Sepsis Clinical Trial
Official title:
Effect of Thiamine on Serum Glucagon And Reactive Oxygen Species (ROS) in Perioperative Stress Response
This research is a clinical trial with a Randomized Controlled Trial (RCT) design. The purpose is to identify the effect of intravenous thiamine administration compared to normal saline placebo on glucagon levels and ROS levels in patients undergoing general anesthesia surgery
Surgery may increase postoperative cortisol and blood glucose levels. Changes in normal metabolic patterns due to surgery stimulate gluconeogenesis, glycogenolysis, proteolysis, lipolysis, and cytogenesis. These result in hyperglycemia and ketosis conditions. Surgery and anesthesia lead to an immunosuppressive effect. Increased secretion of proinflammatory cytokines may also occur after the surgery. Besides an increase in cortisol levels, surgery can also increase cytokine response and ROS production in patients who have undergone surgery under general anesthesia after 72 hours. ROS production can also be a useful indicator in assessing the severity of surgical trauma. In surgical procedures, there is an acute increase in reactive oxidative stress (ROS). This occurs when ischemia is followed by reperfusion. ROS can trigger tissue injury seen in transplantation (liver and heart), the release of aortic clamps during abdominal and thoracic aortic surgery, the release of limb tourniquets during orthopedic surgery, and reperfusion during and after cardiopulmonary bypass. There is a thiamine deficiency in 20% of patients treated in the intensive care unit (ICU). Thiamine deficiency is a source of lactic acidosis that does not seem in severe sepsis and septic shock. An imbalance between the formation and removal of free radicals causes a pathological condition called oxidative stress. However, the human body uses antioxidants to suppress these free radicals. One of the antioxidants that can reduce oxidative stress is thiamine. Previous studies proved this finding. Thiamine has also been able to significantly prevent the expression of inflammatory cytokines and chemokines, depending on NF-B induced by thromboxane and PGI2 synthase. ;
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