OMEGA 3 MITIGATION ON DEFICIENT HYPOXIC-VENTILATORY RESPONSE (HVR) INDUCED BY MODERATE ETHANOL DOSES IN AN ANIMAL MODEL EQUIVALENT TO THE THIRD TRIMESTER OF HUMAN PREGNANCY

SEGOVIA, MM; BALASZCZUK,V; MACCHIONE,AF

Mar del Plata

Congreso; Annual Meeting of Bioscience Societies 2022; 2022

SAIC-SAI-FAIC-SAFIS

Maternal ethanol (EtOH) intake during pregnancy and lactation is a highly frequent “social” behaviour in Argentine, exposing fetus or neonates to moderate EtOH intoxication through amniotic fluid and maternal milk. Earlyexposure to EtOH triggers in the organism a spectrum of neurobehavioral dysfunctions affecting, also, the breathing response. Hypoxia acts as an environmental stressor eliciting breathing adaptations, like Hypoxic VentilatoryResponses-HVR, that may be altered by the EtOH exposure. One of the detrimental effects of early EtOH exposure is the reduction of the Omega3-O3 levels in theCNS. Experiment 1: Pups were intoxicated with 2.0g/kgor 0.0g/kg of EtOH, ig at postnatal days (PDs) 3-5-7-9.At PD9, also were subjected to a hypoxic event [5 min of initial normoxia, followed by 3 episodes of hypoxia (O28%) of 5 min, separated by periods of recovery-normoxia of the same duration]. Breathing frequencies and apneaswere recorded in a whole-body plethysmograph at PDs3-5-7 x 5 min and at PD9 x 35 min of test. Experiment2: The same experimental protocol of EtOH exposure atPDs 3-5-7-9 was employed. However, at PDs 3-5-7, pupsreceived 0.0 or 720 mg/kg O3 (ig), 20 min after EtOHadministration. At PDs 5 and 7, EtOH-intoxicated pups elicited a breathing depression that was not affected by the O3 administration. During the hypoxic challenge,EtOH-exposed pups expressed a significant breathing depression during initial normoxia and also at each hypoxic event (i.e. a reduced HVR) relative to it expressed in vehicle-exposed pups (p