Data "Nasal and tracheobronchial nitric oxide production and its influence on oxygenation in horses undergoing intravenous anaesthesia"

Background: In many species a major part of physiological nitric oxide (NO) production takes place in the nasopharynx. Inhaled NO acts as a pulmonary vasodilator and regulates lung perfusion and endotracheal intubation bypasses the nasopharynx. Objective: To investigate the effect of endotracheal intubation on nasal and tracheal NO concentrations, gas exchange and oxygenation in horses undergoing general anaesthesia. Study design: Prospective, randomized, experimental cross-over study. Methods: Six horses were randomly assigned to “intubated” (INT) and “non-intubated” (nINT) treatment groups. Horses were premedicated with dexmedetomidine (5 µg/kg IV). Anaesthesia was induced with 2.5 mg/kg ketamine and 0.05 mg/kg diazepam IV and was maintained by triple-drip (100 mg/kg/h guaifenesin, 4 mg/kg/h ketamine, 7 µg/kg/h dexmedetomidine). The horses were spontaneously breathing room air. Heart rate, cardiac output, arterial blood pressure, pulmonary arterial blood pressures and respiratory rate were recorded during a 100-minute anaesthesia period. Arterial, venous and mixed venous blood samples were taken every ten minutes and analysed for partial pressure of oxygen (PO2) and carbon dioxide (PCO2), oxygen saturation and haemoglobin content. Standard oxygenation indices were calculated. Nasal and tracheal NO concentration was determined by chemiluminescence. Results: Cardiovascular variables, respiratory rate, PO2, PCO2, oxygen saturation, haemoglobin content, CaO2, O2ER, P(a-ET)CO2 and Qs/Qt did not differ significantly between the two treatment groups. The P(A-a)O2 was significantly higher in INT (6.1 ± 0.3 kPa) compared to nINT (4.9 ± 0.1 kPa) (p = 0.045), respectively. The nasal (8.0 ± 6.2 ppb) and tracheal (13.0 ± 6.3 ppb) NO concentration differed significantly in INT (p = 0.036), but not in nINT (nasal: 16.9 ± 9.0 ppb; tracheal: 18.5 ± 9.5 ppb) (p = 0.215). Conclusion: Endotracheal intubation reduces the nasal and tracheal NO concentration. The influence on pulmonary gas exchange and oxygenation is neglectable in horses breathing room air.

背景：在众多物种中，生理性一氧化氮（nitric oxide, NO）的主要生成部位为鼻咽部。吸入性NO可作为肺血管扩张剂调节肺灌注，而气管插管会绕过鼻咽部。
目的：探究气管插管对接受全身麻醉的马匹的鼻、气管一氧化氮浓度、气体交换及氧合的影响。
研究设计：前瞻性随机交叉实验研究。
方法：将6匹马匹随机分为气管插管组（intubated, INT）与非气管插管组（non-intubated, nINT）。马匹预先经静脉注射右美托咪定（dexmedetomidine, 5 µg/kg）进行镇静预处理。麻醉诱导采用静脉注射2.5 mg/kg氯胺酮（ketamine）与0.05 mg/kg地西泮（diazepam），并通过三联输注维持麻醉：100 mg/kg/h愈创甘油醚（guaifenesin）、4 mg/kg/h氯胺酮、7 µg/kg/h右美托咪定。马匹自主呼吸室内空气。在100分钟的麻醉周期内，记录心率、心输出量、动脉血压、肺动脉压及呼吸频率。每10分钟采集动脉血、静脉血及混合静脉血样本，分析氧分压（partial pressure of oxygen, PO2）、二氧化碳分压（partial pressure of carbon dioxide, PCO2）、血氧饱和度及血红蛋白含量，计算标准氧合指数。采用化学发光法（chemiluminescence）测定鼻及气管内一氧化氮浓度。
结果：两组间心血管变量、呼吸频率、PO2、PCO2、血氧饱和度、血红蛋白含量、动脉血氧含量（CaO2）、氧提取率（O2ER）、动脉-呼气末二氧化碳分压差（P(a-ET)CO2）及肺内分流率（Qs/Qt）均无显著差异。气管插管组的肺泡动脉氧分压差（P(A-a)O2）为6.1 ± 0.3 kPa，显著高于非气管插管组的4.9 ± 0.1 kPa（p = 0.045）。气管插管组的鼻一氧化氮浓度（8.0 ± 6.2 ppb）与气管内一氧化氮浓度（13.0 ± 6.3 ppb）存在显著差异（p = 0.036），而非气管插管组的鼻一氧化氮浓度（16.9 ± 9.0 ppb）与气管内一氧化氮浓度（18.5 ± 9.5 ppb）则无显著差异（p = 0.215）。
结论：气管插管可降低鼻及气管内一氧化氮浓度。对于呼吸室内空气的马匹而言，气管插管对肺气体交换与氧合的影响可忽略不计。