Department of Molecular Pharmacology & Physiology, Hyperbaric Biomedical Research Laboratory, University of South Florida, Morsani College of Medicine, Tampa, FL 33612, USA.
J Appl Physiol (1985). 2013 Apr;114(8):1009-20. doi: 10.1152/japplphysiol.01326.2012. Epub 2013 Feb 21.
Hyperbaric oxygen (HBO(2)) stimulates presumptive central CO2-chemoreceptor neurons, increases minute ventilation (V(min)), decreases heart rate (HR) and, if breathed sufficiently long, produces central nervous system oxygen toxicity (CNS-OT; i.e., seizures). The risk of seizures when breathing HBO(2) is variable between individuals and its onset is difficult to predict. We have tested the hypothesis that a predictable pattern of cardiorespiration precedes an impending seizure when breathing HBO2. To test this hypothesis, 27 adult male Sprague-Dawley rats were implanted with radiotelemetry transmitters to assess diaphragmatic/abdominal electromyogram, electrocardiogram, and electroencephalogram. Seven days after surgery, each rat was placed in a sealed, continuously ventilated animal chamber inside a hyperbaric chamber. Both chambers were pressurized in parallel using poikilocapnic 100% O(2) (animal chamber) and air (hyperbaric chamber) to 4, 5, or 6 atmospheres absolute (ATA). Breathing 1 ATA O(2) initially decreased V(min) and HR (Phase 1 of the compound hyperoxic ventilatory response). With continued exposure to normobaric hyperoxia, however, V(min) began increasing toward the end of exposure in one-third of the animals tested. Breathing HBO2 induced an early transient increase in V(min) (Phase 2) and HR during the chamber pressurization, followed by a second significant increase of V(min) ≤8 min prior to seizure (Phase 3). HR, which subsequently decreased during sustained hyperoxia, showed no additional changes prior to seizure. We conclude that hyperoxic hyperpnea (Phase 3 of the compound hyperoxic ventilatory response) is a predictor of an impending seizure while breathing poikilocapnic HBO(2) at rest in unanesthetized rats.
高压氧（HBO(2)）刺激假定的中枢 CO2 感受器神经元，增加分钟通气量（V(min)），降低心率（HR），并且如果呼吸足够长的时间，会导致中枢神经系统氧中毒（CNS-OT；即癫痫发作）。在呼吸 HBO(2)时发生癫痫发作的风险在个体之间是不同的，其发作很难预测。我们已经测试了一个假设，即在呼吸 HBO2 时，一种可预测的心肺呼吸模式先于即将发生的癫痫发作。为了验证这一假设，我们对 27 只成年雄性 Sprague-Dawley 大鼠进行了无线电遥测发射器植入手术，以评估膈肌/腹部肌电图、心电图和脑电图。手术后 7 天，每只大鼠都被放置在一个密封的、连续通风的动物室内，该动物室位于高压室内。两个室都通过使用变惰性 100% O(2)（动物室）和空气（高压室）以 4、5 或 6 个大气压（ATA）并行加压。最初，呼吸 1 ATA O(2)会降低 V(min)和 HR（复合高氧通气反应的第一阶段）。然而，随着持续暴露于常压高氧，在三分之一的测试动物中，V(min)在暴露结束时开始增加。呼吸 HBO2 在加压期间会引起 V(min)（第二阶段）和 HR 的早期短暂增加，随后在癫痫发作前 8 分钟内会引起第二次显著的 V(min)增加（第三阶段）。随后在持续高氧期间降低的 HR 在癫痫发作前没有显示出其他变化。我们得出结论，高氧性过度通气（复合高氧通气反应的第三阶段）是在未麻醉大鼠休息时呼吸变惰性 HBO(2)时即将发生癫痫发作的预测指标。
