Model Of Abdominal Compartment Syndrome Research Articles

A Custom-Tailored Multichannel Pressure Monitoring System Designed for Experimental Surgical Model of Abdominal Compartment Syndrome.

In experimental medicine, a wide variety of sensory measurements are used. One of these is real-time precision pressure measurement. For comparative studies of the complex pathophysiology and surgical management of abdominal compartment syndrome, a multichannel pressure measurement system is essential. An important aspect is that this multichannel pressure measurement system should be able to monitor the pressure conditions in different tissue layers, and compartments, under different settings. We created a 12-channel positive-negative sensor system for simultaneous detection of pressure conditions in the abdominal cavity, the intestines, and the circulatory system. The same pressure sensor was used with different measurement ranges. In this paper, we describe the device and major experiences, advantages, and disadvantages. The sensory systems are capable of real-time, variable frequency sampling and data collection. It is also important to note that the pressure measurement system should be able to measure pressure with high sensitivity, independently of the filling medium (gas, liquid). The multichannel pressure measurement system we developed was well suited for abdominal compartment syndrome experiments and provided data for optimizing the method of negative pressure wound management. The system is also suitable for direct blood pressure measurement, making it appropriate for use in additional experimental surgical models.

Comparison of Three Devices to Measure Pressure for Acute Compartment Syndrome.

Acute compartment syndrome (ACS) is a well-recognized and common emergency. Undiagnosed ACS leads to muscle necrosis, limb contracture, intractable pain, and may even result in amputation. Three devices (Synthes, Stryker, and MY01) were compared in a pre-clinical rat abdominal compartment syndrome simulation. Simultaneous measurements of intracompartmental pressures allowed concurrent comparison among all devices. Large variations from the reference values are seen with the Synthes and Stryker devices. Variances are large in these two devices even under ideal conditions. The MY01 device was the truest indicator of reference pressure in this ACS model (over 600% more accurate). The MY01 device was the most accurate device in tracking pressure changes in this rat model of abdominal compartment syndrome.

Experimental study on the pathological changes in lung of abdominal compartment syndrome model rabbits

To investigate the secondary pathological changes in lung of abdominal compartment syndrome (ACS). Twenty-five healthy adult clean New Zealand rabbits were randomly divided into control group (n = 5) and experimental group (n = 20) according to the random number table method. The experimental group was subdivided into two subgroups according to the observation time: 24 hours and 48 hours, with 10 rabbits in each subgroup. A high pressure liquid animal model of abdominal cavity was reproduced by water bag superposition pressurization. In the control group, the pressurized water bag did not inject liquid, and intra-abdominal pressure (IAP) was maintained at 0; while in the experimental group, pressurized water infusion was performed, and IAP was maintained at 25 mmHg (1 mmHg = 0.133 kPa). The rabbits in the control group were sacrificed at 48 hours, those in the experimental group were sacrificed at 24 hours and 48 hours respectively, and the lungs were harvested completely. The pathological changes were observed under light microscope after hematoxylin-eosin (HE) staining. In the control group, the activity of the rabbits was decreased, the food intake was decreased, and all the 5 animals survived; in the experimental group, the activity was decreased significantly, little food intake or not, the urine output was decreased significantly, and 1 rabbit died at 22, 27 and 37 hours respectively, and 17 survived. Light microscopy showed that there were terminal bronchioles and a large number of alveoli in the lung tissue of the control group, and small vessels dilated in the interstitium. In the experimental group, alveolar epithelial hyperplasia, alveolar septum of different sizes, alveolar fusion, alveolar septal bleeding, interstitial heart failure cells with phagocytosis of hemosiderin, bronchiolectasis, a large number of inflammatory cell infiltration near the bronchi, thrombosis in the blood vessels were found at 24 hours. A large number of erythrocyte and cellulose-like exudates were seen in the lumen of terminal bronchioles, alveolar dilatation and fusion were aggravated, and old hemorrhage in the lumen of the alveoli was observed, hemosiderosis containing hemosiderin was observed at 48 hours. ACS could cause severe lung injury and aggravate as time goes on.

Biochemical Changes in Experimental Rat Model of Abdominal Compartment Syndrome.

