47: Proinflammatory cytokines and splanchnic blood flow in acute pancreatitis

Abstract

Changes in splanchnic arteries in acute necrotizing pancreatitis are the consequence of the release of proinflammatory cytokines and vasoactive mediators that attract white blood cells in the pathological process and activate vascular endothelium. All this leads to endothelial and microcirculating dysfunction. Disorders of microcirculation are a major step from mild (preserved microcirculation, edematous pancreatitis) to severe disease. Experimental and clinical observations suggest that proinflammatory cytokines and oxidative stress involved in the development of local and systemic complications especially in patients with acute necrotizing pancreatitis. We examined 53 patients with acute pancreatitis and 14 healthy volunteers. According to the criteria of Atlanta (1992) in 28 patients diagnosed severe acute pancreatitis, in 25 – mild. We studied the serum levels of proinflammatory (IL-6, IL-18) cytokines in patients with acute pancreatitis. In patients with acute pancreatitis on admission identified an increase in interleukin-6 and interleukin-18. A significant increase of both pro-inflammatory cytokines determined only in severe acute pancreatitis. There was a significant direct correlation concentrations of IL-6 with peak systolic velocity in the superior mesenteric artery (R = 0.502941, p = 0.047063), with an index of resistance in common hepatic (R = 0.532845, p = 0.033574), splenic (R = 0.511125, p = 0.043028) and superior mesenteric (R = 0.563200, p = 0.023107) arteries. The level of IL-18 was significantly correlated with peak systolic velocity in the common hepatic artery (R = 0.589102, p = 0.016342), splenic artery (R = 0.547865, p = 0.028022) and superior mesenteric artery (R = 0.504783, p = 0.046131), as well as the resistance index in the common hepatic artery (R = 0.524375, p = 0.037051) and superior mesenteric artery (R = 0.573230, p = 0.020271). In patients with acute necrotizing pancreatitis were significant disturbances in microcirculation, resulting vasospasm and endothelial dysfunction resulting from exposure to high concentrations of proinflammatory cytokines.