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Intermittent hyperoxia attenuates the hypoxic ventilatory response in neonatal rats

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Sustained exposure to 30–60% O 2 from birth reduces the hypoxic ventilatory response (HVR) in rats, primarily through abnormal development of the carotid body. We hypothesized that a more clinically relevant intermittent hyperoxia exposure would produce similar changes to the HVR. Rats were continuously exposed to intermittent 30% O 2 or intermittent 60% O 2 from birth through 14–15 days of age (i.e., 4.5‐min bouts of hyperoxia separated by 7.5 min of normoxia, 24 h day −1 ); Control rats were reared in room air. Ventilation was measured at 14–15 days of age by head‐body plethysmography (n=15–18 per group). No differences were detected among treatment groups while breathing 21% O 2 . However, ventilation was significantly lower in both groups of intermittent hyperoxia rats during acute exposure to 12% O 2 (143±8 and 154±4 ml min −1 100g −1 , respectively) than in Control rats (172±6 ml min −1 100g −1 ; both P <0.05). Although attenuation of the HVR was modest relative to that observed after similar durations of sustained hyperoxia, these data indicate that intermittent exposure to hyperoxia can alter the normal development of ventilatory chemoreflexes. Supported in part by NIH grant P20 RR‐016463 (Maine INBRE).
Title: Intermittent hyperoxia attenuates the hypoxic ventilatory response in neonatal rats
Description:
Sustained exposure to 30–60% O 2 from birth reduces the hypoxic ventilatory response (HVR) in rats, primarily through abnormal development of the carotid body.
We hypothesized that a more clinically relevant intermittent hyperoxia exposure would produce similar changes to the HVR.
Rats were continuously exposed to intermittent 30% O 2 or intermittent 60% O 2 from birth through 14–15 days of age (i.
e.
, 4.
5‐min bouts of hyperoxia separated by 7.
5 min of normoxia, 24 h day −1 ); Control rats were reared in room air.
Ventilation was measured at 14–15 days of age by head‐body plethysmography (n=15–18 per group).
No differences were detected among treatment groups while breathing 21% O 2 .
However, ventilation was significantly lower in both groups of intermittent hyperoxia rats during acute exposure to 12% O 2 (143±8 and 154±4 ml min −1 100g −1 , respectively) than in Control rats (172±6 ml min −1 100g −1 ; both P <0.
05).
Although attenuation of the HVR was modest relative to that observed after similar durations of sustained hyperoxia, these data indicate that intermittent exposure to hyperoxia can alter the normal development of ventilatory chemoreflexes.
Supported in part by NIH grant P20 RR‐016463 (Maine INBRE).

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