The effects of esophageal cooling on lung injury and systemic inflammatory response after cardiopulmonary resuscitation in swine_West China Medical Journal

Authors：

XU Jiefeng ¹ , WU Chunshuang ¹ , CHEN Qijiang ² , JIN Xiaohong ³ ,  ZHANG Mao ¹

1. Department of Emergency Medicine, the Second Affiliated Hospital of Zhejiang University School of Medicine / Institute of Emergency Medicine, Zhejiang University, Hangzhou, Zhejiang 310009, P. R. China;
2. Department of Intensive Care Medicine, the First Hospital of Ninghai, Ningbo, Zhejiang 315600, P. R. China;
3. Department of Emergency Medicine, the First People’s Hospital of Wenling, Taizhou, Zhejiang 317500, P. R. China;

Corresponding author：

ZHANG Mao, Email: z2jzk@zju.edu.cn

Keywords：

Cardiac arrest; Cardiopulmonary resuscitation; Lung injury; Inflammatory response; Therapeutic hypothermia; Esophageal cooling

DOI：

10.7507/1002-0179.201911020

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Objective To investigate the effects of esophageal cooling (EC) on lung injury and systemic inflammatory response after cardiopulmonary resuscitation in swine.Methods Thirty-two domestic male white pigs were randomly divided into sham group (S group, n=5), normothermia group (NT group, n=9), surface cooling group (SC group, n=9), and EC group (n=9). The animals in the S group only experienced the animal preparation. The animal model was established by 8 min of ventricular fibrillation and then 5 min of cardiopulmonary resuscitation in the other three groups. A normal temperature of (38.0±0.5)℃ was maintained by surface blanket throughout the experiment in the S and NT groups. At 5 min after resuscitation, therapeutic hypothermia was implemented via surface blanket or EC catheter to reach a target temperature of 33℃, and then maintained until 24 h post resuscitation, and followed by a rewarming rate of 1℃/h for 5 h in the SC and EC groups. At 1, 6, 12, 24 and 30 h after resuscitation, the values of extra-vascular lung water index (ELWI) and pulmonary vascular permeability index (PVPI) were measured, and meanwhile arterial blood samples were collected to measure the values of oxygenation index (OI) and venous blood samples were collected to measure the serum levels of tumor necrosis factor-α (TNF-α) and inerleukin-6 (IL-6). At 30 h after resuscitation, the animals were euthanized, and then the lung tissue contents of TNF-α, IL-6 and malondialdehyde, and the activities of superoxide dismutase (SOD) were detected.Results After resuscitation, the induction of hypothermia was significantly faster in the EC group than that in the SC group (2.8 vs. 1.5℃/h, P<0.05), and then its maintenance and rewarming were equally achieved in the two groups. The values of ELWI and PVPI significantly decreased and the values of OI significantly increased from 6 h after resuscitation in the EC group and from 12 h after resuscitation in the SC group compared with the NT group (all P<0.05). Additionally, the values of ELWI and PVPI were significantly lower and the values of OI were significantly higher from 12 h after resuscitation in the EC group than those in the SC group [ELWI: (13.4±3.1) vs. (16.8±2.7) mL/kg at 12 h, (12.4±3.0) vs. (16.0±3.6) mL/kg at 24 h, (11.1±2.4) vs. (13.9±1.9) mL/kg at 30 h; PVPI: 3.7±0.9 vs. 5.0±1.1 at 12 h, 3.4±0.8 vs. 4.6±1.0 at 24 h, 3.1±0.7 vs. 4.2±0.7 at 30 h; OI: (470±41) vs. (417±42) mm Hg (1 mm Hg=0.133 kPa) at 12 h, (462±39) vs. (407±36) mm Hg at 24 h, (438±60) vs. (380±33) mm Hg at 30 h; all P<0.05]. The serum levels of TNF-α and IL-6 significantly decreased from 6 h after resuscitation in the SC and EC groups compared with the NT group (all P<0.05). Additionally, the serum levels of IL-6 from 6 h after resuscitation and the serum levels of TNF-α from 12 h after resuscitation were significantly lower in the EC group than those in the SC group [IL-6: (299±23) vs. (329±30) pg/mL at 6 h, (336±35) vs. (375±30) pg/mL at 12 h, (297±29) vs. (339±36) pg/mL at 24 h, (255±20) vs. (297±33) pg/mL at 30 h; TNF-α: (519±46) vs. (572±49) pg/mL at 12 h, (477±77) vs. (570±64) pg/mL at 24 h, (436±49) vs. (509±51) pg/mL at 30 h; all P<0.05]. The contents of TNF-α, IL-6, and malondialdehyde significantly decreased and the activities of SOD significantly increased in the SC and EC groups compared with the NT group (all P<0.05). Additionally, lung inflammation and oxidative stress were further significantly alleviated in the EC group compared with the SC group [TNF-α: (557±155) vs. (782±154) pg/mg prot; IL-6: (616±134) vs. (868±143) pg/mg prot; malondialdehyde: (4.95±1.53) vs. (7.53±1.77) nmol/mg prot; SOD: (3.18±0.74) vs. (2.14±1.00) U/mg prot; all P<0.05].Conclusion Therapeutic hypothermia could be rapidly induced by EC after resuscitation, and further significantly alleviated post-resuscitation lung injury and systemic inflammatory response compared with conventional surface cooling.

