An average human body contains 15 g of hyaluronan, which is unevenly distributed and mostly found in the skin (56%), skeleton and connective tissues (27%). HMW-HA is very hygroscopic and one gram can bind up to 6 l of water. The functional effects of hyaluronan are size dependent high molecular weight hyaluronan (HMW-HA > 500 kDa) is anti-inflammatory, whereas fragmented hyaluronan is pro-inflammatory and pro-angiogenic. Hyaluronan is a long non-sulfated polysaccharide composed of repeated disaccharide units of glucuronic acid and N-acetyl-glucosamine with a molecular weight that extends up to several million Daltons. The exact mechanisms leading to or any potential consequences of high plasma hyaluronan are poorly understood. Plasma concentrations of hyaluronan are up to twenty times higher in septic patients compared with healthy individuals and correlate with organ dysfunction and mortality. Current therapeutic options are limited and treatment is mainly based on early detection, broad-spectrum antibiotics, fluid resuscitation, vasopressors and organ support. The pathophysiology is complex and still largely unknown making sepsis a challenge for clinicians and researchers alike. Sepsis is a life-threatening syndrome with high incidence, morbidity and mortality. The results suggest that plasma HYAL does not act as sheddase in sepsis or pancreatitis. In acute pancreatitis, effective plasma HYAL activity was decreased which was not associated with increased plasma hyaluronan concentrations or endogenous HYAL inhibition. ConclusionĮlevated plasma hyaluronan levels coincided with a concomitant decrease in effective plasma HYAL activity and increase of endogenous plasma HYAL inhibition both in experimental and clinical sepsis. Effective plasma HYAL was lower in septic shock and acute pancreatitis as compared to healthy volunteers, while plasma HYAL inhibition was only increased in septic shock. Plasma hyaluronan increased in patients with septic shock but not in acute pancreatitis. coli porcine sepsis and in time controls, plasma hyaluronan increases with concomitant decrease in effective plasma HYAL activity and increase of endogenous HYAL inhibition. coli 1 × 10 8 CFU/h of 6 h followed by 1 × 10 9 CFU/h of the remaining 6 h ( n = 5) or Control with no E. Sixteen pigs were allocated (unblinded, open label) into three groups: Sepsis-1 with infusion of live Escherichia coli ( E. Plasma hyaluronan, effective HYAL activity and HYAL inhibition were measured in healthy volunteers ( n = 20), in patients with septic shock ( n = 17, day 1 and day 4), in patients with acute pancreatitis ( n = 7, day 1 and day 4) and in anesthetized and mechanically ventilated pigs ( n = 16). We specifically hypothesized that plasma HYAL acts as endothelial glycocalyx shedding enzyme, sheddase. In this study we evaluate the roles of plasma hyaluronan, effective plasma hyaluronidase (HYAL) activity and its endogenous plasma inhibition in clinical and experimental sepsis. Plasma hyaluronan concentrations are increased during sepsis but underlying mechanisms leading to high plasma hyaluronan concentration are poorly understood.
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