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首页> 外文期刊>EBioMedicine >Chronic intermittent hypoxia disrupts cardiorespiratory homeostasis and gut microbiota composition in adult male guinea-pigs
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Chronic intermittent hypoxia disrupts cardiorespiratory homeostasis and gut microbiota composition in adult male guinea-pigs

机译：慢性间歇性缺氧破坏成年雄性豚鼠的心肺稳态和肠道菌群组成

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Background Carotid body (peripheral oxygen sensor) sensitisation is pivotal in the development of chronic intermittent hypoxia (CIH)-induced hypertension. We sought to determine if exposure to CIH, modelling human sleep apnoea, adversely affects cardiorespiratory control in guinea-pigs, a species with hypoxia-insensitive carotid bodies. We reasoned that CIH-induced disruption of gut microbiota would evoke cardiorespiratory morbidity. Methods Adult male guinea-pigs were exposed to CIH (6.5% Osub2/sub at nadir, 6?cycles.hoursup?1/sup) for 8?h.daysup?1/sup for 12 consecutive days. Findings CIH-exposed animals established reduced faecal microbiota species richness, with increased relative abundance of Bacteroidetes and reduced relative abundance of Firmicutes bacteria. Urinary corticosterone and noradrenaline levels were unchanged in CIH-exposed animals, but brainstem noradrenaline concentrations were lower compared with sham. Baseline ventilation was equivalent in CIH-exposed and sham animals; however, respiratory timing variability, sigh frequency and ventilation during hypoxic breathing were all lower in CIH-exposed animals. Baseline arterial blood pressure was unaffected by exposure to CIH, but β-adrenoceptor-dependent tachycardia and blunted bradycardia during phenylephrine-induced pressor responses was evident compared with sham controls. Interpretation Increased carotid body chemo-afferent signalling appears obligatory for the development of CIH-induced hypertension and elevated chemoreflex control of breathing commonly reported in mammals, with hypoxia-sensitive carotid bodies. However, we reveal that exposure to modest CIH alters gut microbiota richness and composition, brainstem neurochemistry, and autonomic control of heart rate, independent of carotid body sensitisation, suggesting modulation of breathing and autonomic homeostasis via the microbiota-gut-brainstem axis. The findings have relevance to human sleep-disordered breathing. Funding The Department of Physiology, and APC Microbiome Ireland, UCC.
机译：背景技术颈动脉体（外周血氧传感器）敏化在慢性间歇性缺氧（CIH）诱发的高血压的发展中至关重要。我们试图确定暴露于模拟人类睡眠呼吸暂停的CIH是否会对豚鼠（一种对缺氧不敏感的颈动脉体的物种）的心肺控制产生不利影响。我们认为，CIH引起的肠道菌群破坏会引起心肺疾病。方法成年雄性豚鼠暴露于CIH（最低点6.5％O 2 ，6？cycle.hour ？1 ）暴露8？h.day ？ 1 ，连续12天。研究发现，暴露于CIH的动物减少了粪便微生物群的丰富度，增加了拟杆菌的相对丰度，并减少了Firmicutes细菌的相对丰度。在暴露于CIH的动物中，尿皮质激素和去甲肾上腺素水平没有变化，但是脑干去甲肾上腺素的浓度低于假手术。暴露于CIH和假动物中的基线通气是等效的;但是，暴露于CIH的动物的呼吸时间变化，叹息频率和低氧呼吸期间的通气均较低。基线动脉血压不受暴露于CIH的影响，但与假对照组相比，苯肾上腺素诱导的升压反应期间β-肾上腺素受体依赖性心动过速和钝性心动过缓明显。解释对于在缺氧敏感的颈动脉体中常见的哺乳动物，CIH诱发的高血压的发展和对呼吸的化学反射控制的升高似乎是增加颈动脉体化学活性信号传递所必需的。但是，我们发现，暴露于适度的CIH会改变肠道菌群的丰富度和组成，脑干神经化学以及对心律的自主控制，而与颈动脉机体的敏感性无关，这表明通过微生物-肠-脑干轴调节呼吸和自主稳态。这些发现与人类睡眠呼吸紊乱有关。资金UCC生理学系和爱尔兰APC微生物组。

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