Increased intra-abdominal pressure (IAP) causes tissue ischemia, subsequent hypoxia, and impairment of normal tissue metabolism. Elevation of IAP above 20 mmHg leads to progression of abdominal compartment syndrome (ACS) that is associated with organ dysfunction or failure not previously manifested. To evaluate the eff ects of diff erent grades and time of exposure to IAP on biochemical parameters and oxidative stress in organs aff ected by ischemia using previously developed rat model. Three experimental groups exposed to diff erent IAP and time frames were tested for liver, kidney, and pancreas injury by measuring the activities of tissue specifi c enzymes in blood serum. Elevated activities of aspartate aminotransferase, pancreatic amylase, lipase, and higher concentrations of D-lactate, urea, and creatinine were found in some of the experimental groups compared to a control group of animals not subjected to increased IAP. Increased levels of biomarkers of oxidative stress as well as decrease in concentration of the major cellular antioxidant glutathione indicated the presence of oxidative injury as a result of elevated IAP. The developed rat model is appropriate to study the mechanism and manifestation of tissue injury during diff erent grades of elevated IAP but also to test approaches aimed to attenuate the detrimental eff ects of ACS. This study also underlines the necessity of using not a single but a set of biochemical parameters in order to assess the severity of tissue injury during elevated IAP and progression to ACS.

Hypoxic renal injury in newborns with abdominal compartment syndrome (clinical and experimental study).

BackgroundSurgical treatment for gastroschisis and congenital diaphragmatic hernia (CDH) commonly leads to abdominal compartment syndrome (ACS) associated with hypoxic renal injury. We hypothesized that measurement of urinary and serum concentrations of vascular endothelial growth factor (VEGF), π-glutathione S-transferase (π-GST), and monocyte chemoattractant protein-1 (MCP-1) may serve for noninvasive detection of hypoxic renal injury in such patients.MethodsIntra-abdominal pressure (IAP), renal excretory function, and the biomarker levels were analyzed before, 4, and 10 days after surgery. Association between the biomarker levels and renal histology was investigated using an original model of ACS in newborn rats.ResultsFour days after surgery, IAP increased, renal excretory function decreased, and the levels of VEGF, π-GST, and MCP-1 increased, indicating renal injury. Ten days after surgery, IAP partially decreased, renal excretory function completely restored, but the biomarker levels remained elevated, suggesting the ongoing kidney injury. In the model of ACS, increase in the biomarker levels was associated with progressing kidney morphological alteration.ConclusionSurgical treatment for gastroschisis and CDH is associated with prolonged hypoxic kidney injury despite complete restoration of renal excretory function. Follow-up measurement of VEGF, π-GST, and MCP-1 levels may provide a better tool for noninvasive assessment of renal parenchyma in newborns with ACS.

Early impact of abdominal compartment syndrome on liver, kidney and lung damage in a rodent model.

Abdominal compartment syndrome (ACS) sometimes occurs in critically ill patients following damage control surgery. The purpose of the present study was to develop a model of ACS and to evaluate its pathologic impact on liver, kidney, and lung morphology. Twenty Wistar rats (mass 300-350 g) were randomly divided into four groups: 1) intra-abdominal hypertension (IAH): a laparotomy was performed and the abdomen packed with cotton until an intra-abdominal pressure (IAP) of 15 mm Hg was reached; 2) hypovolemia (HYPO): blood was withdrawn until a mean arterial pressure ~60 mm Hg was reached; 3) IAH + HYPO (to resemble clinical ACS); and 4) sham surgery. After 3 hours of protective mechanical ventilation, the animals were euthanized and the liver, kidney and lungs removed to examine the degree of tissue damage. IAH resulted in the following: oedema and neutrophil infiltration in the kidney; necrosis, congestion, and microsteatosis in the liver; and alveolar collapse, haemorrhage, interstitial oedema, and neutrophil infiltration in the lungs. Furthermore, IAH was associated with greater cell apoptosis in the kidney, liver and lungs compared to sham surgery. HYPO led to oedema and neutrophil infiltration in the kidney. The combination of IAH and HYPO resulted in all the aforementioned changes in lung, kidney and liver tissue, as well as exacerbation of the inflammatory process in the kidney and liver and kidney cell necrosis and apoptosis. Intra-abdominal hypertension by itself is associated with kidney, liver and lung damage; when combined with hypovolemia, it leads to further impairment and organ damage.

