ClinicalTrials.gov number: NCT00273377.

This prospective, interventional observer-blinded study demonstrates that SVV obtained by APCO, using the FloTrac/Vigileo system, is not a reliable predictor of fluid responsiveness in the setting of major abdominal surgery.

We systematically evaluated the effects of test temperature and storage temperature on platelet aggregation using flow cytometry and impedance aggregometry. Aliquots of citrated whole blood from 27 healthy adult male volunteers were stored at 37 degrees C and 22 degrees C. Aliquots were subjected to impedance aggregometry in response to collagen, adenosine diphosphate, ristocetin, and arachidonic acid performed at 22 degrees C, 34 degrees C, 37 degrees C, and 40 degrees C. The expression of activated fibrinogen receptor was determined on adenosine diphosphate-activated platelets at 22 degrees C and 37 degrees C by whole blood flow cytometry using PAC-1 for fluorescent staining. Aggregation induced by collagen, ristocetin, and arachidonic acid was not significantly different at the test temperatures of 34 degrees C and 37 degrees C but was significantly impaired at 22 degrees C. In contrast, adenosine diphosphate-induced aggregation was significantly increased at both 34 degrees C and 22 degrees C. Hyperthermia exclusively impaired collagen-induced aggregation. Storage temperature of 22 degrees C exclusively enhanced adenosine diphosphate- and collagen-induced aggregation compared with storage at 37 degrees C. The binding of PAC-1 was enhanced at test temperatures below 37 degrees C. Prewarming the antibody above 22 degrees C significantly decreased binding. Our results suggest that mild hypothermic test conditions have no relevant effect, whereas profound hypothermia induces defects in adhesion, thromboxane generation, and activation. The pathomechanism for the increased response to adenosine diphosphate at mild and profound hypothermia remains unclear. Storage temperature considerably affects the aggregation response to the agonists adenosine diphosphate and collagen but not to arachidonic acid and ristocetin. Flow cytometry using the temperature-labile antibody PAC-1 fails to assess temperature effects on platelet aggregability.

Introduction:Zonulin is a eukaryotic protein structurally similar to Vibrio cholerae’s zonula occludens toxin. It plays an important role in the opening of small intestine tight junctions. The loss of gut wall integrity during sepsis might be pivotal and has been described in various experimental as well as human studies. Increased levels of zonulin could be demonstrated in diseases associated with increased intestinal inflammation, such as celiac disease and type 1 diabetes. We therefore investigated the role of plasma levels of zonulin in patients with sepsis as a non-invasive marker of gut wall integrity.Materials and methods:Plasma level of zonulin was measured in 25 patients with sepsis, severe sepsis or septic shock according to ACCP/SCCM criteria at the first day of diagnosed sepsis. 18 non-septic post-surgical ICU-patients and 20 healthy volunteers served as control. Plasma levels were determined by using commercially available ELISA kit. Data are given as median and interquartile range (IQR).Results:Significantly higher plasma concentration of zonulin were found in the sepsis group: 6.61 ng/mL (IQR 3.51–9.46), as compared to the to the post-surgical control group: 3.40 ng/mL (IQR 2.14–5.70) (P = 0.025), as well as to the healthy group: 3.55 ng/mL (IQR 3.14–4.14) (P = 0.008).Conclusion:We were able demonstrate elevated levels of plasma zonulin, a potential marker of intestinal permeability in septic patients. Increased zonulin may serve as an additional mechanism for the observed increased intestinal permeability during sepsis and SIRS.