Influence of levels of carbon dioxide and oxygen upon gasping in perfused rat preparation

Walter M St.-John , Ilya A Rybak
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引用次数: 15

Abstract

In vivo, the augmenting pattern of integrated phrenic nerve discharge of eupnea is altered to the decrementing pattern of gasping in severe hypoxia or ischaemia. Identical alterations in phrenic discharge are found in perfused in situ preparations of the juvenile rat. In this preparation, gasping was produced by equilibration of the perfusate with various levels of carbon dioxide and oxygen. The duration of the phrenic burst, the interval between bursts and the burst amplitude were not significantly different following equilibration with 21–6%O2 at 5% CO2 or with 0–9% CO2 at 6% O2, with the exception that the burst amplitude was significantly greater in hypercapnic-hypoxia (9% CO2 at 6% O2). It is proposed that hypoxia-induced gasping results from the release of an endogenous pacemaker activity of rostral medullary neurons. This release is caused by cellular mechanisms that change the balance between membrane ionic currents. Moreover, these cellular mechanisms may be explicitly induced by alterations in the ionic and metabolic homeostasis.

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大鼠灌注制剂中二氧化碳和氧气水平对呼吸的影响
在体内,呼吸暂停时膈神经整体放电的增强模式在严重缺氧或缺血时改变为喘息的减弱模式。在幼年大鼠的原位灌注制剂中发现了相同的膈放电改变。在这种制备中,通过灌注液与不同水平的二氧化碳和氧气的平衡产生喘息。在5% CO2浓度为21 - 6%或6% CO2浓度为0-9%的平衡状态下,膈肌爆发的持续时间、爆发间隔和爆发幅度没有显著差异,但在高碳酸血症-低氧状态下(6% CO2浓度为9%),膈肌爆发幅度明显更大。据推测,缺氧引起的喘息是由于吻侧髓神经元内源性起搏器活动的释放。这种释放是由改变膜离子电流平衡的细胞机制引起的。此外,这些细胞机制可能是由离子和代谢稳态的改变明确诱导的。
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