159 SE) was unchanged. With hypercapnia (PCO₂ 69 mm Hg) the responses were less (840 mm Hg/sec) than with low PCO₂ (1,300 mm Hg/sec, p<0.01). Responses during hypoxemia (PO₂ 33 mm Hg) were indentical to those with normal PO₂. Cardiac slowing in response to stimulation of the right distal vagus N was measured at several frequencies (F) from 1-15/sec, duration 5msec, and 10-15 V. slowing was a function of F, but was unaltered by changes of PO₂, PCO₂ of pH up to an F of 10/sec. At F 15 the bradycardia was often enhanced by hypercapnia. It is co ncluded that hypoxemia and lactic acidemia do not alter adrenergic (A) or cholinergic (C) transmission, but that hypercapnic acidosis may reduce A, and enhance C during maximal stimulation. This suggests a mechanism whereby autonomic control of the heart may be altered in neonatal asphyxia.

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