Journal Article

Cardiorespiratory control and cytokine profile in response to heat stress, hypoxia, and lipopolysaccharide (LPS) exposure during early neonatal period

Hasan, Shabih U., Wilson, Richard J.A., Chandrasekharan, Kumaran, McDonald, Fiona B.

2016

Overview

Sudden infant death syndrome (SIDS) is one of the most common causes of postneonatal infant mortality in the developed world. An insufficient cardiorespiratory response to multiple environmental stressors (such as prone sleeping positioning, overwrapping, and infection), during a critical period of development in a vulnerable infant, may result in SIDS. However, the effect of multiple risk factors on cardiorespiratory responses has rarely been tested experimentally. Therefore, this study aimed to quantify the independent and possible interactive effects of infection, hyperthermia, and hypoxia on cardiorespiratory control in rats during the neonatal period. We hypothesized that lipopolysaccharide (LPS) administration will negatively impact cardiorespiratory responses to increased ambient temperature and hypoxia in neonatal rats. Sprague–Dawley neonatal rat pups were studied at postnatal day 6–8. Rats were examined at an ambient temperature of 33°C or 38°C. Within each group, rats were allocated to control, saline, or LPS (200 μg/kg) treatments. Cardiorespiratory and thermal responses were recorded and analyzed before, during, and after a hypoxic exposure (10% O2). Serum samples were taken at the end of each experiment to measure cytokine concentrations. LPS significantly increased cytokine concentrations (such as TNFα, IL‐1β, MCP‐1, and IL‐10) compared to control. Our results do not support a three‐way interaction between experimental factors on cardiorespiratory control. However, independently, heat stress decreased minute ventilation during normoxia and increased the hypoxic ventilatory response. Furthermore, LPS decreased hypoxia‐induced tachycardia. Herein, we provide an extensive serum cytokine profile under various experimental conditions and new evidence that neonatal cardiorespiratory responses are adversely affected by dual interactions of environmental stress factors. An insufficient cardiorespiratory response to multiple environmental stressors during a critical period of development in a vulnerable infant, may result in SIDS. This study provides an extensive serum cytokine profile under various experimental conditions and new evidence that neonatal cardiorespiratory responses are adversely affected by dual interactions of environmental stress factors.

• Publisher: John Wiley & Sons, Inc,John Wiley and Sons Inc
• Subject: Animals / Animals, Newborn / Babies / Cardiorespiratory / Critical period / Cytokines / Cytokines - analysis / Cytokines - biosynthesis / Disease Models, Animal / Environmental Physiology / Environmental risk / Environmental stress / Fever / Fever - complications / Fever - physiopathology / Heart Rate - physiology / Heat / Heat stress / Humans / Hyperthermia / Hypoxia / Hypoxia - complications / Hypoxia - physiopathology / Immunology / infant / Infant mortality / Infant, Newborn / infection / Infections / Infections - complications / Infections - physiopathology / Inflammation / Lipopolysaccharides / Lipopolysaccharides - toxicity / Multiplex Polymerase Chain Reaction / neonate / Neonates / Original Research / Pathology / Physiology / Plethysmography / Pulmonary Ventilation - physiology / Rats / Rats, Sprague-Dawley / Reproductive Conditions, Disorders and Treatments / Risk factors / SIDS / Studies / Sudden Infant Death - etiology / Sudden infant death syndrome / Tachycardia / Tumor necrosis factor-α / Ventilators / Ventilatory behavior