Laboratório de Investigação Pulmonar, Instituto de Biofísica Carlos Chagas Filho, CCS, Universidade Federal do Rio de Janeiro, Ilha do Fundão, Rio de Janeiro 21941-902, Brazil.
Intensive Care Med. 2012 Mar;38(3):499-508. doi: 10.1007/s00134-011-2451-6. Epub 2012 Jan 11.
We hypothesized that: (1) intraabdominal hypertension increases pulmonary inflammatory and fibrogenic responses in acute lung injury (ALI); (2) in the presence of intraabdominal hypertension, higher tidal volume reduces lung damage in extrapulmonary ALI, but not in pulmonary ALI.
Wistar rats were randomly allocated to receive Escherichia coli lipopolysaccharide intratracheally (pulmonary ALI) or intraperitoneally (extrapulmonary ALI). After 24 h, animals were randomized into subgroups without or with intraabdominal hypertension (15 mmHg) and ventilated with positive end expiratory pressure = 5 cmH(2)O and tidal volume of 6 or 10 ml/kg during 1 h. Lung and chest wall mechanics, arterial blood gases, lung and distal organ histology, and interleukin (IL)-1β, IL-6, caspase-3 and type III procollagen (PCIII) mRNA expressions in lung tissue were analyzed.
With intraabdominal hypertension, (1) chest-wall static elastance increased, and PCIII, IL-1β, IL-6, and caspase-3 expressions were more pronounced than in animals with normal intraabdominal pressure in both ALI groups; (2) in extrapulmonary ALI, higher tidal volume was associated with decreased atelectasis, and lower IL-6 and caspase-3 expressions; (3) in pulmonary ALI, higher tidal volume led to higher IL-6 expression; and (4) in pulmonary ALI, liver, kidney, and villi cell apoptosis was increased, but not affected by tidal volume.
Intraabdominal hypertension increased inflammation and fibrogenesis in the lung independent of ALI etiology. In extrapulmonary ALI associated with intraabdominal hypertension, higher tidal volume improved lung morphometry with lower inflammation in lung tissue. Conversely, in pulmonary ALI associated with intraabdominal hypertension, higher tidal volume increased IL-6 expression.
我们假设:(1)腹腔内高压会增加急性肺损伤(ALI)中的肺炎症和纤维形成反应;(2)在存在腹腔内高压的情况下,较高的潮气量会减轻非肺源性 ALI 中的肺损伤,但不会减轻肺源性 ALI 中的肺损伤。
将 Wistar 大鼠随机分配接受大肠杆菌脂多糖气管内(肺源性 ALI)或腹腔内(非肺源性 ALI)给药。24 小时后,动物随机分为无或有腹腔内高压(15mmHg)亚组,并在呼气末正压=5cmH₂O 和潮气量 6 或 10ml/kg 的条件下通气 1 小时。分析肺和胸壁力学、动脉血气、肺和远隔器官组织学以及肺组织中白细胞介素(IL)-1β、IL-6、半胱氨酸天冬氨酸蛋白酶-3 和 III 型前胶原(PCIII)mRNA 表达。
在腹腔内高压时,(1)胸壁静态弹性增加,且 PCIII、IL-1β、IL-6 和半胱氨酸天冬氨酸蛋白酶-3 的表达在两种 ALI 组中均比正常腹腔内压时更为显著;(2)在非肺源性 ALI 中,较高的潮气量与肺不张减少和较低的 IL-6 和半胱氨酸天冬氨酸蛋白酶-3 表达相关;(3)在肺源性 ALI 中,较高的潮气量导致更高的 IL-6 表达;以及(4)在肺源性 ALI 中,肝脏、肾脏和绒毛细胞凋亡增加,但不受潮气量影响。
腹腔内高压增加了与 ALI 病因无关的肺部炎症和纤维化。在与腹腔内高压相关的非肺源性 ALI 中,较高的潮气量改善了肺形态计量学,使肺组织中的炎症减轻。相反,在与腹腔内高压相关的肺源性 ALI 中,较高的潮气量增加了 IL-6 表达。