ABSTRACT
OBJECTIVE: To determine the main trigger mechanisms of multiple organ failure in acute severe pancreatitis. MATERIAL AND METHODS: An experimental study included 26 dogs with pancreatic necrosis. We assessed homeostasis disorders and functional changes in the pancreas, bowel, liver, kidneys, lungs and heart. Forty-six patients with severe acute pancreatitis were examined. We studied homeostasis disorders and functional state of the organs, endotoxemia, lipid peroxidation, phospholipase activity, coagulation system and hypoxia. RESULTS: Injury of various organs and systems due to systemic inflammatory response at the early stage of disease is an important aspect in progression of acute pancreatitis. Membrane destabilizing phenomena and disturbances in tissue component of coagulation system are the most significant factors. Patients with severe acute pancreatitis had significant changes in homeostasis. We distinguished two subgroups of patients. The course of disease was different. In the first subgroup, changes in homeostatic parameters were 15.4-24.2% less than in the second subgroup. This largely determined treatment outcomes as a whole. In the first subgroup, therapy was effective in most cases, in the second one - less effective that required surgical interventions. In the first subgroup, mortality and hospital-stay were less compared to the second subgroup. CONCLUSION: Oxidative stress, hypoxia, activation of phospholipases, and coagulation abnormalities are important in the development of systemic inflammatory response syndrome following acute pancreatitis. These factors are triggers for a cascade of the same kind of pathophysiological phenomena contributing to multiple organ failure and pancreatitis. In the tissues of various organs, proportional growth of these markers is observed until the 6th day, while in the blood - until the 4th day.
Subject(s)
Multiple Organ Failure , Pancreatitis, Acute Necrotizing , Systemic Inflammatory Response Syndrome , Animals , Disease Progression , Dogs , Homeostasis , Humans , Multiple Organ Failure/etiology , Multiple Organ Failure/physiopathology , Pancreatitis, Acute Necrotizing/complications , Pancreatitis, Acute Necrotizing/diagnosis , Pancreatitis, Acute Necrotizing/physiopathology , Systemic Inflammatory Response Syndrome/etiology , Systemic Inflammatory Response Syndrome/physiopathologyABSTRACT
Combined application of photohemotherapy and antihypoxant reamberin for the treatment of endogenous intoxication favors fast (within one day) restoration of the functional condition of lungs and prevents the development of respiratory distress syndrome. High efficiency of the combined therapy is related to a fast stabilization of membranes, which is determined by the ability to correct lipid metabolism in lung tissues.
Subject(s)
Lipid Metabolism/drug effects , Lung/metabolism , Meglumine/analogs & derivatives , Pancreatitis, Acute Necrotizing/drug therapy , Respiratory Distress Syndrome/prevention & control , Succinates/pharmacology , Animals , Disease Models, Animal , Dogs , Female , Lung/physiopathology , Male , Meglumine/pharmacology , Pancreatitis, Acute Necrotizing/blood , Pancreatitis, Acute Necrotizing/complications , Pancreatitis, Acute Necrotizing/physiopathology , Photochemotherapy/methods , Respiratory Distress Syndrome/blood , Respiratory Distress Syndrome/etiology , Respiratory Distress Syndrome/physiopathologyABSTRACT
This clinico-laboratory study showed that antihypoxant remaxol promoted normalization of lipid metabolism in acute peritonitis and significantly reduced membrane-destabilizing events. This resulted in rapid elimination of the inflammatory process in the abdominal cavity and lowering of the intensity of endogenous intoxication. This beneficial effect decreased the severity of myocardial lesions and resulted in the normalization of erythrocyte function. It is concluded that the regulatory action of remaxol on lipid metabolism is due to its ability to control free radicals in lipid peroxidation and reduce phospholipase A2 activity.