Effects of pentoxifylline on oxidative stress in rats with abdominal compartment syndrome model

BackgroundAbdominal compartment syndrome (ACS) causes severe pathology in the cardiovascular, renal and pulmonary systems. Recent studies showed that pentoxifylline (PTX) has effects on increasing tissue oxygenation, healing capillary refill and reducing superoxides and hydroxyl radicals by inhibiting xanthine oxidase. In this study, our aim was to study the effects of PTX on free oxygen radicals and oxidative damage in rats with ACS model. Materials and methodsACS model was created in 32 male Wistar-Albino-rats, which were randomized into one of the four study groups: Group A (n:8), having ACS; Group B (n:8), having ACS and receiving PTX (50 mg/kg/day) intraperitoneal for 10 days; Group C (n:8), receiving PTX (50 mg/kg/day) intraperitoneal for 10 days without having ACS; Group D (n:8), having no ACS and not receiving PTX. On the 11th day blood samples were collected to measure alanine-amino-acid-transferase (ALT) and aspartate-amino-acid-transferase (AST) in the heart, malondialdehyde (MDA), myeloperoxidase (MPO) and glutathione (GSH) in the liver, lung and small bowel. Histopathologic injury scoring was done. ResultsGroups were compared in pairs. Group A compared to Group B: ALT increase, liver MDA, lung GSH and MPO decrease were statistically meaningful in Group B. Group A compared to Group C: ALT and liver MPO decrease and liver MDA increase were statistically meaningful in Group A. Group B compared to Group C: ALT increase, MDA and GSH decrease in the lung were statistically meaningful in Group B. Group B compared to Group D: ALT and MPO increase in the small bowel and MPO decrease in the lung were statistically meaningful in Group B. Group A had the highest histopathologic injury scoring. ConclusionHistopathologically confirmed pentoxifylline was effective in the treatment of ACS in these rat models.

Abnormal Expression of Urea Transporter Protein in a Rat Model of Hepatorenal Syndrome Induced by Succinylated Gelatin.

BackgroundHepatorenal syndrome (HRS) is a serious complication of advanced chronic liver disease. Abdominal compartment syndrome (ACS) occurs with dysfunction of multiple organs when abdominal pressure increases. Here, we report on a novel model of ACS with ascites and a model of HRS in rats to observe the urea transporter protein (UT) expression in the 2 models.Material/MethodsA liver cirrhosis model was induced by CCl4. After changes of liver histopathology were observed, rats were injected intraperitoneally with succinylated gelatin to establish a model of ACS and HRS. Then, changes in BUN, Cr, and renal histopathology were detected. Moreover, the UT in ACS and HRS were also quantified.ResultsThe surfaces of liver in the cirrhotic group became coarse, with visible small nodules and became yellow and greasy. The normal structure of the hepatic lobules were destroyed, and hyperplasia of fibrotic tissue and pseudo-lobe was observed. The levels of BUN and Cr were significantly increased in rats suffering from ACS and HRS, respectively, compared to their control groups. In addition, the mRNA levels of UT-A2 and UT-A3 decreased in rats with HRS compared to cirrhotic rats. However, there was no significant difference between the mRNA levels of UT-A2, UT-A3, and UT-B in rats with ACS vs. normal rats.ConclusionsIt is feasible to model ACS in rats by injecting succinylated gelatin into the abdominal cavity. Increasing the intra-abdominal pressure by succinylated gelatin is also a novel approach for modeling HRS in cirrhotic rats. Compared with control rats, there is an abnormal mRNA expression of UT in ACS rats and HRS rats.

Physiologic changes with abdominal wall reconstruction in a porcine abdominal compartment syndrome model.

