Chronic moderate hypercapnia suppresses ventilatory responses to acute CO<sub>2</sub> challenges.
Chronic moderate hypercapnia suppresses ventilatory responses to acute CO<sub>2</sub> challenges.
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慢性中度高碳酸血症抑制对急性 CO 的通气反应
DOI：
10.1152/japplphysiol.00407.2022
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发表时间：
2022
期刊：
影响因子：
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通讯作者：
Forster,HubertV
中科院分区：
文献类型：
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作者：
Buchholz,KirstynJ;Neumueller,SuzanneE;Burgraff,NicholasJ;Hodges,MatthewR;Pan,Lawrence;Forster,HubertV
慢性高碳酸血症（CH）是慢性肺部疾病的一个标志，CH增加了急性慢性加重的风险，导致更严重的低氧血症/高碳酸血症和不良的健康结果。然而，高碳酸血症本身（持续时间和严重程度）在决定个体耐受进一步高碳酸血症恶化的能力中的作用尚不清楚。我们在此的主要目的是验证轻度至中度CH（动脉PCO2 ~ 50-70 mmHg）增加对严重急性co2挑战的病理生理反应的易感性的假设。研究人员对三组成年母山羊进行了为期14天的室内空气暴露（GR 1，对照组）或6%吸入二氧化碳（GR 2，轻度甲烷），或7天6%吸入二氧化碳，然后7天8%吸入二氧化碳（GR 3，中度甲烷）的研究。与之前的报道一致，生理参数ingr1 （RA对照）没有变化，但轻度CH （GR 2）增加了稳态通气，并短暂抑制了CO2/[H+]化学敏感性。进一步将inco2从6%增加到8% (GR 3)，可短暂增加通气和动脉[H+]。与轻度CH相似，中度CH使通气量增加到比预期更高的水平。然而，与轻度CH相比，急性通气化学敏感性在中度CH持续期间受到抑制，动脉-混合过期co2梯度变为阴性。这些数据表明，中度CH限制了对急性严重加重的生理反应，并提供了在中重度高碳酸血症期间肺外系统（即胃二氧化碳消除）的补充的证据。健康成年母山羊的中度慢性高碳酸血症（CH; ~ 70 mmHg）与轻度CH （~ 55 mmHg）相比，引起了相似的稳态生理适应。然而，与轻度CH不同，中度CH慢性抑制急性CO2/[H+]化学敏感性，逆转动脉到混合过期CO2梯度。这些发现表明，适度的CH抑制通气控制的重要机制，并招募额外的生理系统（即胃二氧化碳释放）来帮助缓冲过量的二氧化碳。
Chronic hypercapnia (CH) is a hallmark of chronic lung disease, and CH increases the risk for acute-on-chronic exacerbations leading to greater hypoxemia/hypercapnia and poor health outcomes. However, the role of hypercapnia per se (duration and severity) in determining an individual’s ability to tolerate further hypercapnic exacerbations is unknown. Our primary objective herein was to test the hypothesis that mild-to-moderate CH (arterial PCO2 ∼50–70 mmHg) increases susceptibility to pathophysiological responses to severe acute CO2challenges. Three groups (GR) of adult female goats were studied during 14 days of exposure to room air (GR 1; control) or 6% inspired CO2(GR 2; mild CH), or 7 days of 6% inspired CO2followed by 7 days of 8% inspired CO2(GR 3; moderate CH). Consistent with previous reports, there were no changes in physiological parameters inGR 1(RA control), but mild CH (GR 2) increased steady-state ventilation and transiently suppressed CO2/[H+] chemosensitivity. Further increasing InCO2from 6% to 8% (GR 3) transiently increased ventilation and arterial [H+]. Similar to mild CH, moderate CH increased ventilation to levels greater than predicted. However, in contrast to mild CH, acute ventilatory chemosensitivity was suppressed throughout the duration of moderate CH, and the arterial − mixed expired CO2gradient became negative. These data suggest that moderate CH limits physiological responses to acute severe exacerbations and provide evidence of recruitment of extrapulmonary systems (i.e., gastric CO2elimination) during times of moderate-severe hypercapnia.NEW & NOTEWORTHYModerate levels of chronic hypercapnia (CH; ∼70 mmHg) in healthy adult female goats elicited similar steady-state physiological adaptations compared with mild CH (∼55 mmHg). However, unlike mild CH, moderate CH chronically suppressed acute CO2/[H+] chemosensitivity and reversed the arterial to mixed expired CO2gradient. These findings suggest that moderate CH suppresses vital mechanisms of ventilatory control and recruits additional physiological systems (i.e., gastric CO2release) to help buffer excess CO2.