| Introduction The development and persisting of Intra-abdominal hypertension (IAH) is the main cause to induce abdominal compartment syndrome (ACS), which was first mentioned by Kron in 1984 to describe the pathophysiology resulting from IAH secondary to aortic aneurysm surgery. This uncontrolled increase in intra-abdominal pressure (IAP) from a myriad of disorders can eventually lead to multiple organ dysfunction. IAH and ACS have a high incidence in severely burned patients and other patients from intensive care units. Ivy ME and his colleagues in a prospective study on major burn patients showed that 70% of them had IAH and 20% eventually developed to ACS. Based on a report from NewYork Presbyterian Hospital in the 11th international burn congress (Seattle, Aug. 2002), 18 cases burned patients in the "911" event admitted to the hospital, among them 4 cases developed IAH and ACS who needed decompression immediately. As a result of insufficient scientific proofs, this grave syndrome had long been ignored. In recent years, there is a significant increase in clinical reports and scientific research on IAH and ACS. Perhaps this is why experts in the 11th international burn congress appeal to pay much attention to this lethal syndrome. Previous studies showed that IAH and ACS had detrimental effects on splanchnic perfusion and could result multiple organ dysfunction, but the reason is still obscure. We hypothesized that, IAH could affect redox status of the gut and result redox imbalance, this may contribute to cell apoptosis and eventually lead to intestinal barrier injury.Objective To observe the influence of different levels of intra-abdominal pressure and persisting times on intestinal barrier function, and the changes of redox status, cell apoptosis in intestinal mucosa; To discuss the relationship between redox imbalance, apoptosis and intestinal barrier dysfunction caused by intra-abdominal hypertension. Methods In first part of the study, rabbit model of Pneumoperitoneum intra-abdominal hypertension were established using nitrogen gas. According to pressure and maintaining time, New Zealand white rabbits were randomly divided into 0,10,20,30 mmHg and 1, 2, 4 hours. Heart rate (HR), mean blood pressure (MAP), respiratory rate(RR), and arterial blood gas analysis were examined during IAH. In the second part, Intestinal mucosa blood flow was detected using laser doppler instrument; Intestinal permeability was examined using Fluorescein isothiocyanate- dextran and Horseradish peroxidase typeâ…¡ molecular probes; The mucosa injury was defined by examination of D-lactate, diamine oxidase (DAO) in circulation, and by light microscope, electron microscope; We also examined endotoxin/bacteria translocation. In the third part, the changes of redox status in intestinal mucosa were examined by detection of malondialdehyde (MDA), reduced glutathione (GSH), oxidized glutathione (GSSG), enzyme activities of catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx); we also examined the mRNA gene expression of GPx and peroxisome proliferator activated receptor (PPAR) using RT-PCR. In the fourth part, in situ apoptosis was detected using TUNEL methods; Apoptosis inhibition gene bcl-xl was examined using RT-PCR, and the protein expression of Bcl-xl was also examined using Western blot method.Results 1. HR, MAP and RR had no significant changes when IAP below 20 mmHg, IAP 30 mmHg caused a decrease either in HR, MAP, or RR; PO2 dropped significant from normally 98.8 to 89, 74.5, 59.3 mmHg when IAP increased from 10, 20, to 30 mmHg maintaining 1 hour. Meanwhile, PCO2 is increased from normal control 39.2 to 39, 49, 65 mmHg respectively. 2. Intestinal mucosa blood flow decreased 45%, 80% respectively when IAP increased to 20, 30 mmHg compared to normal control group; When IAP > 20 mmHg, both FITC-D and HRP-â…¡ increased in portal vein; Endotoxin concentration in portal vein increased with elevated IAP and maintaining time; The ratio of bacteria translocation to mesenteric lymph node under IAP o...
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