Insulin, C‐peptide, Glucose, and Heart Rate Responses to Acute Intermittent Hypoxia in the Neonatal Rat: Body Temperature and Chemical Sympathectomy

Abstract

Apnea due to immature respiratory control is a common cause of neonatal intermittent hypoxia (IH). We hypothesized that IH disrupts glucose homeostasis and is a metabolic stressor. Rats at postnatal days (PD) 2–3, 7–8, or 11–12 were exposed to 6 @ 30‐sec cycles of IH (3% O2) over 1 hr. An additional group of PD7‐8 pups underwent IH for 3 cycles over 0.5 hr, but were pretreated (on PD3, 5, and 6) with guanethidine (chemical sympathectomy). In PD2‐3 rats, plasma glucose, insulin, and C‐peptide were increased at the 6th cycle of IH. In PD7‐8 rats, plasma glucose, insulin, and C‐peptide increased by the 3rd cycle, but by the 6th cycle, glucose had returned to baseline. PD11‐12 pups experienced a similar increase in plasma glucose, but a much larger increase in insulin and C‐peptide compared to PD7‐8. IH caused bradycardia and a decrease in body temperature. Pretreatment with guanethidine in PD7‐8 rats augmented the increase in insulin and C‐peptide; heart rate at baseline, and heart rate and body temperature at their nadirs during IH were lower after guanethidine pretreatment. We conclude that IH alters glucose homeostasis and induces bradycardia in neonates. The sympathetic nervous system restrains the insulin response and maintains heart rate during IH in the neonate.