Abdominal compartment syndrome (ACS) is a severe complication of ventral hernia repair. The aims of this study were to investigate the effects of intra-abdominal pressure on the physiologic changes of abdominal wall reconstruction and component separation in a porcine model. Ventral hernia repair (VHR) was simulated by abdominal fascial imbrication of a 10 × 15 cm defect in 45 Yorkshire pigs assigned to five experimental groups. ACS was simulated by a Stryker endoscopy insufflator with intra-abdominal pressure elevated to 20 mmHg in two groups. Component separation was performed in one of these groups and in one group without ACS. Physiological parameters were measured before and after the procedures and monitored for 4 h. The animals were euthanized for histologic analysis of organ damage. VHR led to an increase in intra-abdominal pressure, bladder pressure, and central venous pressure by an average of 14.89, 13.93, and 14.69 mmHg (p < 0.001) in all animals. Component separation was performed in 25 animals and the three pressures reduced by 9.11, 8.00, 7.89 mmHg (p < 0.001). ACS correlated with higher percentages of large and small bowel necrosis compared to groups without abdominal compartment syndrome. The results confirm that primary repair of large abdominal wall defects leads to increased intra-abdominal pressure, which can be reduced with component separation. In animals with ACS, component separation may reduce the risk of organ damage. Central venous pressure, bladder pressure, and other physiologic parameters accurately correlated with elevated intra-abdominal pressure and may have utility as markers for diagnosis of ACS.

The effect of glutamine on oxidative damage in an experimental abdominal compartment syndrome model in rats

The aim was to investigate whether or not glutamine, an antioxidant effective amino acid, improves the reperfusion-induced oxidative injury of abdominal hypertension. Wistar Albino rats were used. Group 1: Abdominal compartment syndrome alone: With the rats under anesthesia, intraabdominal pressure was obtained. Three days later, the rats were sacrificed, and intestine, lung and liver samples were removed for determination of tissue malondialdehyde (MDA) and glutathione (GSH) levels as oxidative injury parameters and of myeloperoxidase (MPO) activity as an inflammatory parameter. Trunk blood was analyzed for the alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. Group 2: Abdominal compartment syndrome and glutamine: intragastric glutamine was given for seven days before and three days following establishment of the abdominal compartment syndrome model. The same examination procedure was then performed. Group 3: Glutamine administration alone. Group 4: Control group. Intraabdominal pressure significantly increased the intestine, lung and liver MDA levels and MPO activities in comparison to the control group. Glutamine was associated with decreased MDA levels and MPO activities and increased GSH levels. Glutamine appears to have protective effects against reperfusion-induced oxidative damage via its anti-inflammatory and antioxidant effect.

The effect of glutamine on oxidative damage in an experimental abdominal compartment syndrome model in rats

The effect of glutamine on oxidative damage in an experimental abdominal compartment syndrome model in rats

Effects of doxycycline on intestinal ischemia reperfusion injury induced by abdominal compartment syndrome in a rat model

Background: Abdominal compartment syndrome (ACS) refers to organ dysfunction and ischemia resulting from intra-abdominal hypertension (IAH). Ischemia of the gut results in the triggering of a systemic inflammatory response by releasing cytokines which, in turn, causes capillary leakage leading to bowel edema, further increasing intra-abdominal pressure and resulting in a morbid cycle of ischemia and edema. Objective: The aim of this study was to determine the effects of doxycycline on intestinal ischemia reperfusion (I/R) injury in a rat model of ACS. Methods: Sprague-Dawley rats were divided into 5 equal groups. In groups 1 and 2, saline (1 cc IP) was administered during induction of ACS and intestinal samples were removed at 1 and 24 hours, respectively, after decompression. In groups 3 and 4, doxycycline (10 mg/kg IP) was injected during induction of ACS and, similarly, intestinal samples were removed at 1 and 24 hours after decompression. In the control group (group 5), intestinal samples were collected without induction of ACS. Malon-dialdehyde (MDA), interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, matrix metalloproteinase-2 (MMP-2), and tissue inhibitor of metalloproteinase-1 were studied and the apoptotic cells were enumerated histopathologically. Apoptosis and β-cell lymphoma 2 (βcl-2) expression were assessed immunohistochemically. Results: Thirty-five rats were evenly divided into 5 groups of 7 rats each. MDA, IL-1β, IL-6, TNF-α, and MMP-2 levels were significantly higher in group 1 one hour after the reperfusion period compared with the control group ( P < 0.001, P < 0.001, P < 0.05, P < 0.001, and P < 0.01, respectively). The same parameters were significantly lower in group 3, in which doxycycline was administered, than in group 1 ( P < 0.001, P < 0.05, P < 0.05, P < 0.001, and P < 0.01, respectively). However, there was no significant difference between groups 2 and 4 in the 24th hour (all, P > 0.05). The mean (SD) number of apoptotic cells and the expression of βcl-2 was highest in group 2 at 24 hours after the reperfusion period (92.5 [11.4] and 35.9 [5.0], respectively) and significantly greater than that in group 4 ( P < 0.001 and P < 0.05, respectively). Conclusion: Doxycycline was associated with protective effects against I/R injury through decreasing apoptosis via attenuating the response of proinflammatory cytokines and inhibiting the activity of MMP-2 in this rat model.

