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首页> 外文期刊>American Journal of Physiology >Adenosine depletion alters postictal hypoxic cerebral vasodilation in the newborn pig.
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Adenosine depletion alters postictal hypoxic cerebral vasodilation in the newborn pig.

机译：腺苷耗竭会改变新生猪的缺氧后脑血管舒张。

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Altered postictal cerebral blood flow dilatory responses may contribute to brain injury following neonatal seizures. We developed an initial series of experiments to characterize the effects of seizure activity on cerebral vascular dilatory responses during the immediate postictal period. Significant attenuation of postictal hypoxic cerebral vasodilation was noted. We hypothesize that this diminished cerebral dilator response to hypoxia involves depletion of adenosine (Ado) activity resulting from seizure ictus. Additional experiments were designed to evaluate whether the altered postictal responses were related to a depletion of Ado stores or a decreased response to Ado in the postictal state. Farm-bred piglets were equipped with closed cranial windows. Responses to hypercapnia (10% CO2), hypoxia (fractional inspired O2 = 0.10), and topical sodium nitroprusside (10(-6) M) were compared before and after bicuculline-induced seizures (1 mg/kg). Hypoxia-induced cerebral vasodilation was significantly attenuated in the first 90 min postictal (control: 56.5 +/- 6%, 10 min postictal: 6.3 +/- 2%, 60 min postictal: 21.7 +/- 6%, and 90 min postictal: 21.6 +/- 5%; P < 0.01), whereas the dilator responses to hypercapnia and topical sodium nitroprusside remained intact. In a separate group of piglets, both a dilating (10(-5) M) and a nondilating concentration of Ado (10(-11) M) were topically administered postictally to measure their effects on pial vessel dilatory response to hypoxia. Dilation to topical Ado (10(-5) M) was not altered postictally compared with control. Ado (10(-11) M) restored hypoxia-induced vasodilation to preseizure control values in the immediate postictal period (control: 51.0 +/- 8%, postictal: 46.7 +/- 8%, P > 0.05). Postictal administration of Ado will restore hypoxia-induced cerebral vasodilation in piglets even when a nondilating concentration is employed. This suggests that depletion of Ado with seizure activity is a mechanism for the loss of postictal cerebral vasodilation to hypoxia, and the role of Ado in hypoxic cerebral vasodilation is permissive.
机译：阵发性脑血管血流扩张反应的改变可能会导致新生儿癫痫发作后的脑损伤。我们开发了一系列初始实验，以表征发作后即刻癫痫发作活动对脑血管扩张反应的影响。注意到显着减弱了术后缺氧性脑血管舒张。我们假设这种大脑扩张器对缺氧的反应减弱涉及癫痫发作导致的腺苷（Ado）活性减少。设计了其他实验以评估改变的姿势反应是否与Ado存储库的耗尽或姿势状态下对Ado的反应减少有关。农场饲养的仔猪配有封闭的颅窗。在比库卡林诱发癫痫发作（1 mg / kg）之前和之后，比较了对高碳酸血症（10％CO2），低氧（分数激发的O2 = 0.10）和局部硝普钠（10（-6）M）的反应。缺氧引起的脑血管扩张在发作后的前90分钟显着减弱（对照：56.5 +/- 6％，发作后10分钟：6.3 +/- 2％，发作后60分钟：21.7 +/- 6％和发作后90分钟：21.6 +/- 5％; P <0.01），而扩张剂对高碳酸血症和局部硝普钠的反应仍然完整。在单独的一组仔猪中，局部施用局部扩张剂量的（10（-5）M）和非扩张浓度的Ado（10（-11）M），以测量它们对低氧时脊髓血管扩张反应的影响。与对照组相比，局部Ado扩张（10（-5）M）的姿势没有改变。 Ado（10（-11）M）在发作后即刻恢复低氧诱导的血管舒张至发作前的控制值（对照：51.0 +/- 8％，发作后：46.7 +/- 8％，P> 0.05）。即使使用非扩张浓度，Ado的术后给药也可恢复缺氧引起的仔猪脑血管舒张。这表明，具有癫痫发作活动的Ado耗竭是使缺氧后的脑血管舒张丧失的一种机制，并且Ado在低氧性脑血管舒张中的作用是允许的。

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