Iwase M, Izumizaki M, Tsuchiya N, Homma I.
Iwase M, Izumizaki M, Tsuchiya N, Homma I.
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岩濑 M、泉崎 M、土屋 N、本间 I。
DOI：
10.1113/expphysiol.2012.068312
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发表时间：
2013
期刊：
影响因子：
2.7
通讯作者：
Dopamine D1 receptors control exercise hyperpnoea in mice.
中科院分区：
文献类型：
--
作者：
兵頭昌樹;柏木陽子;儀間温子;花山耕三;正門由久;Dopamine D1 receptors control exercise hyperpnoea in mice.
新发现·本研究的中心问题是什么？运动小鼠的通气量测量（以及通气量和肺气体交换的同时记录）尚未得到彻底研究。我们评估了小鼠在恒定负荷运动期间与代谢变化相关的通气，并检查了D1受体以及先前研究的D2受体的作用。这种可靠的方法可用于基因操作小鼠。·主要发现及其重要性是什么？我们发现，D1受体参与静息通气和运动呼吸过度与代谢的变化在小鼠稳态平行。D1受体的代谢控制对于维持稳态是重要的，以前，我们同时记录了小鼠的通气和肺气体交换，并发现多巴胺D2受体通过行为控制通气与不变的肺气体交换参与运动呼吸过度。在这里，我们检查了假设，D1受体也有助于运动呼吸过度使用D1受体拮抗剂（SCH 23390; SCH），通过血脑屏障，与以前的研究中相同的记录技术和协议。注射生理盐水或SCH（50 μg（kg体重）-1，i. p.）在6 m min-1的恒定负荷运动中进行比较。将每只小鼠置于配备有压差传感器和带质谱仪的开路系统的气密跑步机室中。与注射生理盐水的小鼠相比，注射SCH的小鼠在休息时呼吸频率、每分钟通气量和肺气体交换显著降低。高氧气体吸入期间的通气和高碳酸血症缓解反应组间相似。在两组小鼠中，通过跑步机运动产生了突然增加和连续下降至稳态水平。SCH治疗降低了稳态期间呼吸频率、潮气量和每分钟通气量的增加水平，并降低了整个跑步机运动期间的O2摄取、CO2排出和体温。这些数据表明，D1受体有助于静息通气水平和运动呼吸过度，在稳态与代谢变化平行。值得注意的是，D1受体的代谢控制是重要的稳态的维持，和D1受体在下丘脑核可能参与这种调制。
New findings•What is the central question of this study?Measurement of ventilation (as well as simultaneous recording of ventilation and pulmonary gas exchange) in exercising mice has not been studied thoroughly. We evaluated ventilation in association with metabolic changes during constant‐load exercise in mice and examined the role of D1receptors in addition to the D2receptors previously studied. This reliable method can be used in gene‐manipulated mice.•What is the main finding and its importance?We showed that the D1receptors participate in resting ventilation and exercise hyperpnoea in parallel with metabolic changes during the steady state in mice. The metabolic control of D1receptors was important for maintenance of the steady state.Previously, we undertook simultaneous recording of ventilation and pulmonary gas exchange in mice and revealed that dopamine D2receptors participate in exercise hyperpnoea via behavioural control of ventilation with unchanged pulmonary gas exchange. Here, we examined the hypothesis that D1receptors also contribute to exercise hyperpnoea using a D1receptor antagonist (SCH 23390; SCH) that crosses the blood–brain barrier, with the same recording technique and protocol as in the previous study. The respiratory responses of mice injected with saline or SCH (50 μg (kg body weight)−1,i.p.) were compared during constant‐load exercise at 6 m min−1. Each mouse was set in an airtight treadmill chamber equipped with a differential pressure transducer and open‐circuit system with a mass spectrometer. At rest, SCH‐injected mice had significantly reduced respiratory frequency, minute ventilation and pulmonary gas exchange compared with saline‐injected mice. Ventilation during hyperoxic gas inhalation and hypercapnic ventilatory responses between groups were similar. Abrupt increases and sequential declines to the steady‐state level were produced by treadmill exercise in both groups of mice. Treatment with SCH lowered the increased levels of respiratory frequency, tidal volume and minute ventilation during the steady state, as well as reducing the O2uptake, CO2output and body temperature throughout treadmill exercise. These data suggest that D1receptors contribute to a resting ventilation level and exercise hyperpnoea during the steady state in parallel with metabolic changes. Notably, the metabolic control of D1receptors was important for maintenance of the steady state, and D1receptors in hypothalamic nuclei could be involved in this modulation.