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Contribution of hypercapnia and trigeminal stimulation to cerebrovascular dilation during simulated diving.

机译:模拟潜水期间高碳酸血症和三叉神经刺激对脑血管扩张的贡献。

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摘要

We investigated the relative contribution of humoral (carbon dioxide) and neural (trigeminal stimulation) inputs in the cerebrovasodilatory response to simulated diving in the rat. The cerebral hemodynamic profile of rats was determined using the brain blood flow tracer N-[14C]isopropyl-p-iodoamphetamine. During a simulated dive response, cerebral vascular resistance (CVR) decreased 63.1%, resulting in a 1.5-fold increase in cerebral blood flow (CBF). To investigate the contribution of hypercapnia to the decrease in CVR during simulated diving, we measured CBF during simulated diving in rats with preexisting hypocapnia. To investigate the contribution of trigeminal input, we measured CBF during periods of trigeminal stimulation alone with continued ventilation. Preexisting hypocapnia abolished the cerebrovasodilatory response to simulated diving. Trigeminal stimulation alone did not produce a significant increase in CBF from control values in any brain region, suggesting that trigeminal input does not contribute to the cerebrovascular response to simulated diving in rats. These results suggest that the cerebrovasodilatory response observed during diving in small mammals is driven primarily by progressive hypercapnia associated with asphyxia.
机译:我们调查了在模拟大鼠中脑血管舒张反应中体液(二氧化碳)和神经(三叉神经刺激)输入的相对贡献。使用脑血流示踪剂N- [14C]异丙基-对-碘苯丙胺测定大鼠的脑血流动力学特征。在模拟潜水反应期间,脑血管阻力(CVR)下降63.1%,导致脑血流量(CBF)增长1.5倍。为了调查高碳酸血症对模拟潜水过程中CVR降低的影响,我们在模拟碳酸潜水中已存在低碳酸血症的大鼠中测量了CBF。为了研究三叉神经输入的贡献,我们在持续通气的情况下测量了三叉神经刺激期间的CBF。先前存在的低碳酸血症消除了对模拟潜水的脑血管舒张反应。单靠三叉神经刺激并没有在任何大脑区域的控制值上使CBF显着增加,这表明三叉神经输入对大鼠模拟潜水的脑血管反应没有贡献。这些结果表明,在小型哺乳动物的潜水过程中观察到的脑血管舒张反应主要是由与窒息有关的进行性高碳酸血症引起的。

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