Changes in respiratory timing induced by hypercapnia in maturing rats
Changes in respiratory timing induced by hypercapnia in maturing rats
复制标题
DOI：
10.1152/jappl.1999.87.2.484
复制
发表时间：
1999-08-01
影响因子：
3.3
通讯作者：
Martin, RJ
中科院分区：
文献类型：
--
作者：
Abu-Shaweesh, JM;Dreshaj, IA;Martin, RJ
早产儿对高碳酸血症的反应是通气反应减弱，其特征是呼吸频率降低。我们假设这种受损的高碳酸血症通气反应是中枢起源的，并且是通过γ-氨基丁酸能（GABA能）途径介导的。因此，我们研究了两组成熟的 Sprague-Dawley 大鼠：在出生后四个年龄（5、16-17、22-23 和 41-42 天）进行全身体积描记的无约束大鼠；以及以及通气、去大脑、迷走神经切断、瘫痪的大鼠，在4-6天和37-39天龄时测量膈神经对高碳酸血症的反应。在不受限制的组中，高碳酸血症引起的每分通气量增加在 5 天时显着低于 16 天后。尽管所有年龄段的潮气量均有所增加，但频率在 5 天时较基线显着下降，而在 16-17、22-23 和 41-42 天则显着增加。 5日龄时频率的下降主要是由于呼气持续时间（TE）显着延长。在通气组中，高碳酸血症还会导致 4-6 天龄的 TE 延长，但不会导致 37-39 天龄的 TE 延长。静脉注射荷包牡丹碱（GABA(A) 受体阻滞剂）可消除新生大鼠因高碳酸血症而导致的 TE 延长。我们得出结论，新生大鼠幼崽表现出对 CO2 的特征性通气反应，表现为中枢介导的 TE 延长，这似乎是由 GABA 能机制介导的。
Premature infants respond to hypercapnia by an attenuated ventilatory response that is characterized by a decrease in respiratory frequency. We hypothesized that this impaired hypercapnic ventilatory response is of central origin and is mediated via gamma-aminobutyric acid-ergic (GABAergic) pathways. We therefore studied two groups of maturing Sprague-Dawley rats: unrestrained rats in a whole body plethysmograph at four postnatal ages (5, 16-17, 22-23, and 41-42 days); and ventilated, decerebrate, vagotomized, paralyzed rats in which phrenic nerve responses to hypercapnia were measured at 4-6 and 37-39 days of age. In the unrestrained group, the increase in minute ventilation induced by hypercapnia was significantly lower at 5 days vs. beyond 16 days. Although there was an increase in tidal volume at all ages, frequency decreased significantly from baseline at 5 days, whereas it increased significantly at 16-17, 22-23, and 41-42 days. The decrease in frequency at 5 days of age was mainly due to a significant prolongation in expiratory duration (TE). In the ventilated group, hypercapnia also caused prolongation in TE at 4-6 days but not at 37-39 days of age. Intravenous administration of bicuculline (GABA(A)-receptor blocker) abolished the prolongation of TE in response to hypercapnia in the newborn rats. We conclude that newborn rat pups exhibit a characteristic ventilatory response to CO2 expressed as a centrally mediated prolongation of TE that appears to be mediated by GABAergic mechanisms.