A SYNERGISM BETWEEN HYPOXIC EPISODES AND LOW ETHANOL DOSES TRIGGERS DELETERIOUS EFFECTS UPON NEONATAL BREATHING PATTERNS.

TRUJILLO, VERÓNICA; MACCHIONE, A.F.; ANUNZIATA, F; HAYMAL, O.B.; MOLINA, J.C.

MAR DEL PLATA

Congreso; SAIC-SAI-SAFIS-2018; 2018

SOCIEDAD ARGENTINA DE FISIOLOGÌA

A SYNERGISM BETWEEN HYPOXIC EPISODES AND LOW ETHANOL DOSES TRIGGERS DELETERIOUS EFFECTS UPON NEONATAL BREATHING PATTERNS. Ana Fabiola Macchione1 , Florencia Anunziata1 , Verónica Trujillo1 , Olga Beatriz Haymal1 , Juan Molina1, 2 1 Instituto M. M. Ferreyra, INIMEC-CONICET-UNC. , 2 Facultad de Psicología, Universidad Nacional de Córdoba Effects of early ethanol exposure upon neonatal respiratory plasticity have received progressive attention given a multifactorial perspective related with sudden infant death syndrome or hypoxia-associated syndromes. In this preclinical study we examine how low doses of ethanol potentiate the effects induced by sequential exposures to hypoxia in 3?9-day-old pups, period equivalent to the 3rd human gestational trimester. At postnatal days (PDs) 3, 5 and 7, pups received 1.0 g/kg ethanol (ip) or vehicle and later were exposed to normoxia or hypoxia (8%O2) during 15min. At testing day (PD9), pups were exposed to normoxia/hypoxia/recovery-normoxia under the effects of 0.0, 1.0 or 2.0 g/kg EtOH. Breathing frequencies and apneas were recorded by plethysmography. The duration of hyperventilation induced by hypoxia progressively increased. At PD7 pups were able to maintain hyperventilation along the entire hypoxic-test. At PDs 5-7, hyperventilation was altered by ethanol intoxication. While vehicle-pups hyperventilate efficiently, intoxicated-pups were only able to maintain hyperventilation during a short temporal interval. Immediately after these pups showed a significant respiratory depression comparable to the breathing rates obtained during normoxia. At PD3, hypoxia generated a significant number of apneic episodes. At PD9, the hyperventilation was significantly mediated by the state of intoxication. Pups treated with 2.0 g/kg EtOH exhibited a very low capability in terms of generating adequate hyperventilation. During recovery-normoxia, intoxicated-males (2.0g/kg) presented an abrupt respiratory depression coupled with heightened levels of apnea. These results indicate that a relatively low ethanol dose coupled with a hypoxic event disrupts early respiratory plasticity. Furthermore, ethanol intoxication paired with hypoxia alters the capability of the organism to exhibit compensatory breathing patterns when defied with the lack of ambient oxygen. The results also indicate that males are more vulnerable to the deleterious effects of the synergism comprising hypoxia and ethanol particularly during the phase of recovery-normoxia.