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腹腔内压升高对中枢神经系统细胞因子、乳酸和灌注压的影响可能导致缺血。

Ischemia as a possible effect of increased intra-abdominal pressure on central nervous system cytokines, lactate and perfusion pressures.

机构信息

Second Department of Surgery, Aretaieion University Hospital, 76 Vassilisis Sofia's Av, Athens, Greece.

出版信息

Crit Care. 2010;14(2):R31. doi: 10.1186/cc8908. Epub 2010 Mar 15.

DOI:10.1186/cc8908
PMID:20230612
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2887137/
Abstract

INTRODUCTION

The aims of our study were to evaluate the impact of increased intra-abdominal pressure (IAP) on central nervous system (CNS) cytokines (Interleukin 6 and tumor necrosis factor), lactate and perfusion pressures, testing the hypothesis that intra-abdominal hypertension (IAH) may possibly lead to CNS ischemia.

METHODS

Fifteen pigs were studied. Helium pneumoperitoneum was established and IAP was increased initially at 20 mmHg and subsequently at 45 mmHg, which was finally followed by abdominal desufflation. Interleukin 6 (IL-6), tumor necrosis factor alpha (TNFa) and lactate were measured in the cerebrospinal fluid (CSF) and intracranial (ICP), intraspinal (ISP), cerebral perfusion (CPP) and spinal perfusion (SPP) pressures recorded.

RESULTS

Increased IAP (20 mmHg) was followed by a statistically significant increase in IL-6 (p = 0.028), lactate (p = 0.017), ICP (p < 0.001) and ISP (p = 0.001) and a significant decrease in CPP (p = 0.013) and SPP (p = 0.002). However, further increase of IAP (45 mmHg) was accompanied by an increase in mean arterial pressure due to compensatory tachycardia, followed by an increase in CPP and SPP and a decrease of cytokines and lactate.

CONCLUSIONS

IAH resulted in a decrease of CPP and SPP lower than 60 mmHg and an increase of all ischemic mediators, indicating CNS ischemia; on the other hand, restoration of perfusion pressures above this threshold decreased all ischemic indicators, irrespective of the level of IAH.

摘要

简介

本研究旨在评估腹内压（IAP）升高对中枢神经系统（CNS）细胞因子（白细胞介素 6 和肿瘤坏死因子）、乳酸和灌注压的影响，检验腹内高压（IAH）可能导致中枢神经系统缺血的假说。

方法

研究纳入 15 头猪。建立氦气气腹，初始 IAP 增加至 20mmHg，随后增加至 45mmHg，最后行腹部放气。测量脑脊液（CSF）和颅内（ICP）、椎管内（ISP）、脑灌注（CPP）和脊髓灌注（SPP）压力中的白细胞介素 6（IL-6）、肿瘤坏死因子-α（TNF-α）和乳酸。

结果

IAP 升高（20mmHg）后，IL-6（p=0.028）、乳酸（p=0.017）、ICP（p<0.001）和 ISP（p=0.001）显著升高，CPP（p=0.013）和 SPP（p=0.002）显著降低。然而，进一步升高 IAP（45mmHg）会因代偿性心动过速导致平均动脉压升高，随后 CPP 和 SPP 升高，细胞因子和乳酸降低。

结论

IAH 导致 CPP 和 SPP 降低至 60mmHg 以下，并增加所有缺血性介质，提示中枢神经系统缺血；另一方面，灌注压恢复至该阈值以上可降低所有缺血性指标，而与 IAH 水平无关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc81/2887137/c8b2c7e6e2d6/cc8908-7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc81/2887137/903d7a32e15f/cc8908-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc81/2887137/6e6690347fdf/cc8908-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc81/2887137/584b56227942/cc8908-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc81/2887137/638ad3dbef74/cc8908-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc81/2887137/d6ae2e3a29a2/cc8908-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc81/2887137/5ce3a84dc896/cc8908-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc81/2887137/c8b2c7e6e2d6/cc8908-7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc81/2887137/903d7a32e15f/cc8908-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc81/2887137/6e6690347fdf/cc8908-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc81/2887137/584b56227942/cc8908-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc81/2887137/638ad3dbef74/cc8908-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc81/2887137/d6ae2e3a29a2/cc8908-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc81/2887137/5ce3a84dc896/cc8908-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc81/2887137/c8b2c7e6e2d6/cc8908-7.jpg

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