The cardiovascular system of vertebrates, including humans, is well known to respond to hyperoxia by vasoconstriction, bradycardia and decreased contractility of the left heart ventricle. We hypothesized that all of these responses are components of the baroreflex that regulates blood pressure and circulation in hyperoxia. To test this hypothesis, we carried out experiments on awake rats in which the dynamics of arterial blood pressure, organ blood flow (brain, kidney, lower limbs) and ECG was tracked in response to oxygen breathing at 1, 3 and 5 ATA. The afferent and efferent baroreflex pathways were studied using denervation of the carotid baroreceptors and transection of the aortic depressor nerves and vagus nerve. The baroreflex effectiveness was assessed using phenylephrine injections or spontaneous changes in blood pressure. To activate the GABAergic system, nipecotic acid was injected into the lateral ventricle of the brain. Our studies demonstrated the presence of all the baroreflex components in hyperoxia which were triggered by a sharp rise in blood pressure due to systemic vasoconstriction. Hyperoxic vasoconstriction, in turn, arose due to endothelium-derived nitric oxide (NO) which binds to superoxide anions followed by a loss of the vasodilator component of vascular tone. Aortic and carotid sinus baroreceptors with ascending nerve fibers were identified as an afferent component of the hyperoxic baroreflex. Bradycardia and a decrease in cardiac output, resulting from baroreflex activation by hyperoxia, are actualized via efferent sympathetic and parasympathetic pathways. At 1 and 3 ATA the baroreflex effectiveness increased compared to atmospheric air breathing, but extreme hyperoxia (5 ATA) suppressed the baroreflex mechanism. Activation of the GABAergic system in the cerebral cortex by nipecotic acid prevented the loss of the hyperoxic baroreflex. In hyperoxia, the baroreflex mechanism realizes adaptive responses of the cardiovascular system aimed at restraining the delivery of excess oxygen to an organism and mitigates activation of the sympathetic nervous system.

中文翻译：

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极端高氧条件下心血管系统压力反射调节的适应性机制

众所周知，包括人类在内的脊椎动物的心血管系统通过血管收缩、心动过缓和左心室收缩力降低对高氧作出反应。我们假设所有这些反应都是在高氧条件下调节血压和循环的压力反射的组成部分。为了验证这一假设，我们对清醒的大鼠进行了实验，其中跟踪动脉血压、器官血流（大脑、肾脏、下肢）和 ECG 的动态，以响应 1、3 和 5 ATA 的氧气呼吸。使用颈动脉压力感受器的去神经支配和主动脉抑制神经和迷走神经的横断来研究传入和传出压力反射通路。使用去氧肾上腺素注射液或血压的自发变化来评估压力反射的有效性。为了激活 GABAergic 系统，将尼泊替克酸注射到大脑的侧脑室中。我们的研究表明，由于全身血管收缩导致血压急剧上升，高氧中存在所有压力反射成分。反过来，高氧血管收缩是由于内皮衍生的一氧化氮 (NO) 与超氧阴离子结合，随后血管张力的血管舒张成分丧失所致。具有上行神经纤维的主动脉和颈动脉窦压力感受器被确定为高氧压力反射的传入成分。由高氧引起的压力反射激活引起的心动过缓和心输出量减少是通过传出交感神经和副交感神经通路实现的。在 1 和 3 ATA 时，与大气空气呼吸相比，压力反射效率增加，但极度高氧（5 ATA）抑制了压力反射机制。烟油酸对大脑皮层中 GABA 能系统的激活防止了高氧压力反射的丧失。在高氧条件下，压力反射机制实现了心血管系统的适应性反应，旨在抑制向生物体输送过量氧气并减轻交感神经系统的激活。