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Ventilatory and carotid body responses to acute hypoxia in rats exposed to chronic hypoxia during the first and second postnatal weeks.
Respiratory Physiology & Neurobiology ( IF 1.9 ) Pub Date : 2020-01-30 , DOI: 10.1016/j.resp.2020.103400
Ryan W Bavis 1 , Monata J Song 1 , Julia P Smachlo 1 , Alexander Hulse 1 , Holli R Kenison 1 , Jose N Peralta 1 , Jennifer T Place 1 , Sam Triebwasser 1 , Sarah E Warden 1 , Amy B McDonough 1
Affiliation  

Chronic hypoxia (CH) during postnatal development causes a blunted hypoxic ventilatory response (HVR) in neonatal mammals. The magnitude of the HVR generally increases with age, so CH could blunt the HVR by delaying this process. Accordingly, we predicted that CH would have different effects on the respiratory control of neonatal rats if initiated at birth versus initiated later in postnatal development (i.e., after the HVR has had time to mature). Rats had blunted ventilatory and carotid body responses to hypoxia whether CH (12 % O2) occurred for the first postnatal week (P0 to P7) or second postnatal week (P7 to P14). However, if initiated at P0, CH also caused the HVR to retain the "biphasic" shape characteristic of newborn mammals; CH during the second postnatal week did not result in a biphasic HVR. CH from birth delayed the transition from a biphasic HVR to a sustained HVR until at least P9-11, but the HVR attained a sustained (albeit blunted) phenotype by P13-15. Since delayed maturation of the HVR did not completely explain the blunted HVR, we tested the alternative hypothesis that the blunted HVR was caused by an inflammatory response to CH. Daily administration of the anti-inflammatory drug ibuprofen (4 mg kg-1, i.p.) did not alter the effects of CH on the HVR. Collectively, these data suggest that CH blunts the HVR in neonatal rats by impairing carotid body responses to hypoxia and by delaying (but not preventing) postnatal maturation of the biphasic HVR. The mechanisms underlying this plasticity require further investigation.

中文翻译:

出生后第一周和第二周暴露于慢性缺氧的大鼠的通气和颈动脉体对急性缺氧的反应。

产后发育过程中的慢性缺氧(CH)在新生哺乳动物中导致钝性低氧通气反应(HVR)。HVR的大小通常会随着年龄的增长而增加,因此CH可能会通过延迟该过程而使HVR钝化。因此,我们预测,如果在出生时开始与出生后后期(即在HVR有时间成熟之后)开始,CH对新生大鼠的呼吸控制会有不同的影响。无论是在出生后第一周(P0至P7)还是在出生后第二周(P7至P14)发生CH(12%O2),大鼠对缺氧的通气和颈动脉体反应均变钝。但是,如果在P0开始,CH也会使HVR保持新生哺乳动物的“双相”形状特征。产后第二周的CH并未导致双相HVR。CH的出生延迟了从双相性HVR到持续性HVR的转变,直到至少P9-11为止,但是HVR在P13-15之前达到了持续性(尽管变钝)表型。由于HVR的延迟成熟不能完全解释钝化的HVR,因此我们测试了另一种假说,即钝化的HVR是由对CH的炎症反应引起的。每天服用抗炎药布洛芬(4 mg kg-1,ip)不会改变CH对HVR的影响。总体而言,这些数据表明,CH通过削弱颈动脉体对缺氧的反应以及延迟(但不能阻止)双相HVR的出生后而使新生大鼠的HVR变钝。这种可塑性的基础机制需要进一步研究。但是HVR在P13-15上获得了持续的(尽管变钝)表型。由于HVR的延迟成熟不能完全解释钝化的HVR,因此我们测试了另一种假说,即钝化的HVR是由对CH的炎症反应引起的。每天服用抗炎药布洛芬(4 mg kg-1,ip)不会改变CH对HVR的影响。总体而言,这些数据表明,CH通过削弱颈动脉体对缺氧的反应以及延迟(但不能阻止)双相HVR的出生后而使新生大鼠的HVR变钝。这种可塑性的潜在机制需要进一步研究。但是HVR在P13-15上获得了持续的(尽管变钝)表型。由于HVR的延迟成熟不能完全解释钝化的HVR,因此我们测试了另一种假说,即钝化的HVR是由对CH的炎症反应引起的。每天服用抗炎药布洛芬(4 mg kg-1,ip)不会改变CH对HVR的影响。总体而言,这些数据表明,CH通过削弱颈动脉体对缺氧的反应以及延迟(但不能阻止)双相HVR的出生后而使新生大鼠的HVR变钝。这种可塑性的潜在机制需要进一步研究。每天服用抗炎药布洛芬(4 mg kg-1,ip)不会改变CH对HVR的影响。总体而言,这些数据表明,CH通过削弱颈动脉体对缺氧的反应以及延迟(但不能阻止)双相HVR的出生后而使新生大鼠的HVR变钝。这种可塑性的潜在机制需要进一步研究。每天服用抗炎药布洛芬(4 mg kg-1,ip)不会改变CH对HVR的影响。总体而言,这些数据表明,CH通过削弱颈动脉体对缺氧的反应以及延迟(但不能阻止)双相HVR的出生后而使新生大鼠的HVR变钝。这种可塑性的潜在机制需要进一步研究。
更新日期:2020-01-30
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