Ventilatory response to intravenous methionine enkephalin in awake dogs.
Ventilatory response to intravenous methionine enkephalin in awake dogs.
复制标题
清醒狗对静脉注射蛋氨酸脑啡肽的通气反应。
DOI：
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发表时间：
1985
期刊：
影响因子：
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通讯作者：
T. Giles
中科院分区：
文献类型：
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作者：
M. J. Evanich;G. Sander;J. Rice;T. Giles
在有意识、无微丝虫的成年杂种狗中，静脉注射蛋氨酸脑啡肽（Met5-ENK）可使吸气分气量（VI）和心率（HR）短暂升高。在6 - 18微克/千克的剂量范围内，随着Met5-ENK剂量的增加，VI和HR逐渐增加，然后在剂量达到36微克/千克时趋于稳定。注射后30 - 45秒内，VI和HR发生最大变化，两项指标在约2分钟内恢复到控制水平。在五分之四的狗中，平均吸气流量（潮气量/吸气时间），因此，潮气量，解释了脑啡肽介导的通气增加。其中一只狗在服用Met5-ENK后，呼吸频率而不是潮气量增加。呼吸频率的变化是由于呼吸周期“有效计时”的增加，后者被定义为吸气时间与总呼吸时间之比。静脉注射Met5-ENK后，尽管VI和HR有显著变化，但末潮氧和二氧化碳水平与对照组没有显著差异。甲基溴纳曲酮是一种不穿过血脑屏障的季阿片拮抗剂，预处理后可消除脑啡肽诱导的所有VI和HR变化，从而提示全身性脑啡肽通过血脑屏障外的阿片受体调节通气。这些受体的激活会增加心血管和呼吸活动，正如人们在压力条件下所期望的那样。这些数据进一步支持外周脑啡肽作为兴奋性应激激素的潜在作用。
In conscious, microfilaria-free, adult mongrel dogs, i.v. bolus administration of methionine enkephalin (Met5-ENK) produced a transient elevation of both inspiratory minute ventilation (VI) and heart rate (HR). Both VI and HR increased progressively with increasing doses of Met5-ENK over the range of 6 to 18 micrograms/kg, thereafter plateauing at doses up to 36 micrograms/kg. Maximum changes in VI and HR occurred within 30 to 45 sec after injection, both variables returning to control levels in approximately 2 min. In four out of five dogs, mean inspiratory flow (tidal volume/inspiratory time), and consequently, tidal volume, accounted for this enkephalin-mediated increase in ventilation. In one of the dogs, respiratory rate, rather than tidal volume, increased after Met5-ENK. This change in respiratory rate was due to an increase in "effective timing" of the respiratory cycle, the latter defined as the ratio of inspiratory time to total respiratory time. Despite significant changes in VI and HR, neither end tidal oxygen nor carbon dioxide levels were significantly different from control after i.v. injections of Met5-ENK. Pretreatment with naltrexone methylbromide, a quaternary opiate antagonist that does not cross the blood-brain barrier, abolished all enkephalin-induced changes in VI and HR, thus suggesting that systemic enkephalins modulate ventilation via opiate receptors outside the blood-brain barrier. Activation of these receptors produce an increase in both cardiovascular and respiratory activity, as one might expect during stress conditions. These data further support a potential role for peripheral enkephalins as excitatory stress hormones.