A novel mechanism for neutrophil priming in trauma: Potential role of peritoneal fluid

We sought to determine the effect of peritoneal fluid from a novel animal model of abdominal compartment syndrome (ACS) on the proinflammatory status of polymorphonuclear leukocytes (PMNs) and monocytes. We hypothesize that peritoneal fluid is a potential priming and/or activating agent for PMNs/monocytes. ACS was induced in female Yorkshire swine, and peritoneal fluid was collected at the time of decompressive laparotomy. Naïve PMNs/monocytes were primed and/or activated with peritoneal fluid, phosphatidylcholine (PAF) plus peritoneal fluid, peritoneal fluid plus n-formyl-met-leu-phe (fMLP), and peritoneal fluid plus phorbol 12-myristate 13-acetate (PMA). Activation was determined by surface marker expression of integrins (CD11b an CD18) and selectins (CD62L). Additionally, proinflammatory cytokines in peritoneal fluid were analyzed. Peritoneal fluid did not activate PMNs but increased CD11b expression on monocytes. When used as a primer for fMLP- or PMA-induced activation, peritoneal fluid significantly increased CD11b and CD18 expression on PMNs and monocytes. Peritoneal fluid collected at 6 and 12 h post decompressive laparotomy had similar effects. Interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) levels were increased in peritoneal fluid. Peritoneal fluid represents a primer for PMNs/monocytes and seems to act through receptor-dependent and receptor-independent pathways. Strategies to reduce the amount of peritoneal fluid may decrease the locoregional and systemic inflammatory response by reducing priming and activation of neutrophils/monocytes.

A Novel Physiologic Model for the Study of Abdominal Compartment Syndrome (ACS)

: Current abdominal compartment syndrome (ACS) models rely on intraperitoneal instillation of fluid, air, and other space-occupying substances. Although this allows for the study of the effects of increased abdominal pressure, it poorly mimics its pathogenesis. We have developed the first reported large animal model of ACS incorporating hemorrhagic shock/resuscitation. : Hemorrhagic shock was induced and maintained (1 hour) in 12 Yorkshire swine by bleeding to a mean arterial pressure (MAP) of 50 mm Hg. The collected blood plus two additional volumes of crystalloid was then reinfused. Mesenteric venous hypertension was induced by tightening a previously placed portal vein snare in a nonocclusive manner to mimic the effects of abdominal packing. Crystalloids were infused to maintain MAP. Hemodynamic measurements, abdominal pressure, peak inspiratory pressures, urine output, and blood chemistries were measured sequentially. Animals were studied for 36 hours after decompression. : ACS (intra-abdominal pressure of > or =20 mm Hg with new organ dysfunction) developed in all animals. There were significant increases in peak inspiratory pressure, central venous pressure, and pulmonary artery pressure and decreases in MAP upon development of ACS. Urine output was significantly decreased before decompression. Mean blood lactate decreased and base excess increased significantly after decompression. : We have created the first reported physiologic animal ACS model incorporating hemorrhagic shock/resuscitation and the effects of damage control surgery.

Peritoneal Fluid Induces Priming of Naive Neutrophils in an Animal Model of Abdominal Compartment Syndrome

Introduction: Translocation of fluid into the peritoneal cavity contributes, in part, to the development of ACS (abdominal compartment syndrome). The purpose of this experiment was to determine the effect of exposure of peritoneal fluid from an animal model of ACS on the pro-inflammatory status of naïve PMNs (polymorphonuclear leukocytes) as measured by oxidative burst and adhesion molecule expression. Methods: ACS was induced in 6 female Yorkshire swine, utilizing a hemorrhagic shock/resuscitation and mesenteric venous pressure elevation model.

