ATTENUATION OF THE HYPOXIC VENTILATORY RESPONSE IN ADULT-RATS FOLLOWING ONE MONTH OF PERINATAL HYPEROXIA

1. This study was designed to test the hypothesis that perinatal suppr ession of peripheral arterial chemoreceptor inputs attenuates the hypo xic ventilatory response in adult rats. Perinatal suppression of perip heral chemoreceptor activity was achieved by exposing rats to hyperoxi a throughout the first month of life. 2. Late gestation pregnant rats were housed in a 60% O-2 environment, exposing the pups to hyperoxia f rom several days prior to birth until they were returned to normoxia o n postnatal day 28. These perinatally treated rats were then reared to adulthood (3-5 months old) in normoxia. In addition to the mother rat s, adult-male rats were also exposed to hyperoxia, creating an adult-t reated control group. Two to four months after the hyperoxic exposure, treated rats were compared with untreated male rats of similar age. 3 . A whole-body, flow-through plethysmograph was used to measure hyrpox ic and hypercapnic ventilatory responses of the unanaesthetized adult rats. In moderate hypoxia (arterial oxygen partial pressure, P-a,P-O2 similar to 48 mmHg), V-E (minute ventilation) and the ratio V-E/V-CO2 (ventilation relative to CO2 production) increased by 16.7 +/- 4.0 and 35.4 +/- 3.4%, respectively, in perinatal-treated rats (means +/- S.E .M), but increased more in untreated control rats (51.4 +/- 2.8 and 83 .1 +/- 4.3%; both P < 10(-6)). 4. In contrast to the impaired hypoxic ventilatory response, ventilatory responses to hypercapnia (5% CO2) we re similar between untreated control and perinatal-treated rats. 5. Im paired hypoxic responsiveness was unique to the perinatal-treated rats since hypoxic ventilatory responses were not attenuated in adult-trea ted rats. 6. The results indicate that ventilatory responses to hypoxa emia are greatly attenuated in adult rats that had experienced hyperox ia during their first month of life, and suggest that normal hypoxic v entilatory control mechanisms are susceptible to developmental plastic ity.