Objective To summarize the research progress of CO2 pneumoperitoneum impacts on invasiveness of cancer cells. Methods Currently published experimental and clinical researches related to the effect of CO2 pneumoperitoneum on invasiveness of cancer cells were reviewed. Results CO2 pneumoperitoneum may affect the invasiveness of cancer cell through several ways， such as changing the structure and function of mesothelial cell， changing microenvironment of peritoneum， influencing the expression of oncogen， affecting the secretion of cell factor， and changing the adhesion of cancer cell. Conclusions The consequences of these alterations to cancer cell and the microenvironment are not well understood， but they may facilitate tumor invasion and implantation. Further investigations in this area are very urgent.
Objective To study whether carbon dioxide used to establish pneumoperitoneum has an influence on port-site and intraperitoneal implantation and metastasis of tumor cells. Methods R15 hepatic cancer cells were injected into 30 Wistar rats’ peritoneal cavities 1 hour before operation, then the 30 Wistar rats were randomly divided into 3 groups: gasless group, helium group and carbon dioxide group. The suspension was exposed to the gas environment for 2 hours, all animals were killed after 28 days and the port-site and intraperitoneal implantation and metastasis of tumor cells were examined. Results On port-site, intestinal serous coat, mesentery, greater omentum and diaphragm, the weights of tumor cells, in carbon dioxide group were (326.7±230.3) mg， （626.2±215.9） mg，（476.2±204.8） mg，（2 536.5±906.7） mg and （384.5±149.9） mg respectively； in helium group were (235.6±107.3) mg， （414.2±148.4） mg, （261.8±92.6） mg, （1 633.4±247.3） mg and（220.0±57.9） mg； in gasless group were (145.0±42.4) mg， （221.5±108.2） mg， （212.5±109.6） mg, （797.5±335.9） mg and 113.0 mg.The weights of carbon dioxide group showed a significant increase, compared with helium group and gasless group (P＜0.05). The weights of helium group were greater than gasless group，but there was no significance in statistics (Pgt;0.05). Conclusion The insufflation of carbon dioxide promotes intraperitoneal tumor implantation and growth compared with helium and gaslessness in a rat model.
Objective To investigate the effect of CO2 pneumoperitoneum on the tumor cell port site implantation in laparoscopic surgery. Methods Male SpraqueDawley rats were intraperitoneally injected with gastric cancer cells (cell line SGC-7901). Continuous CO2 pneumo of 15 mm Hg or 30 mm Hg were established for 5 mins, 60 mins, 120 mins and 180 mins with the injection of different concentrations of tumor cells (104/ml, 106/ml respectively). Several samples of peritoneal washing served as positive control. All collecting dishes were incubated at 37℃ with 5% CO2 concentration for one week and then examined for the presence of tumor cell under microscope. Results After one week of incubation, some of the dishes with continuous flow of CO2 gas (5 L/min) at pneumo 30 mm Hg for 60 mins or longer demonstrated tumor growth, and all peritoneal washing samples showed tumor growth, while other dishes showed negative. Conclusion The research suggests that gastric cancer cells can cause port site implantation and the concentration of tumor cells, pneumoperitoneum pressure and duration may affect the occurrence of port site implantation. It may help to find a suitable way to prevent the port site implantation in operations.
ObjectiveTo investigate the changes of peritoneal macrophages function of mice with gastric cancer in the CO2 pneumoperitoneum environment, as well as its effect on the peritoneal metastasis of gastric cancer. MethodsAn orthotopic implantation model of mouse forestomach cancer was established using the 615 mouse. The mice bearing tumors were randomly divided into five groups (n=30): anesthesia alone, laparotomy, and 2, 4, and 6 mm Hg CO2 insufflation groups. Peritoneal macrophages were collected from six mice in each group and cultured. The macrophage phagocytic function on neutral red and the levels of NO and TNF-α produced by macrophages were measured after 12, 24, 48, and 72 h of culture. The remaining mice were observed after two weeks for the rate of peritoneal metastasis of forestomach cancer cells and the total weight of implanted nodules. ResultsNo death and ascites were found and the difference of weight body was not significant in all mice (Pgt;0.05). The uptake of neutral red by peritoneal macrophages and the levels of NO and TNF-α secreted by peritoneal macrophages in the laparotomy group after 12 h of culture were all significantly higher than those in other four groups (Plt;0.05). The corresponding values in the 2, 4， and 6 mm Hg CO2 insufflation groups after 12 h were all significantly lower than those in the anesthesia alone group (Plt;0.05). Among three insufflation groups, the corresponding values in the 2 mm Hg after 12 h were significantly higher than those in the 4 and 6 mm Hg CO2 insufflation group, though the difference in the two latter was not significant (Pgt;0.05). The uptake of neutral red by peritoneal macrophages and the levels of NO and TNF-α secreted by peritoneal macrophages in the 6 mm Hg CO2 insufflation group after 24 h of culture were all significantly lower than those in other four groups (Plt;0.05), while the difference in the four groups was not significant (Pgt;0.05). The uptake of neutral red by peritoneal macrophages and the levels of NO and TNF-α secreted by peritoneal macrophages after 48 h and 72 h were not significantly different in the five groups (Pgt;0.05). The rate of peritoneal metastasis of mice was significantly lower in the 6 mm Hg insufflation CO2 group (75.0%, 15/20) than that in the anesthesia alone group (100%, 24/24), Plt;0.05, but higher than other three groups(Plt;0.05), which was not different in 2 mm Hg (47.8%, 11/23), 4 mm Hg insufflation group (45.45%, 10/22) and laparotomy group (50.0%, 10/20), Pgt;0.05. The total weight of implanted nodules of mouse forestomach cancer was (1.24±0.48) g, (1.02±0.38) g, (0.96±0.33) g, (0.93±0.45) g, and (1.18±0.37) g in the anesthesia alone group, the laparotomy group, and 2, 4, and 6 mm Hg CO2 insufflation group, and the difference was not significant (Pgt;0.05). ConclusionHigh pressure (6 mm Hg) CO2 pneumoperitoneum can constantly inhibit the phagocytosis and cytokine secretion functions of peritoneal macrophages in gastric cancer-bearing mice and promote peritoneal implantation of gastric cancer.
