Hypercapnia-induced long-term depression of respiratory activity requires α2-adrenergic receptors
Hypercapnia-induced long-term depression of respiratory activity requires α2-adrenergic receptors
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DOI：
10.1152/jappl.1998.84.6.2099
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发表时间：
1998-06-01
影响因子：
3.3
通讯作者：
Mitchell, GS
中科院分区：
文献类型：
--
作者：
Bach, KB;Mitchell, GS
我们研究了反复高碳酸血症发作(吸入二氧化碳分数=0.10)对甲状旁腺后呼吸神经放电的影响。麻醉(乌拉坦)、迷走神经切断和人工呼吸的大鼠连续三次发生5分钟的高氧性高碳酸血症，中间隔5分钟的高氧性常压(吸入O-2分数=0.5)。记录末次高碳酸血症发作前、发作后30分钟和60分钟的呼吸神经放电和血气。高碳酸血症后，动脉血P-CO2维持在初始基线值的1Torr以内。合并的膈和舌下爆发波幅在高碳酸血症后分别降低了基线的46+/-17和55+/-13%，并保持下降至少1小时[长期抑郁(LTD)]。用az-肾上腺素能拮抗剂盐酸育亨宾(0.5 mg/kg；n=7)或2-[2-(2-甲氧基-1，4-苯二氧基)]咪唑啉(RX-821002)盐酸盐(0.25 mg/kg；n=3)预先处理大鼠，重复上述方案。这两种药物都使LTD的膈神经和舌下神经图变弱。结果表明，发作性高碳酸血症引起大鼠呼吸神经活动对育亨宾和RX-821002敏感的LTD，提示LTD需要α(2)受体激活。
We investigated the effects of repeated hypercapnic episodes (inspired CO2 fraction = 0.10) on posthypercapnic respiratory nerve discharge. Anesthetized (urethan), vagotomized, and artificially ventilated rats were presented with three consecutive 5-min episodes of hyperoxic hypercapnia, separated by 5 min of hyperoxic normocapnia (inspired O-2 fraction = 0.5). Respiratory nerve discharge and blood gases were recorded before and 30 and 60 min after the final hypercapnic episode. Posthypercapnia, arterial P-CO2 was maintained within 1 Torr of initial baseline values. Integrated phrenic and hypoglossal burst amplitudes decreased posthypercapnia by up to 46 +/- 17 and 55 +/- 13% of baseline values, respectively, and remained reduced for at least 1 h [long-term depression (LTD)]. The protocol was repeated in rats pretreated with the az-adrenergic antagonists yohimbine HCl (0.5 mg/kg; n = 7) or 2-[2-(2-methoxy-1,4-benzodioanyl)]imidazoline (RX-821002) HCl (0.25 mg/kg; n = 3). Both drugs attenuated LTD in the phrenic and hypoglossal neurograms. Results indicate that episodic hypercapnia elicits a yohimbine- and RX-821002-sensitive LTD of respiratory nerve activity in rats, suggesting that LTD requires alpha(2)-receptor activation.