Deneysel Abdominal Kompartman Sendromu Oluşturulan Sıçanlarda Serum Malondialdehid Düzeyi ile Seruloplazmin Oksidaz Aktivitesi

Objective: The aim of this study was to investigate serum ceruloplasmin (Cp) oxidase activity and malondialdehyde (MDA) levels in a rat model of abdominal compartment syndrome (ACS). Material and Methods: There were four groups consisting of eight rats per group. Group 1 (Control group): After anesthesia, 3 ml of blood were taken from the heart of these rats. Group 2 (Sham group): Under anesthesia, an injector needle was inserted intraperitoneally and left there. After 3 h, 3 ml of blood was taken from the heart of these rats. Group 3 (First study group): Under anesthesia, an injector needle (number 16) was inserted intraperitoneally and a standard insufflator (Karl Storz, Germany) was connected. At the end of this procedure, the abdomen was decompressed and 3 ml of blood was collected as descried above. Group 4 (Second study group): The abdomen was compressed as Group 3. However, the intraabdominal hypertension was established by keeping the pressure constant at 25 mmHg for 3 h in this group. At the end of this procedure, the abdomen was decompressed and 3 ml of blood was collected as descried above. Results: Cp oxidase activities and MDA levels significantly increased in first and second study groups when compared to the control group. Cp oxidase activities and MDA levels were significantly higher in second study group than those of the first study group. MDA levels were significantly higher in first study group than those of the sham group. Conclusion: We found increased serum Cp oxidase activity and MDA level in experimental abdominal compartment syndrome-induced rats. These findings show that oxidative stress increase ACS in rats.

Effects of Doxycycline on Renal Ischemia Reperfusion Injury Induced by Abdominal Compartment Syndrome

The aim of this study was to determine the effects of doxycycline on renal ischemia reperfusion (I/R) injury in a rat model of abdominal compartment syndrome (ACS). Forty-two Sprague-Dawley rats were divided into six groups. In the control group (group 1), kidney samples were collected with no manipulation; in the sham group (group 2) induction of ACS was followed by decompression. In groups 3 and 4, 1 cc of saline was administered intraperitoneally (i.p.) during the induction of ACS, and the kidneys were removed 1 and 24h after decompression, respectively. In groups 5 and 6, doxycycline (10mg/kg i.p.) was injected during the induction of ACS, and similarly all tissue samples were removed 1 and 24h after decompression, respectively. MDA, IL-1β, IL-6, TNF-α, MMP-2, and TIMP-1 were studied, and the apoptotic cells were enumerated histopathologically, and apoptosis and bcl-2 expression were assessed immunohistochemically. Creatinine, MDA, IL-1β, and IL-6 levels were significantly higher in group 3, 1h after the reperfusion period compared with the control group, and the same parameters were significantly lower in the groups in which doxycycline was administered, 1 hour after decompression. However, there remained no difference between groups at 24h, except IL-1β, which was decreased to even lower values. TNF-α and TIMP-1 levels were not statistically different in all groups. The MMP-2 level was significantly higher in group 4 by 24h, and there remained no difference between groups 1, 2, and 6. In group 6, there were not any apoptotic cells as were observed in the other groups. The number of apoptotic cells and the expression of bcl-2 was significantly less in the groups in which doxycycline was administered. Doxycycline had protective effects on I/R injury by decreasing apoptosis via reducing the level of pro-inflammatory cytokines, increasing the level of TIMP-1, and inhibiting the activity of MMP-2.

Effect of Elevated Intra-Abdominal Pressure and Hyperoxia on Portal Vein Blood Flow, Hepatocyte Proliferation and Apoptosis in a Rat Model

