Figure 1

Disputable mechanisms of the addition of N ₂ O to the CO ₂ pneumoperitoneum impact on adhesion formation. A) Traditional mechanism of multiple severe adhesion formation, which is not related with N₂O. B) The antiadhesiogenic impact of N₂O. Metabolic pathways affected by N₂O included interactions with the cobalt atom (Co), betaine, methyltransferase, methionine synthase with increased homocysteine (Hcys) and decreased methionine [5, 6]. Then, several enzyme deficiencies can also be a pathway for decreased postsurgical adhesions such as acystathionine synthetase, tetrahydrofolate methyltransferase and 5,10-methylenetetrahydrofolate reductase (MTHFR), which catalyze the synthesis of cystathionine from Hcys [5, 6] with subsequent increased cysteine concentration, which then results in weakened collagen cross-linking [7] in the collagen network between fibroblasts; N₂O induced-oxidative stress, DNA damage [8] and apoptosis by caspase-3 activation [9] in these virgin adhesion fibroblasts with increased genome instability. C) A possible mechanism of the adhesiogenic impact of N₂O: The following changes are associated with increased Hcys concentration: shift of vascular endothelium surface from anti- to pro-coagulant status; reactivation of blood platelets; alterations of several intrinsic and extrinsic targets in the coagulation and fibrinolysis system with modification of the blood clot/fibrin clot structure; increased resistance of fibrin clot to fibrinolysis [13] with increased adhesion formation potential.