Spinelli Elena, Pesenti Antonio, Lopez Gianluca, Damia Anna, Damarco Francesco, Garbelli Erica, Dal Santo Gaia, Caccioppola Alessio, Giudici Giorgio, Figgiaconi Virginia, Biancolilli Osvaldo, Battistin Michele, Lonati Caterina, Vaira Valentina, Rosso Lorenzo, Ferrero Stefano, Gatti Stefano, Mauri Tommaso
Department of Anesthesia, Critical Care and Emergency, Fondazione Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy.
Department of Pathophysiology and Transplantation, University of Milan, Milan, Italy.
Front Med (Lausanne). 2022 May 20;9:901809. doi: 10.3389/fmed.2022.901809. eCollection 2022.
Unilateral ligation of the pulmonary artery (UPAL) induces bilateral lung injury in pigs undergoing controlled mechanical ventilation. Possible mechanisms include redistribution of ventilation toward the non-ligated lung and hypoperfusion of the ligated lung. The addition of 5% CO to the inspiratory gas (FiCO) prevents the injury, but it is not clear whether lung protection is a direct effect of CO inhalation or it is mediated by plasmatic hypercapnia. This study aims to compare the effects and mechanisms of FiCO . hypercapnia induced by low tidal volume ventilation or instrumental dead space.
Healthy pigs underwent left UPAL and were allocated for 48 h to the following: Volume-controlled ventilation (VCV) with V 10 ml/kg (injury, = 6); VCV plus 5% FiCO (FiCO, = 7); VCV with V 6 ml/kg (low V, = 6); VCV plus additional circuit dead space (instrumental V, = 6). Histological score, regional compliance, wet-to-dry ratio, and inflammatory infiltrate were assessed to evaluate lung injury at the end of the study. To investigate the mechanisms of protection, we quantified the redistribution of ventilation to the non-ligated lung, as the ratio between the percentage of tidal volume to the right and to the left lung (V), and the hypoperfusion of the ligated lung as the percentage of blood flow reaching the left lung (Perfusion).
In the left ligated lung, injury was prevented only in the FiCO group, as indicated by lower histological score, higher regional compliance, lower wet-to-dry ratio and lower density of inflammatory cells compared to other groups. For the right lung, the histological score was lower both in the FiCO and in the low V groups, but the other measures of injury showed lower intensity only in the FiCO group. V was lower and Perfusion was higher in the FiCO group compared to other groups.
In a model of UPAL, inhaled CO but not hypercapnia grants bilateral lung protection. Mechanisms of protection include reduced overdistension of the non-ligated and increased perfusion of the ligated lung.
在接受控制性机械通气的猪中,单侧肺动脉结扎(UPAL)可导致双侧肺损伤。可能的机制包括通气向未结扎肺的重新分布以及结扎肺的灌注不足。在吸入气体中添加5%的一氧化碳(FiCO)可预防这种损伤,但尚不清楚肺保护是一氧化碳吸入的直接作用还是由血浆高碳酸血症介导。本研究旨在比较FiCO、低潮气量通气或器械死腔引起的高碳酸血症的效果和机制。
健康猪接受左UPAL手术,并在48小时内分为以下几组:潮气量为10 ml/kg的容量控制通气(VCV)(损伤组,n = 6);VCV加5% FiCO(FiCO组,n = 7);潮气量为6 ml/kg的VCV(低V组,n = 6);VCV加额外的回路死腔(器械V组,n = 6)。在研究结束时,评估组织学评分、区域顺应性、湿干比和炎症浸润以评估肺损伤。为了研究保护机制,我们量化了通气向未结扎肺的重新分布,即右肺与左肺潮气量百分比的比值(V),以及结扎肺的灌注不足,即到达左肺的血流百分比(灌注)。
在左结扎肺中,仅FiCO组的损伤得到预防,与其他组相比,其组织学评分更低、区域顺应性更高、湿干比更低且炎症细胞密度更低。对于右肺,FiCO组和低V组的组织学评分均较低,但其他损伤指标仅在FiCO组显示强度较低。与其他组相比,FiCO组的V更低且灌注更高。
在UPAL模型中,吸入一氧化碳而非高碳酸血症可提供双侧肺保护。保护机制包括减少未结扎肺的过度膨胀和增加结扎肺的灌注。