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首页> 外文期刊>American Journal of Physiology >Opiate slowing of feline respiratory rhythm and effects on putative medullary phase-regulating neurons.
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Opiate slowing of feline respiratory rhythm and effects on putative medullary phase-regulating neurons.

机译：阿片类药物会降低猫的呼吸节奏，并影响假定的髓样相调节神经元。

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摘要

Opiates have effects on respiratory neurons that depress tidal volume and air exchange, reduce chest wall compliance, and slow rhythm. The most dose-sensitive opioid effect is slowing of the respiratory rhythm through mechanisms that have not been thoroughly investigated. An in vivo dose-response analysis was performed on medullary respiratory neurons of adult cats to investigate two untested hypotheses related to mechanisms of opioid-mediated rhythm slowing: 1) Opiates suppress intrinsic conductances that limit discharge duration in medullary inspiratory and expiratory neurons, and 2) opiates delay the onset and lengthen the duration of discharges postsynaptically in phase-regulating postinspiratory and late-inspiratory neurons. In anesthetized and unanesthetized decerebrate cats, a threshold dose (3 microg/kg) of the mu-opioid receptor agonist fentanyl slowed respiratory rhythm by prolonging discharges of inspiratory and expiratory bulbospinal neurons. Additional doses (2-4 microg/kg) of fentanyl also lengthened the interburst silent periods in each type of neuron and delayed the rate of membrane depolarization to firing threshold without altering synaptic drive potential amplitude, input resistance, peak action potential frequency, action potential shape, or afterhyperpolarization. Fentanyl also prolonged discharges of postinspiratory and late-inspiratory neurons in doses that slowed the rhythm of inspiratory and expiratory neurons without altering peak membrane depolarization and hyperpolarization, input resistance, or action potential properties. The temporal changes evoked in the tested neurons can explain the slowing of network respiratory rhythm, but the lack of significant, direct opioid-mediated membrane effects suggests that actions emanating from other types of upstream bulbar respiratory neurons account for rhythm slowing.
机译：阿片类物质对呼吸神经元有影响，可抑制潮气量和空气交换，降低胸壁顺应性并减慢心律。对剂量最敏感的阿片类药物作用是通过尚未彻底研究的机制减慢呼吸节律。对成年猫的髓样呼吸神经元进行了体内剂量反应分析，以研究两个与阿片类药物介导的节律减慢机制有关的未经检验的假说：1）阿片类药物抑制内在电导，限制了髓样吸气和呼气神经元的放电持续时间，以及2鸦片制剂会在呼吸后和吸气后神经元的相位调节中延迟突触发作并延长突触后放电的持续时间。在麻醉和未麻醉的去脑猫中，μ阿片类受体激动剂芬太尼的阈值剂量（3 microg / kg）通过延长吸气和呼气性脊髓神经元的放电而减慢了呼吸节律。额外剂量（2-4微克/千克）的芬太尼还延长了每种神经元中的突触沉默期，并延迟了膜去极化的速率至激发阈值，而不会改变突触驱动电位幅度，输入阻力，峰值动作电位频率，动作电位形状或超极化后。芬太尼还可以延长吸气后和吸气后神经元的放电速度，减慢吸气和呼气神经元的节律，而不会改变峰值膜去极化和超极化，输入阻力或动作电位特性。受测神经元引起的时间变化可以解释网络呼吸节律的减慢，但是缺乏明显的，直接的阿片样物质介导的膜效应表明，其他类型的上游延髓性呼吸神经元所产生的作用导致节律减慢。

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