Objective To examine the effects of carbon dioxide (CO2) pneumoperitoneum on local pancreas pathological changes, serum levels of amylase, IL-1, IL-6, and the positive rate of dissolubility adhesion molecule (CD11a/CD18 and CD11b/CD18) expression in rats with severe acute pancreatitis (SAP). Methods Fifty healthy male SpragueDawley (SD) rats were randomly divided into 3 groups: CO2 pneumoperitoneum group (n=20): SAP was induced by injecting 5% sodium taurocholate through retrogradely common biliopancreatic ducts via duodenal papilla， and then CO2 pneumoperitoneum was established at a pressure of 12 mm Hg (1 mm Hg=0.133 kPa) for 30 min; SAP group (n=20): The rats were treated as same as CO2 pneumoperitoneum group, except CO2 pneumoperitoneum； Simple operation group (n=10): Laparotomy was performed and nothing was done to duodenum and pancreas except for moving them softly. The blood samples were collected for examining serum levels of amylase, IL-1, IL-6, and the positive rates of CD11a/CD18 and CD11b/CD18 expression, and histopathologic examination of pancreas was performed. Results Compared with simple operation group, the pancreatic pathologic histology score, serum levels of amylase, IL-1, IL-6, and the positive rates of CD11a/CD18 and CD11b/CD18 expression were significantly higher in CO2 pneumoperitoneum group and SAP group (P=0.000). The levels of IL-1 and IL-6 were significantly lower in CO2 pneumoperitoneum group as compared to SAP group (P=0.000). There was no significant difference between CO2 pneumoperitoneum group and SAP group in pancreatic pathologic histology score (P=0.294), the level of serum amylase (P=0.073), the positive rates of CD11a/CD18 (P=0.155) and CD11b/CD18 expression (P=0.201). Conclusion CO2 pneumoperitoneum has inhibitory effect on the levels of IL-1 and IL-6, rather than the positive rates of CD11a/CD18 and CD11b/CD18 expression in SD rats with SAP.
Objective To investigate the influence of different pressures and duration of CO2 pneumoperitoneum on the adhesive and invasive ability of gastric cancer cells based on the expressions of adhesive and invasive molecules. Methods With an artificial CO2 pneumoperitoneum model in vitro, human gastric cancer cell lines including MKN-45, SGC-7901, and MKN-28 were exposed to CO2 in different environments: 0 mm Hg （1 mm Hg=0.133 kPa）, 9 mm Hg （2 h, 4 h）, and 15 mm Hg （2 h, 4 h）. The expressions of mRNA of E-cadherin, intercellular adhesion molecule-1 (ICAM-1), matrix metalloproteinase-2 (MMP-2), and vascular endothelial growth factor-A (VEGF-A) in the different environments were measured by RT-PCR. The expressions of protein of E-cadherin and ICAM-1 in the environments of 0 mm Hg and 15 mm Hg （4 h） were measured by FCM. Results With the increase of duration or pressure, RT-PCR showed that there was a downward trend in the expression of E-cadherin mRNA as well as there were upward trends in the expressions of ICAM-1, MMP-2, and VEGF-A mRNA; FCM showed that there was a downward trend in the expression of E-cadherin protein while the expression of ICAM-1 protein showed the opposite change. But there were no obvious differences under different environment (P＞0.05). Conclusions Under low pressure (≤15 mm Hg) and short time (≤4 h) of CO2 pneumoperitoneum, the adhesive and invasive ability of gastric cancer cells could not be affected, which means that under this environment, CO2 pneumoperitoneum will not increase the possibility of neoplasm metastasis.