Effect of Pneumoperitoneum on Oxidative Stress and Inflammation via the Arginase Pathway in Rats

Abstract

PurposeOxidative stress during CO2 pneumoperitoneum is reported to be associated with decreased bioactivity of nitric oxide (NO). However, the changes in endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), and arginase during CO2 pneumoperitoneum have not been elucidated.Materials and MethodsThirty male Sprague-Dawley rats were randomized into three groups. After anesthesia induction, the abdominal cavities of the rats of groups intra-abdominal pressure (IAP)-10 and IAP-20 were insufflated with CO2 at pressures of 10 mm Hg and 20 mm Hg, respectively, for 2 hours. The rats of group IAP-0 were not insufflated. After deflation, plasma NO was measured, while protein expression levels and activity of eNOS, iNOS, arginase (Arg) I, and Arg II were analyzed with aorta and lung tissue samples.ResultsPlasma nitrite concentration and eNOS expression were significantly suppressed in groups IAP-10 and IAP-20 compared to IAP-0. While expression of iNOS and Arg I were comparable between the three groups, Arg II expression was significantly greater in group IAP-20 than in group IAP-0. Activity of eNOS was significantly lower in groups IAP-10 and IAP-20 than in group IAP-0, while iNOS activity was significantly greater in group IAP-20 than in groups IAP-0 and IAP-10. Arginase activity was significantly greater in group IAP-20 than in groups IAP-0 and IAP-10.ConclusionThe activity of eNOS decreases during CO2 pneumoperitoneum, while iNOS activity is significantly increased, a change that contributes to increased oxidative stress and inflammation. Moreover, arginase expression and activity is increased during CO2 pneumoperitoneum, which seems to act inversely to the NO system.

Interaction of AR and iNOS in lens epithelial cell: A new pathogenesis and potential therapeutic targets of diabetic cataract

“…The FRET efficiencies were calculated by curve fitting analysis of Cy3 fluorescence changes. The interaction distance between the donor and the acceptor (R) was calculated using the equation [40]: E -1 = 1+ (R/R0) 6 , wherein R0 is the Foster distance when the energy transfer efficiency between donor and acceptor is 50%, and R represents the actual distance between donor and acceptor. The FRET efficiency formula is as follows [41]: 2Where I DD is the fluorescence intensity of the donor channel under the excitation wavelength of the donor before bleaching, is the fluorescence intensity of the donor channel after donor excitation, and the PB denotes the degree of bleaching.…”

“…In Figure 6, the energy transfer rate of transfection group was 38.37 ± 4.76 %, compared with the control group at 4.23 ± 1.04 %, with significant differences (p < 0.01). We computed the energy transfer rate using the formula E -1 = 1+ (R / R0) 6 to calculate the interaction distance between AR and iNOS, as shown in Figure 7. The transfection group distance R was 6.50 ± 0.22 nm, and compared with the control group distance R was 10.14 ± 0.44 nm; the differences were statistically significant (p < 0.01).…”

“…It is well known that the major recognized pathogenesis of DC is polyol pathway, oxidative stress pathway and glycosylation pathway [5][6][7]. In polyol pathway, the intracellular increase of fluid in response to AR-mediated accumulation in LEC makes lens with complex biochemical changes ultimately leading to cataract formation; in oxidative stress pathway, diabetic lenses show an impaired antioxidant capacity, a susceptibility to oxidative stress, and inactivation of lens antioxidant enzymes like superoxide dismutases or activation of iNOS leads to the oxidative stress of lens; in glycosylation pathway, the increased glucose levels in lens induce glycation of lens proteins and result in generation of superoxide radicals and advanced glycation end products (AGE) in this process [8][9][10].…”

“…Aldose reductase (AR) is a key enzyme in polyol pathway, leads to accumulation of sorbitol and changes of intracellular osmotic pressure, which damages the LEC eventually [5,11,13]. And inducible nitric oxide synthase (iNOS), an isoform of nitric oxide synthase, catalyzes the oxidation of L-arginine, and the expression of iNOS in LEC can bring a lot of NO, further activates the oxidative stress response to damage LEC [6,12,[14][15]. In LEC, AR and iNOS are both up regulated with hyperglycemia in DC [16][17][18].…”

Effects of propofol on the inflammatory response during robot-assisted laparoscopic radical prostatectomy: a prospective randomized controlled study

“…Compared with conventional open surgery, laparoscopic surgery is associated with smaller incisions, reduced intraoperative bleeding, and lesser postoperative pain; however, it may result in increased trauma due to peritoneal insufflation and increased intra-abdominal pressure. In addition, hemodynamic changes and the presence of CO 2 may further contribute to inflammation and oxidative stress during pneumoperitoneum, which result in acute-phase responses such as the release of proinflammatory cytokines and acute-phase proteins 16–20 . Postoperative increases in inflammatory markers, including cytokines and CRP, are associated with tissue damage, postoperative morbidity, and cancer recurrence 21–23 .…”