Citation： XU Jiefeng, WU Chunshuang, CHEN Qijiang, JIN Xiaohong, ZHANG Mao. The effects of esophageal cooling on lung injury and systemic inflammatory response after cardiopulmonary resuscitation in swine. West China Medical Journal, 2019, 34(11): 1261-1267. doi: 10.7507/1002-0179.201911020 Copy

1.	Neumar RW, Nolan JP, Adrie C, et al. Post-cardiac arrest syndrome: epidemiology, pathophysiology, treatment, and prognostication. Circulation, 2008, 118(23): 2452-2483.
2.	Laver S, Farrow C, Turner D, et al. Mode of death after admission to an intensive care unit following cardiac arrest. Intensive Care Med, 2004, 30(11): 2126-2128.
3.	Callaway CW, Donnino MW, Fink EL, et al. Part 8: post-cardiac arrest care: 2015 American heart association guidelines update for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation, 2015, 132(18 Suppl 2): S465-S482.
4.	Adrie C, Adib-Conquy M, Laurent I, et al. Successful cardiopulmonary resuscitation after cardiac arrest as a " sepsis-like” syndrome. Circulation, 2002, 106(5): 562-568.
5.	张东, 赵淑杰, 李南, 等. 心搏骤停后综合征预后相关影响因素的分析. 中华危重病急救医学, 2015, 27(3): 175-179.
6.	李培杰, 杨小华, 张立平, 等. 心肺复苏后血浆可溶性选择素及基质金属蛋白酶-9测定的临床意义. 中国危重病急救医学, 2004, 16(3): 137-141.
7.	Miller AC, Rosati SF, Suffredini AF, et al. A systematic review and pooled analysis of CPR-associated cardiovascular and thoracic injuries. Resuscitation, 2014, 85(6): 724-731.
8.	Weisfeldt ML, Becker LB. Resuscitation after cardiac arrest: a 3-phase time-sensitive model. JAMA, 2002, 288(23): 3035-3038.
9.	Chenoune M, Lidouren F, Adam C, et al. Ultrafast and whole-body cooling with total liquid ventilation induces favorable neurological and cardiac outcomes after cardiac arrest in rabbits. Circulation, 2011, 124(8): 901-911.
10.	Xu J, Chen Q, Jin X, et al. Early initiation of continuous renal replacement therapy induces fast hypothermia and improves post-cardiac arrest syndrome in a porcine model. Shock, 2019, 52(4): 456-467.
11.	Suh GJ, Kwon WY, Kim KS, et al. Prolonged therapeutic hypothermia is more effective in attenuating brain apoptosis in a swine cardiac arrest model. Crit Care Med, 2014, 42(2): e132-e142.
12.	Lu X, Ma L, Sun S, et al. The effects of the rate of post-resuscitation rewarming following hypothermia on outcomes of cardiopulmonary resuscitation in a rat model. Crit Care Med, 2014, 42(2): e106-e113.
13.	Xu JF, Jin XH, Chen QJ, et al. Faster hypothermia induced by esophageal cooling improves early markers of cardiac and neurological injury after cardiac arrest in swine. J Am Heart Assoc, 2018, 7(21): e010283.
14.	Nielsen N, Wetterslev J, Cronberg T, et al. Targeted temperature management at 33℃ versus 36℃ after cardiac arrest. N Engl J Med, 2013, 369(23): 2197-2206.
15.	Fukuda T. Targeted temperature management for adult out-of-hospital cardiac arrest: current concepts and clinical applications. J Intensive Care, 2016, 4: 30.
16.	顾伟, 李春盛, 殷文朋, 等. 转录因子GATA-3和T-bet的表达失衡在复苏后急性肺损伤中的作用. 中华急诊医学杂志, 2014, 23(1): 8-14.
17.	刘忠民, 李南, 于贺, 等. 参麦注射液对家兔心脏骤停后综合征影响的实验研究. 中华危重病急救医学, 2013, 25(11): 664-668.
18.	Qian J, Yang ZF, Cahoon J, et al. Post-resuscitation intestinal microcirculation: its relationship with sublingual microcirculation and the severity of post-resuscitation syndrome. Resuscitation, 2014, 85(6): 833-839.

