Zhu Guang-fa, Zhang Wei, Zong Hua, Liang Ying
Department of Respiratory Medicine, Beijing Anzhen Hospital, Capital University of Medical Science, Beijing 100029, China.
Chin Med J (Engl). 2006 Sep 5;119(17):1415-20.
Pulmonary surfactant dysfunction may contribute to the development of ventilator induced lung injury (VILI). Tracheal gas insufflation (TGI) is a technique in which fresh gas is introduced into the trachea and augment ventilation by reducing the dead space of ventilatory system, reducing ventilatory pressures and tidal volume (V(T)) while maintaining constant partial arterial CO2 pressure (PaCO(2)). We hypothesised that TGI limited peak inspiratory pressure (PIP) and V(T) and would minimize conventional mechanical ventilation (CMV) induced pulmonary surfactant dysfunction and thereby attenuate VILI in rabbits with acute lung injury (ALI).
ALI was induced by intratracheal administration of lipopolysaccharide in anaesthetized, ventilated healthy adult rabbits randomly assigned to continuous TGI at 0.5 L/min (TGI group) or CMV group (n = 8 for each group), and subsequently ventilated with limited PIP and V(T) to maintain PaCO(2) within 35 to 45 mmHg for 4 hours. Physiological dead space to V(T) ratio (V(D)/V(T)), dynamic respiratory compliance (Cdyn) and partial arterial O(2) pressure (PaO(2)) were monitored. After ventilation, lungs were analysed for total phospholipids (TPL), total proteins (TP), pulmonary surfactant small to large aggregates ratio (SA/LA) in bronchoalveolar lavage fluid (BALF) and for determination of alveolar volume density (V(V)), myeloperoxidase and interleukin (IL)-8.
TGI resulted in significant (P < 0.05 or P < 0.01) decrease in PIP [(22.4 +/- 1.8) cmH2O vs (29.5 +/- 1.1) cmH2O], V(T) [(6.9 +/- 1.3) ml/kg vs (9.8 +/- 1.11) ml/kg], V(D)/V(T) [(32 +/- 5)% vs (46 +/- 2)%], TP [(109 +/- 22) mg/kg vs (187 +/- 25) mg/kg], SA/LA (2.5 +/- 0.4 vs 5.4 +/- 0.7), myeloperoxidase [(6.2 +/- 0.5) U/g tissue vs (12.3 +/- 0.8) U/g tissue] and IL-8 [(987 +/- 106) ng/g tissue vs (24 +/- 3) mN/m] of BALF, and significant (P < 0.05) increase in Cdyn [(0.47 +/- 0.02) ml.cmH2O(-1).kg(-1) vs (0.31 +/- 0.02) ml.cmH2O(-1).kg(-1)], PaO(2) [(175 +/- 24) mmHg vs (135 +/- 26) mmHg], TPL/TP (52 +/- 8 vs 33 +/- 11) and Vv (0.65 +/- 0.05 vs 0.44 +/- 0.07) as compared with CMV.
In this animal model of ALI, TGI decreased ventilatory requirements (PIP, V(T) and V(D)/V(T)), resulted in more favourable alveolar pulmonary surfactant composition and function and less severity of lung injury than CMV. TGI in combination with pressure limited ventilation may be a lung protective strategy for ALI.
肺表面活性物质功能障碍可能导致呼吸机诱导性肺损伤（VILI）的发生。气管气体注入（TGI）是一种将新鲜气体引入气管的技术，通过减少通气系统的死腔、降低通气压力和潮气量（V(T)），同时维持动脉血二氧化碳分压（PaCO(2)）恒定来增加通气。我们假设TGI能限制吸气峰压（PIP）和V(T)，并能使传统机械通气（CMV）诱导的肺表面活性物质功能障碍最小化，从而减轻急性肺损伤（ALI）兔的VILI。
在麻醉、通气的健康成年兔中，通过气管内给予脂多糖诱导ALI，将其随机分为持续TGI（0.5 L/min）组（TGI组）或CMV组（每组n = 8），随后以限制的PIP和V(T)进行通气，维持PaCO(2)在35至45 mmHg之间4小时。监测生理死腔与V(T)的比值（V(D)/V(T)）、动态呼吸顺应性（Cdyn）和动脉血氧分压（PaO(2)）。通气后，分析肺组织中的总磷脂（TPL）、总蛋白（TP）、支气管肺泡灌洗液（BALF）中肺表面活性物质小聚集体与大聚集体的比值（SA/LA），并测定肺泡体积密度（V(V)）、髓过氧化物酶和白细胞介素（IL）-8。
与CMV相比，TGI导致PIP显著降低（P < 0.05或P < 0.01）[（22.4 ± 1.8）cmH2O对（29.5 ± 1.1）cmH2O]、V(T)显著降低[（6.9 ± 1.3）ml/kg对（9.8 ± 1.11）ml/kg]、V(D)/V(T)显著降低[（32 ± 5）%对（46 ± 2）%]、TP显著降低[（109 ± 22）mg/kg对（187 ± 25）mg/kg]、SA/LA显著降低（2.5 ± 0.4对5.4 ± 0.7）、BALF中的髓过氧化物酶显著降低[（6.2 ± 0.5）U/g组织对（12.3 ± 0.8）U/g组织]和IL-8显著降低[（987 ± 106）ng/g组织对（24 ± 3）mN/m]，同时Cdyn显著增加（P < 0.05）[（0.47 ± 0.02）ml.cmH2O(-1).kg(-1)对（0.31 ± 0.02）ml.cmH2O(-1).kg(-1)]、PaO(2)显著增加[（175 ± 24）mmHg对（135 ± 26）mmHg]、TPL/TP显著增加（52 ± 8对33 ± 11）和Vv显著增加（0.65 ± 0.05对0.44 ± 0.07）。
在这个ALI动物模型中，与CMV相比，TGI降低了通气需求（PIP、V(T)和V(D)/V(T)），使肺泡肺表面活性物质的组成和功能更有利，肺损伤的严重程度更低。TGI联合压力限制通气可能是ALI的一种肺保护策略。
