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.
The purpose of this study was to compare the air handling capability of five currently used membrane oxygenators: the Avecor Affinity, the Bentley SpiralGold, the Medtronic Maxima Plus, the Sarns Turbo and the Sorin Monolyth M. A circuit was constructed to include a hardshell venous reservoir and roller pump. Pressure monitoring sites and ultrasonic microbubble detection probes were located proximal and distal to the oxygenator. An air injection/infusion site was provided proximal to the roller pump inlet. Each circuit was primed with fresh anticoagulated bovine blood, adjusted to a haematocrit of 25% and maintained at 38 +/- 1 degree C. Three different bolus amounts of air (10, 20 and 40 cm3) were injected at three blood flow rates (3, 4.5 and 6 l/min). A 1-min infusion of air delivered at 1 ml/s was also administered at three blood flow rates (3, 4.5 and 6 l/min). The hardshell reservoir was also completely emptied at each flow rate to simulate a massive air infusion. At any given blood flow, outlet microbubble counts were usually higher with greater bolus amounts of air. When indexed to the inlet bubble counts, the following average percent microbubbles were released from the outlet: Turbo 25%, Affinity 7%, Monolyth 5%, Maxima 3% and SpiralGold 1%. With a constant air infusion of 1 ml/s, greater outlet microbubble counts were associated with higher blood flow rates. Again, when indexed to the inlet bubble counts, the following average percent microbubbles were released from the outlet: Turbo 44%, Affinity 25%, Maxima 19%, Monolyth 16% and SpiralGold 0%. All oxygenators deprimed when the hardshell reservoir was emptied and all shed microbubbles into the outlet blood except the SpiralGold. The results of this study indicate that air handling is not a simple function of blood flow pattern (i.e. top to bottom versus bottom to top), but also includes dynamics associated with oxygenator design, fibre arrangement and flow resistance.
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