1. Neumar RW, Nolan JP, Adrie C, et al. Post-cardiac arrest syndrome: epidemiology, pathophysiology, treatment, and prognostication. Circulation, 2008, 118(23): 2452-2483.
2. Laver S, Farrow C, Turner D, et al. Mode of death after admission to an intensive care unit following cardiac arrest. Intensive Care Med, 2004, 30(11): 2126-2128.
3. Callaway CW, Donnino MW, Fink EL, et al. Part 8: post-cardiac arrest care: 2015 American heart association guidelines update for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation, 2015, 132(18 Suppl 2): S465-S482.
4. Adrie C, Adib-Conquy M, Laurent I, et al. Successful cardiopulmonary resuscitation after cardiac arrest as a " sepsis-like” syndrome. Circulation, 2002, 106(5): 562-568.
5. 张东, 赵淑杰, 李南, 等. 心搏骤停后综合征预后相关影响因素的分析. 中华危重病急救医学, 2015, 27(3): 175-179.
6. 李培杰, 杨小华, 张立平, 等. 心肺复苏后血浆可溶性选择素及基质金属蛋白酶-9测定的临床意义. 中国危重病急救医学, 2004, 16(3): 137-141.
7. Miller AC, Rosati SF, Suffredini AF, et al. A systematic review and pooled analysis of CPR-associated cardiovascular and thoracic injuries. Resuscitation, 2014, 85(6): 724-731.
8. Weisfeldt ML, Becker LB. Resuscitation after cardiac arrest: a 3-phase time-sensitive model. JAMA, 2002, 288(23): 3035-3038.
9. Chenoune M, Lidouren F, Adam C, et al. Ultrafast and whole-body cooling with total liquid ventilation induces favorable neurological and cardiac outcomes after cardiac arrest in rabbits. Circulation, 2011, 124(8): 901-911.
10. Xu J, Chen Q, Jin X, et al. Early initiation of continuous renal replacement therapy induces fast hypothermia and improves post-cardiac arrest syndrome in a porcine model. Shock, 2019, 52(4): 456-467.
11. Suh GJ, Kwon WY, Kim KS, et al. Prolonged therapeutic hypothermia is more effective in attenuating brain apoptosis in a swine cardiac arrest model. Crit Care Med, 2014, 42(2): e132-e142.
12. Lu X, Ma L, Sun S, et al. The effects of the rate of post-resuscitation rewarming following hypothermia on outcomes of cardiopulmonary resuscitation in a rat model. Crit Care Med, 2014, 42(2): e106-e113.
13. Xu JF, Jin XH, Chen QJ, et al. Faster hypothermia induced by esophageal cooling improves early markers of cardiac and neurological injury after cardiac arrest in swine. J Am Heart Assoc, 2018, 7(21): e010283.
14. Nielsen N, Wetterslev J, Cronberg T, et al. Targeted temperature management at 33℃ versus 36℃ after cardiac arrest. N Engl J Med, 2013, 369(23): 2197-2206.
15. Fukuda T. Targeted temperature management for adult out-of-hospital cardiac arrest: current concepts and clinical applications. J Intensive Care, 2016, 4: 30.
16. 顾伟, 李春盛, 殷文朋, 等. 转录因子GATA-3和T-bet的表达失衡在复苏后急性肺损伤中的作用. 中华急诊医学杂志, 2014, 23(1): 8-14.
17. 刘忠民, 李南, 于贺, 等. 参麦注射液对家兔心脏骤停后综合征影响的实验研究. 中华危重病急救医学, 2013, 25(11): 664-668.
18. Qian J, Yang ZF, Cahoon J, et al. Post-resuscitation intestinal microcirculation: its relationship with sublingual microcirculation and the severity of post-resuscitation syndrome. Resuscitation, 2014, 85(6): 833-839.

West China Medical Journal

The effects of esophageal cooling on lung injury and systemic inflammatory response after cardiopulmonary resuscitation in swine

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