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首页> 外文期刊>The European Journal of Neuroscience >Disruption of Kir6.2-containing ATP-sensitive potassium channels impairs maintenance of hypoxic gasping in mice.
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Disruption of Kir6.2-containing ATP-sensitive potassium channels impairs maintenance of hypoxic gasping in mice.

机译：含Kir6.2的ATP敏感性钾通道的破坏损害了小鼠低氧性喘息的维持。

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摘要

Hypoxic gasping emerges under severe hypoxia/ischemia in various species, exerting a life-protective role by assuring minimum ventilation even in loss of consciousness. However, the molecular basis of its generation and maintenance is not well understood. Here we found that mice lacking Kir6.2- but not Kir6.1-containing ATP-sensitive potassium (K(ATP)) channels [knockout (KO) mice] exhibited few gaSPS when subjected to abrupt ischemia by decapitation, whereas wild-type mice all exhibited more than 10 gaSPS. Under anesthesia, wild-type mice initially responded to severe hypoxic insult with augmented breathing (tachypnea) accompanied by sighs and subsequent depression of respiratory frequency. Gasping then emerged and persisted stably (persistent gasping); if the hypoxia continued, several gaSPS with distinct patterns appeared (terminal gasping) before cessation of breathing. KO mice showed similar hypoxic responses but both depression and the two types of gasping were of much shorter duration than in wild-type mice. Moreover, in the unanesthetized condition, the onset of terminal gasping in KO mice, which was always earlier than in wild-type mice, was unaltered by decreasing O(2) concentrations within the severe range (4.5-7.0%), whereas onset in wild-type mice became earlier in response to lowered O(2) concentrations. Thus, the mechanism responsible for regulating the hypoxic response in accordance with the severity of the hypoxia was dysfunctional in these KO mice, suggesting that Kir6.2-containing K(ATP) channels are critically involved in the maintenance rather than the generation of hypoxic gasping and depression of respiratory frequency.
机译：在各种物种的严重缺氧/缺血情况下都会出现低氧喘气，即使在失去知觉的情况下，也可通过确保最少的通气来发挥保护生命的作用。然而，对其产生和维持的分子基础尚不十分了解。在这里，我们发现，缺少Kir6.2-但不含Kir6.1的ATP敏感钾（K（ATP））通道的小鼠[敲除（KO）小鼠]，因断头而遭受突然缺血时，其gaSPS很少，而野生型小鼠均表现出超过10 gaSPS。在麻醉下，野生型小鼠最初对严重的低氧损伤有增强的呼吸反应（呼吸急促），伴有叹气和随后的呼吸频率降低。然后出现喘气并稳定持续（持续喘气）。如果继续缺氧，在停止呼吸之前会出现几种具有不同模式的gaSPS（终末喘气）。 KO小鼠表现出相似的低氧反应，但是抑郁症和两种喘气的持续时间都比野生型小鼠短。此外，在未麻醉的情况下，KO小鼠的终末喘气的发生总是早于野生型小鼠，但在严重范围内（4.5-7.0％）降低O（2）的浓度并没有改变。野生型小鼠响应降低的O（2）浓度变得更早。因此，负责根据缺氧的严重程度来调节缺氧反应的机制在这些KO小鼠中是功能失调的，这表明含有Kir6.2的K（ATP）通道关键地参与了维持而不是产生缺氧性喘气和呼吸频率降低。

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