Hypotension in Fetal and Newborn Lambs; Different Patterns of Reflex Heart Rate Control Revealed by Autonomic Blockade

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Abstract
Reflex heart rate (HR) responses to hypotension were studied in chronically instrumented fetal and newborn lambs. Studies spanned 106–141 days of gestation and 1–22 days after birth. Brief hypotensive stimuli (10 s) were produced by inflation of a cuff implanted around the inferior vena cava; HR and mean arterial pressure (MAP) were recorded from a carotid arterial catheter. Autonomic nervous control of HR was examined using selective sympathetic beta-adrenergic blockade (propranolol 1 mg/kg), cholinergic blockade (atropine 0.2–0.3 mg/kg), and total autonomic blockade (propranolol plus atropine). In newborn lambs (n = 4) HR increased progressively as MAP was reduced in the range 5–50%. Tachycardia during mild hypotension (< 15% MAP fall) was due to sympathetic activation as it was abolished by propranolol. During severe hypotension ( > 30% MAP fall) tachycardia was reduced by selective beta-adrenergic blockade and by cholinergic blockade, and totally abolished by total autonomic blockade; thus withdrawal of vagal tone plus augmentation of sympathetic activity contribute to the increase of HR in response to large MAP falls in the newborn. Fetal lambs (n = 4) responded with tachycardia in mild hypotension (< 15% MAP fall) but this was reversed when hypotension was severe (> 30% MAP fall). The primary tachycardia was due to sympathetic activation and was indistinguishable from the newborn response. Reversal of the tachycardia in severe hypotension was due to increased vagal activity which counteracted the sympathetic acceleration. This pattern of simultaneous activation of the opposing autonomic pathways prevents tachycardia and appears to be a characteristic fetal response to severe hypotensive and hypoxemic stress.