Ethanols disruptive effects on the hypoxic ventilatory response and blood parameters associated with hypercapnia in rat pups

ANUNZIATA, FLORENCIA; AMIGONE, JOSE LUIS; MOLINA, JUAN CARLOS; TEJERINA, DAVID NORBERTO; TRUJILLO, VERÓNICA; ANA FABIOLA MACCHIONE; WILLE-BILLE, ARANZA

SANTIAGO DE CHILE

Jornada; Sociedad Chilena de Ciencias Fisiológicas y Asociación Latinoamericana de Ciencias Fisiológicas Joint Meeting; 2020

Sociedad Chilena de Ciencias Fisiológicas (SCHCF)

Introduction: Prenatal and neonatal ethanol (EtOH) exposure affects neonatal respiratory neuroplasticity; a risk factor related with the Sudden Infant Death Syndrome (SIDS). This association is currently promoting research based on the early effects of the drug upon the respiratory system.Objective: The aim of this study was to examine if early acute and/or chronic EtOH exposure are able to trigger hypoxia-related long term facilitation (LTF) associated with elevated pCO2 levels in blood. Methods: At postnatal day (PD) 9, we analyzed the impact of different EtOH doses (0.75, 1.37 or 2.0 g/kg) upon the respiratory response in pups that were chronically pre-exposed to 0.0 or 2.0 g/kg EtOH during PDs 3, 5, 7. At PD 9 animals were subjected to sequential air conditions defined as initial normoxia, hypoxia and recovery normoxia. Furthermore, we analyzed EtOH-related blood parameters in other neonates that were only exposed to 0.0 or 2.0g/kg of EtOH during PDs 3-9 (not subjected to a hypoxic challenge). All experimental protocols were approved by CICUAL-INIMEC. Between-within ANOVAs were performed and data was reported as mean+/- standard error; n>10 in all experimental groups.Results: Sensitization effects upon initial normoxia and the hypoxic ventilatory response in EtOH pre-treated animals were observed. During hypoxic and recovery normoxic events, EtOH pre-exposure increased respiratory rates across all EtOH doses administered at PD9; a phenomenon probably related with a LTF process. Also, at PD9 we observed that all EtOH doses during recovery normoxia elicited LTF. Blood parameters of acidosis-hypercapnia (lower pH and higher pCO2) were observed as a function of either acute or chronic EtOH exposure. Conclusion: Early EtOH exposure induced acidosis-hypercapnia that may support the LTF process observed in hypoxic and recovery normoxic phases. In summary, early acute or chronic EtOH experience alter the acid-base equilibrium inducing respiratory plasticity such as LTF. Fundings: FONCyT (PICT 2014-1606), SECyT and CONICET.