A synergism between hypoxic episodes and low ethanol doses triggers deleterious effects upon neonatal breathing patterns.

MACCHIONE, A.F.; ANUNZIATA, F; TRUJILLO, V.; HAYMAL, BO; MOLINA, JC

Mar del Plata

Congreso; Reunión Conjunta SAIC, SAI, SAFIS.; 2018

Effects of early ethanol exposure upon neonatal respiratory plasticityhave received progressive attention given a multifactorialperspective related with sudden infant death syndrome or hypoxia-associated syndromes. In this preclinical study we examine howlow doses of ethanol potentiate the effects induced by sequentialexposures to hypoxia in 3?9-day-old pups, period equivalent to the3rd human gestational trimester. At postnatal days (PDs) 3, 5 and7, pups received 1.0 g/kg ethanol (ip) or vehicle and later were exposedto normoxia or hypoxia (8%O2) during 15min. At testing day(PD9), pups were exposed to normoxia/hypoxia/recovery-normoxiaunder the effects of 0.0, 1.0 or 2.0 g/kg EtOH. Breathing frequenciesand apneas were recorded by plethysmography.The duration of hyperventilation induced by hypoxia progressivelyincreased. At PD7 pups were able to maintain hyperventilation alongthe entire hypoxic-test. At PDs 5-7, hyperventilation was altered byethanol intoxication. While vehicle-pups hyperventilate efficiently,intoxicated-pups were only able to maintain hyperventilation duringa short temporal interval. Immediately after these pups showed asignificant respiratory depression comparable to the breathing ratesobtained during normoxia. At PD3, hypoxia generated a significantnumber of apneic episodes. At PD9, the hyperventilation was significantlymediated by the state of intoxication. Pups treated with2.0 g/kg EtOH exhibited a very low capability in terms of generatingadequate hyperventilation. During recovery-normoxia, intoxicated-males (2.0g/kg) presented an abrupt respiratory depressioncoupled with heightened levels of apnea.These results indicate that a relatively low ethanol dose coupledwith a hypoxic event disrupts early respiratory plasticity. Furthermore,ethanol intoxication paired with hypoxia alters the capabilityof the organism to exhibit compensatory breathing patterns whendefied with the lack of ambient oxygen. The results also indicate thatmales are more vulnerable to the deleterious effects of the synergismcomprising hypoxia and ethanol particularly during the phase of recovery-normoxia.