The Microcirculation in Trauma and Sepsis
Abstract: The microcirculation plays a vital part for fluid-, gas- and solute-exchange, and changes in permeability during trauma or sepsis, that are in part necessary for the natural healing process, may also cause hypovolemia and edema formation, leading to disturbances in microvascular exchange. This thesis discusses changes is microvascular flow, permeability and plasma volume (PV) loss after experimental or surgical trauma and experimental sepsis. We evaluated the effect of blunt skeletal muscle trauma itself and thereafter treatment with prostacyclin (PGI2) on PV-loss, transcapillary escape rate (TER) of 125I-albumin and cytokine release. In experimental sepsis, we studied the importance of charge for microvascular permeability and observed the effectiveness of albumin versus Ringer's acetate compared to a hemorrhage model. Perioperatively, we evaluated changes in the sublingual microcirculation in patients undergoing major abdominal surgery, using Sidestream Darkfield-imaging (SDF) in relation to outcome. Skeletal muscle trauma caused PV-loss, increase in permeability and cytokine release and PGI2-treatment attenuated these changes. Sepsis led to a breakdown of the negatively charged glycocalix, which is probably important for the normally low permeability of albumin. The plasma volume expanding effect of albumin as compared to Ringer's acetate was independent of the state of permeability. Perioperative changes in the sublingual microcirculation during major abdominal surgery are minor with no correlation to outcome or parameters reflecting global oxygen delivery.
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