激活咪唑啉1受体维持新生大鼠应用右美托咪定时自主呼吸的呼吸驱动力
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Imidazoline 1 receptor activation preserves respiratory drive in spontaneously breathing newbornrats during dexmedetomidine administration
背景与目的
右美托咪啶是一种用于镇静而不降低呼吸驱动力的α2肾上腺素能受体和咪唑啉1（I1）受体激动剂。本研究的目的是阐明新生自主呼吸大鼠中，α2肾上腺素能受体和I1受体如何参与右美托咪定引起的循环呼吸改变。
方 法
将给药的腹部导管和3个用于记录心电图数据的皮下电极分别插入2到5日龄Wistar经异氟醚吸入麻醉的大鼠中。在单独的房间内，每只大鼠经腹腔给予右美托咪定（50 μg·kg-1），5 min后分别给予生理盐水或者1、5、10 mg·kg-1的阿替美唑（选择性α2肾上腺素能受体拮抗剂）或者依法克生（α2肾上腺素能受体/ I1受体拮抗剂）。用药前、后记录心肺功能指标。
结 果
单独应用右美托咪定造成了心肺功能指标的显著变化。加用5 mg·kg-1或者10 mg·kg-1的阿替美唑，或1 mg·kg-1的依法克生完全改善右美托咪定相关的心率（HR）降低。加用1 mg·kg-1阿替美唑，1 mg·kg-1或5 mg·kg-1的依法克生完全改善右美托咪啶相关的呼吸频降低。平均吸气流速（VT /TI；VT表示潮气量，TI表示吸气时间）作为呼吸驱动的一个指标，并不受单独应用右美托咪定 (P = 0.273) 及右美托咪定合用阿替美唑（P = 0.605, 0.153, 0.138 各自对应 1, 5, 10 mg·kg-1阿替美唑 ）的影响。然而，右美托咪定合用依法克生后平均吸气流速显著降低（P = 0.029, <0.001, <0.001 各自对应 1, 5, 10 mg·kg-1依法克生）。
结 论
我们的研究结果表明，对接受右美托咪定镇静的新生大鼠，是α2肾上腺素能受体而非I1参与心率和呼吸频率的调节，而I1受体的激活在呼吸驱动的维持中起主要作用。
原始文献摘要
Sato N, Saiki C, Tamiya J Imidazoline 1 receptor activation preserves respiratory drive in spontaneously breathing newbornrats during dexmedetomidine administration Paediatr Anaesth. 2017 May;27(5):506-515. doi: 10.1111/pan.13107. Epub 2017 Feb 8
BACKGROUND:
Dexmedetomidine is an alpha-2 (α2 ) adrenoceptor and imidazoline 1 (I1 ) receptor agonist that provides sedation without loss of respiratory drive.
AIMS:
The aim of this study was to elucidate the involvement of α2 -adrenoceptor and I1 receptor in the cardiorespiratory changes induced by dexmedetomidine in spontaneously breathing newborn rats.
METHODS:
An abdominal catheter to administer drugs and three subcutaneous electrodes to record electrocardiographic data were inserted into 2- to 5-day-old Wistar rats under isoflurane anesthesia. In individual chambers, each rat was intraperitoneally administered dexmedetomidine (50 μg·kg-1 ) followed 5 min later by normal saline or 1, 5, or 10 mg·kg-1 atipamezole (selective α2 -adrenoceptor antagonist) or efaroxan (α2 -adrenoceptor/I1 receptor antagonist). Cardiorespiratory indices were recorded before and after drug administration.
RESULTS:
The administration of dexmedetomidine alone resulted in significant changes to most of the cardiorespiratory indices examined. The addition of 5 or 10 mg·kg-1 atipamezole or 1 mg·kg-1 efaroxan completely ameliorated the dexmedetomidine-associated reduction in heart rate (HR). The addition of 1 mg·kg-1 atipamezole or 1 or 5 mg·kg-1 efaroxan completely ameliorated the dexmedetomidine-associated reduction in respiratory frequency. Mean inspiratory flow (VT /TI ; VT is tidal volume and TI is inspiratory time), which is an index of respiratory drive, was not significantly affected by the administration of dexmedetomidine alone (P = 0.273) or dexmedetomidine + atipamezole (P = 0.605, 0.153, 0.138 for 1, 5, 10 mg·kg-1 atipamezole, respectively); however, it was significantly decreased after the administration of dexmedetomidine + efaroxan (P = 0.029, <0.001, <0.001 for 1, 5, 10 mg·kg-1 efaroxan, respectively).
CONCLUSIONS:
Our results suggest that in newborn rats undergoing dexmedetomidine sedation, the α2 -adrenoceptor, but not I1 receptor, is involved in the regulation of HR and respiratory frequency, and that activation of the I1 receptor plays a major role in the maintenance of respiratory drive.
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