Indications for a laparoscopic approach for the management of biliary atresia in children are not clearly defined. We have recently shown that persistent intra-abdominal pressure (IAP) significantly decreased portal vein (PV) flow. Ventilation with a high concentration of oxygen after abdomen deflation raises concerns of increased oxidative stress but has also been shown to exert beneficial effects on splanchnic ischemia/reperfusion. The purpose of the present study was to evaluate the effects of IAP and hyperoxia on liver histology, hepatocyte proliferation and apoptosis in a rat model of abdominal compartment syndrome (ACS). Male Sprague-Dawley rats were anesthetized with intraperitoneal ketamine and xylasine. After a midline laparotomy, the PV was isolated. Ultrasonic blood flow probes were placed on the vessel for continuous measurement of regional blood flow. Mean arterial blood pressure (MABP) was continuously measured. Two large-caliber percutaneous peripheral intravenous catheters were introduced into the peritoneal cavity for inflation of air and measurement of IAP. Rats were divided into three experimental groups: 1) Sham rats were subjected to IAP of 0 mmHg; 2) ACS rats were subjected to IAP of 6 mmHg for 2 hours and were ventilated with air; and 3) ACS-O (2) rats were subjected to IAP of 6 mmHg for 2 hours and were ventilated with 100 % O (2) during the operation and ventilation was continued for 6 hours after operation. Liver structural changes, hepatocyte proliferation (using BrdU assay) and apoptosis (using Tunel assay) were determined 24 hours following operation. IAP at 6 mmHg caused a twofold decrease in PV flow compared to sham animals. Hyperoxia resulted in a less significant decrease in PV flow compared to air-ventilated animals. Despite a significant decrease in PV blood flow, 24 hours after abdominal deflation only a few animals demonstrated histological signs of liver damage. The small histological changes were accompanied by increased hepatocyte apoptosis and enhanced hepatocyte proliferation in 25 % of animals, suggesting a liver repair response. Despite a significant decrease in PV blood flow, persistent IAP for 2 hours results in few changes in liver histology, and stimulates hepatocyte proliferation and apoptosis in only a few animals, supporting the presence of a recovering mechanism. Treatment with hyperoxia did not significantly change hepatocyte proliferation and apoptosis.

Effect of elevated intra-abdominal pressure and 100% oxygen on superior mesenteric artery blood flow and enterocyte turnover in a rat

Elevated intra-abdominal pressure (IAP) has been shown to reduce mesenteric blood flow and cause intestinal damage. The purpose of the present study was to evaluate the effects of IAP and hyperoxia on superior mesenteric artery (SMA) blood flow, enterocyte proliferation and apoptosis in a rat model of abdominal compartment syndrome (ACS). Male rats underwent midline laparotomy. SMA was isolated and ultrasonic blood flow probes were placed on the vessel for continuous measurement of regional blood flow. Two catheters were introduced into the peritoneal cavity for inflation of air and for measurement of IAP. Rats were divided into three experimental groups: (1) Sham rats were subjected to IAP of 0 mmHg, (2) ACS-air rats were subjected to IAP of 6 mmHg for 2 h and were ventilated with air, and (3) ACS-O(2) rats were subjected to IAP of 6 mmHg and were ventilated with 100% oxygen (O(2)) during the operation and for 6 h after the operation. Intestinal structural changes, enterocyte proliferation and enterocyte apoptosis were evaluated at 24 h after operation. A paired Student's t test and the non-parametric Kruskal-Wallis ANOVA test were used as indicated. P < 0.05 was considered statistically significant. IAP at 6 mmHg caused a moderate decrease in SMA blood flow. Inhalation of 100% oxygen resulted in a trend toward an increase in SMA flow when compared to air-ventilated animals. ACS rats demonstrated a significantly lower index of proliferation in jejunum and ileum as well as a significantly greater apoptotic index in jejunum compared to sham animals. Exposure to 100% oxygen resulted in a significant increase in cell proliferation in jejunum and ileum as well as in a significant decrease in cell apoptosis in jejunum compared to air-breathing animals. In a rat model of ACS, elevated IAP decreases SMA blood flow and inhibits enterocyte turnover. Hyperoxia results in a trend toward an increase in SMA blood flow, increases enterocyte proliferation and inhibits cell death via apoptosis. These findings may have significant implications for ventilation strategies during laparoscopy.

Clinically applicable porcine model of abdominal compartment syndrome

Aggressive resuscitation in disease processes such as sepsis, peritonitis, and bowel ischemia can result in elevated intra-abdominal pressure (IAP), leading ultimately to abdominal compartment syndrome (ACS). Clinically, ACS causes organ dysfunction with oliguria, increased airway pressures, reduced oxygenation, and a fall in cardiac output (CO). There are currently no animal models that adequately mimic the complex pathophysiology associated with ACS. We have developed a clinically applicable porcine model that closely mimics the pathology seen in human patients.