Surgery is associated with release of local and systemic mediators which influence vascular and tissue homeostasis. The post-surgical release of acute phase reactants, particularly IL-6 and CRP, is reduced in minimally invasive surgery, compared with conventional surgery. Additionally, there is emerging evidence that leukocytes and Reactive Oxygen Species (ROS) are affected differentially by minimally invasive surgery.
ROS and mediators of oxidative stress influence vascular endothelium, organ perfusion and angiogenesis, and may be critical determinants of survival and outcome. ROS also influence cell proliferation and cell death and have been implicated in neoplastic signalling. Advances in ROS detection and oxidative stress signalling have shown cellular changes affected by minimally invasive surgery. It has been observed that the invasiveness of surgery is proportional to changes in phagocyte and lymphocyte ROS. A potential role for ROS signalling in the immune system is suggested by evidence of closer ROS/leukocyte correlation in patients undergoing minimally invasive surgery. At lower ROS levels, phagocyte and lymphocyte ROS following minimally invasive surgery implicate a homeostatic response with closer leukocyte/ROS correlations, whereas higher ROS in open surgery and greater leukocyte depletion indicate more cytotoxic signalling.
Interactions between humoral and cellular elements suggest that an integrated systems approach, using individual patient responses, should be used to analyse the response to surgical trauma and oxidative stress. These studies are being used to investigate ROS as biomarkers of the effects of surgery on vascular and pulmonary reactivity. ROS signalling may provide insights into post surgical trauma and its underlying pathology.