The abnormal conditions to which blood is subjected during cardiopulmonary bypass (CPB) trigger an activation of the inflammatory response in all patients to varying degrees. Both complement activation and the release of cytokines characterize this response. Most inflammatory mediators have a molecular weight that is below the membrane pore size of commonly used ultrafilters, which should allow them to be freely filtered. However, some mediators have been shown to fail to cross through the membrane even though they are small enough to cross. The purpose of the present study was to determine whether certain inflammatory mediators could be removed by ultrafiltration when performed during the rewarming phase of CPB. Thirty adult patients undergoing a single, open-heart procedure were randomized to either control (no ultrafiltration) or to the zero-balance ultrafiltration (ZBUF) group. ZBUF was performed by removing 3 l/m2 blood using a 65-kDa ultrafilter with 1.3-m2 surface area. A volume of a balanced salt crystalloid solution (Plasmalyte) equal to the filtered blood volume was given to replace the fluid removed. Patient data was taken before CPB (T1), immediately following CPB (T2), and 12 h following the procedure (T3). The average volume of filtrate removed during ZBUF was 6405 ml, which was analyzed for the presence of interleukin (IL)-1, IL-6, tumor necrosis factor-alpha (TNF-alpha), C3a, and C5a. The average concentrations of the mediators measured in the effluent were: IL-1, 0.17 pg/ml; IL-6, 0.64 pg/ml; TNF-alpha, 1.25 ng/ml; C3a, 782.6 ng/ml; C5a, 25.6 ng/ml. In every case except for IL-1, the amounts of mediators removed were significantly greater than zero. This study demonstrates that ultrafiltration is a strategy that can be used during CPB in the adult to remove significant amounts of inflammatory mediators.

Use of hyperthermia in the treatment of cancer and viral infection has received renewed interest. However, the in vivo relationship between hyperthermia and direct versus indirect effects upon hemostasis are incompletely defined, although we do know that disseminated intravascular coagulation (DIC) is a common sequel to heat stroke. The purpose of the present study was to more precisely define the relationship between hyperthermia and derangements of hemostasis, thereby providing a guideline for the development of safe hyperthermia treatment regimens. The present investigation examined the in vivo effects of high-grade whole-body hyperthermia (WBH) (42.5 degrees C, 90 min) on hemostasis in a canine model. Induction of hyperthermia via extracorporeal circulation of heated blood (ECC-WBH) caused thrombocytopenia, increased plasma fibrin degradation products (FDPs), prolonged clotting times, increased serum liver enzymes, and evidence of spontaneous bleeding. However, when WBH was induced by peritoneal lavage (PL-WBH), transient thrombocytopenia was the only significant alteration. Temporal correlation between hemostatic alterations and elevations in serum alanine aminotransferase (ALT) levels in the ECC-WBH treatment group suggested that liver injury is responsible, at least in part, for the coagulopathy associated with high-grade hyperthermia and that in the absence of liver injury, identical degrees of hyperthermia cause only incidental decreases in platelet numbers.

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