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J receptor activity in idiopathic pulmonary hypertension and its expected change in the presence of pulmonary bed vasodilators
Respiratory Physiology & Neurobiology ( IF 2.3 ) Pub Date : 2021-07-21 , DOI: 10.1016/j.resp.2021.103742
Ashima Anand 1 , Rajeev Sharma 2 , Niraj Srivastava 1 , Sivasubramanian Ramakrishnan 2
Affiliation  

Juxtapulmonary receptors (J) lying in the lung parenchyma are stimulated naturally by any condition that produces interstitial oedema, transient increases in interstitial volume and pressure or raised pulmonary capillary pressure. There is no information available about the level of their stimulation in patients with idiopathic pulmonary hypertension (IPH) who have high levels of pulmonary artery systolic pressures.

The aim of the present study therefore was to find the level of these receptors activity in these patients at their prevailing pulmonary artery systolic pressures. This was done by the established method of determining the dose of i.v. lobeline that gives rise to threshold levels of sensations in the upper chest areas and accelerates respiration. In IPH patients it was found to be as high as 31.6 ± 5.6 μg/kg i.e., twice as much as that known for healthy individuals which is 15 μg/kg. This shows an enhanced stimulation of J receptors in IPH patients.

Expectedly when pulmonary artery systolic pressure falls with pulmonary bed vasodilator medication given to IPH patients, a reduction in the natural stimulus of J receptors would also occur leading to a fall in their activity and hence that of the quantum of their reflexes of respiratory acceleration and inhibition of exercise. This finding provides the first insight of a neural mechanism that could be influenced to produce its effects when pulmonary artery systolic pressure falls by pulmonary vasodilator medication.



中文翻译:

特发性肺动脉高压中的 J 受体活性及其在肺床血管扩张剂存在下的预期变化

任何产生间质水肿、间质体积和压力的瞬时增加或肺毛细血管压力升高的情况都会自然地刺激位于肺实质中的近肺受体 (J)。对于肺动脉收缩压水平较高的特发性肺动脉高压 (IPH) 患者,没有关于其刺激水平的信息。

因此,本研究的目的是在这些患者的主要肺动脉收缩压下找出这些受体的活性水平。这是通过确定 iv lobeline 剂量的既定方法完成的,该剂量在上胸部区域引起阈值水平的感觉并加速呼吸。在 IPH 患者中,它被发现高达 31.6 ± 5.6 μg/kg,即是健康个体已知的 15 μg/kg 的两倍。这表明 IPH 患者中 J 受体的刺激增强。

预期当肺动脉收缩压因 IPH 患者的肺床血管扩张药物而下降时,J 受体的自然刺激也会减少,从而导致它们的活动下降,从而导致其呼吸加速和抑制的反射量下降的运动。这一发现首次揭示了一种神经机制,当肺血管扩张剂药物导致肺动脉收缩压下降时,这种神经机制可能会受到影响而产生影响。

更新日期:2021-07-29
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