The effects of hemodynamic shock and increased intra-abdominal pressure on bacterial translocation
The effects of hemodynamic shock and increased intra-abdominal pressure on bacterial translocation
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DOI：
10.1097/00005373-200201000-00005
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发表时间：
2002-01-01
影响因子：
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通讯作者：
Sugerman, HJ
中科院分区：
文献类型：
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作者：
Doty, JM;Oda, J;Sugerman, HJ
背景：我们假设失血性休克继发腹腔室隔综合征(Acs)导致胃肠道细菌易位(BT)。在实验1组(n=10)，动物失血至平均动脉压(MAP)25~30 mm Hg，持续30分钟，复苏至基础MAP。随后，通过向腹膜腔内注入无菌生理盐水，将腹内压(MAP)提高到高于基线的30 mm Hg。IAP维持在这个水平60分钟。测定并记录酸/碱状态、胃粘膜pH值、肠系膜上动脉(SMA)血流量和血流动力学参数。用聚合酶链式反应(PCR)分析血液样本中细菌的存在。24小时后取脾、淋巴结和门静脉血培养。结果用单因素方差分析和均值+/-扫描电子显微镜报告。第二组为对照组。结果：第1组SMA血流量(基线为0.87±0.101次/分)随出血量的增加而减少(0.53±0.101次/分，p=0.0001)，随着腹内高压的加重而持续下降(0.631次/分钟~0.10次/分钟)。P=0.0006)，缓解后恢复至基线水平(1.01+/-0.51min)。与对照组相比，第1组的PHI(基线7.21+/-0.03)在出血时显著降低(7.04+/-0.03，p=0.0003)，在IAH后进一步下降(6.99+/-0.03，p=0.0001)，但在24小时恢复到基线(7.28+/-0.04)。第1组的平均动脉pH从基线的7.43+/-0.01降至最低点的7.27+/-0.01(p=0.0001)，与对照组相比(p=0.0001)。在出血(3.3±0.71vs.0.06+/-0.60vs.0.06+/-0.60vs.0.06+/-0.60vs.3.08+/-0.71vs.1.170.60，p=0.0001)期间，组1和组2之间的碱基过剩也显著减少。第1组10只动物中，8只淋巴结培养阳性，2只脾培养阳性，2只门静脉血革兰氏阴性肠杆菌培养阳性。10只动物中只有2只呈阳性。在第2组中，9只动物中5只淋巴结培养阳性，0只脾培养阳性，1只门静脉血培养阳性。9只动物中有2只的PCRS呈阳性。两组培养和聚合酶链式反应结果无显著差异(Fisher‘s Exact检验，p=0.3)。结论：在本研究中，出血后再灌流和随后IAH的损伤导致了严重的胃肠道粘膜酸中毒、低灌注率以及全身性酸中毒。根据聚合酶链式反应测量、组织或血液培养的判断，这些变化似乎与显著的细菌易位无关。
Background: We hypothesized that hemorrhagic shock followed by the abdominal compartment syndrome (ACS) resulted in bacterial translocation (BT) from the gastrointestinal (GI) tract.Methods: Nineteen Yorkshire swine (20-30 kg) were divided into two groups. In the experimental group, group 1 (n = 10), animals were hemorrhaged to a mean arterial pressure (MAP) of 25-30 mm Hg for a period of 30 minutes and resuscitated to baseline MAP. Subsequently, intra-abdominal pressure (MAP) was increased to 30 mm Hg above baseline by instilling sterile normal saline into the peritoneal cavity. The IAP was maintained at this level for 60 minutes. Acid/ base status, gastric mucosal ph (pHi), superior mesenteric artery (SMA) blood flow, and hemodynamic parameters were measured and recorded. Blood samples were analyzed by polymerase chain reaction (PCR) for the presence of bacteria. Spleen, lymph node, and portal venous blood cultures were obtained at 24 hours. Results were analyzed by ANOVA and are reported as mean +/- SEM. The second group was the control. These animals did not have the hemorrhage, resuscitation, or infra-abdominal hypertension (IAH) but were otherwise similar to the experimental group in terms of laparotomy and measured parameters.Results: SMA blood flow in group 1 (baseline of 0.87 +/- 0.10 1/min) decreased in response to hemorrhage (0.53 +/- 0.10 1/min, p = 0.0001) and remained decreased with IAH (0.63 1/min 1- 0.10, p = 0.0006) as compared to control and returned towards baseline (1.01 +/- 0.5 1/min) on relief of IAH. pHi (baseline of 7.21 +/- 0.03) was significantly decreased with hemorrhage (7.04 +/- 0.03, p = 0.0003) and decreased further after IAH (6.99 +/- 0.03, p = 0.0001) in group 1 compared to control, but returned toward baseline at 24 hours (7.28 +/- 0.04). The mean arterial pH decreased significantly from 7.43 +/- 0.01 at baseline to 7.27 +/- 0.01 at its nadir within group 1 (p = 0.0001) as well as when compared to control (p = 0.0001). Base excess was also significantly decreased between groups 1 and 2 during hemorrhage (3.30 +/- 0.71 vs. 0.06 +/- 0.60,p = 0.001) and IAH (3.08 +/- 0.71 vs. -1.17 0.60, p = 0.0001). In group 1, 8 of the 10 animals bad positive lymph node cultures, 2 of the 10 had positive spleen cultures, and 2 of the 10 had positive portal venous blood cultures for gram-negative enteric bacteria. Only 2 of the 10 animals had a positive PCR. In group 2, five of the nine animals had positive lymph node cultures, zero of the nine had positive spleen cultures, and one of the nine had positive portal venous blood cultures. Two of the nine animals had positive PCRs. There was no significant difference in cultures or PCR results between the two groups (Fisher's exact test, p = 0.3).Conclusion: In this study, hemorrhage followed by reperfusion and a subsequent insult of IAH caused significant GI mucosal acidosis, hypoperfusion, as well as systemic acidosis. These changes did not appear to be associated with a significant bacterial translocation as judged by PCR measurements, tissue, or blood cultures.