Effects Of Perfusion Temperature Research Articles

Debulking and HIPEC for ovarian cancer: effects of perfusion temperature on morbidity and cisplatin pharmacokinetics

Background: In patients with stage III epithelial ovarian cancer (EOC), the addition of hyperthermic intraperitoneal chemoperfusion (HIPEC) to interval debulking was recently shown to improve survival compared to surgery alone. However, the added benefit of hyperthermia remains unknown. Here, we report secondary outcomes of the OvIP study (NCT02567253), a multicenter randomized trial investigating tumor tissue platinum penetration after normothermic (37°C) versus hyperthermic (41°C) chemoperfusion with cisplatin at 75 or 120 mg/m2.

Effect of perfusion temperature on glucose and electrolyte transport during hyperthermic intraperitoneal chemoperfusion (HIPEC) with oxaliplatin

Hyperthermic intraperitoneal chemoperfusion (HIPEC) with oxaliplatin is increasingly used in patients with carcinomatosis from colorectal cancer. For reasons of chemical stability, oxaliplatin can only be administered in a dextrose (D5%) solution, and this causes peroperative glucose and electrolyte shifts. Here, we examined the influence of perfusion temperature on glucose and electrolyte transport, metabolic shifts, and surgical morbidity. Patients with carcinomatosis underwent cytoreduction and HIPEC using oxaliplatin (460 mg/m(2) in D5%, open abdomen) during 30 min at 39°-41 °C. Intraperitoneal (IP) temperature was measured at three locations using thermocouple probes. The area under the temperature versus time curve (AUCt) was calculated using the trapezoid rule. The influence of perfusion temperature on surgical outcome was assessed using linear regression models and the Mann Whitney U test where appropriate. From July 2005 until March 2011, 145 procedures were performed in 139 patients with a diagnosis of CRC (70%), pseudomyxoma peritonei (11%), ovarian cancer (10%), or miscellaneous peritoneal malignancies (9%). Postoperative mortality and major morbidity were 1.4% and 26%, respectively. Higher perfusion temperature was related to more pronounced changes in serum glucose (P = 0.058), sodium (P = 0.017), and lactate (P < 0.001). The median duration of nasogastric drainage was 5 days, and this was unrelated to perfusion temperature (P = 0.76). The GI fistula rate and reoperation rate were 12.4% and 16.5% respectively; neither was related to perfusion temperature. In patients undergoing HIPEC with oxaliplatin, perfusion temperature exacerbates peroperative metabolic shifts but does not affect surgical outcome.

Effects of Perfusion Temperature on Inflammatory Response and Outcome Following Cardiopulmonary Bypass

Effects of Perfusion Temperature on Inflammatory Response and Outcome Following Cardiopulmonary Bypass

Effect of Perfusion Temperature on the Inflammatory Response During Pediatric Cardiac Surgery

Cardiopulmonary bypass (CPB) triggers the whole body inflammatory response, and it has been suggested that the degree of hypothermia may influence these responses. The aim of this prospective study was to compare the inflammatory response in children undergoing CPB for repair of congenital heart defects, randomized to mild or moderate hypothermia. We measured inflammatory markers in blood samples of thirty children with body weight less than 10 kg undergoing open heart surgery randomized to surgery at either mild (32 degrees C) or moderate (25 degrees C) hypothermia. Blood was sampled after induction of anesthesia, at skin closure, 2 hours, 24 hours, and 48 hours postoperatively. Except for an enhanced interleukin-8 response in the moderate hypothermia group, there were no differences in levels of inflammatory mediators between those with mild and those with moderate hypothermia. In contrast to the modest influence of the degree of hypothermia, long CPB time and long aortic cross-clamp time were accompanied by enhanced inflammation involving raised levels of interleukin-8 and myeloperoxidase, as well as increased leukocyte counts. Only minor differences in cytokine levels were detected between those with moderate and those with mild hypothermia during CPB. Ischemic aortic cross-clamp time and time on CBP should be as short as possible to avoid an excessive inflammatory response and possibly adverse clinical effects.

Characterization of the calcium paradox in the isolated perfused frog heart: enzymatic, ionic, contractile and electrophysiological studies

The effect of perfusion temperature and duration of calcium deprivation on the occurrence of the calcium paradox was studied in the isolated frog heart. Loss of electrical and mechanical activity, ion fluxes, creatine kinase and protein release were used to define cell damage. Perfusion was performed at 22, 27, 32, and 37 degrees C, and calcium deprivation lasted 10, 20, 30, or 40 min. At 22 degrees C and 27 degrees C even a prolonged calcium-free perfusion failed to induce a calcium paradox. After 30 min of calcium-free perfusion at 37 degrees C ventricular activity ceased and a major contraction occurred followed by an increase in resting tension. During the 15-min re-perfusion period the release of creatine kinase was 158.24 +/- 2.49 IU.g dry wt-1, and the total amount of protein lost was 70.37 +/- 0.73 mg.g dry wt-1, while lower perfusion temperatures resulted in a decreased loss of protein and creatine kinase. Ion fluxes in the perfusion effluent indicate that during re-perfusion a massive calcium influx accompanied by a potassium and a magnesium efflux, and an apparent sodium efflux, occur at a perfusion temperature of 37 degrees C after 30 min of calcium deprivation. The results suggest that the basic principles and damaging effects of calcium overloading are common to both mammalian and frog hearts.

Effects of ischemia and perfusion temperature on the synthesis of stress-induced (heart shock) proteins in isolated and perfused rat hearts

Isolated and perfused rat hearts were examined by 2-dimensional gel electrophoresis and liquid scintillation counting to determine the effect of ischemia or perfusion temperature on protein synthesis. Isolated hearts were subjected to ischemia at either 4 degrees, 20 degrees, or 30 degrees C and then perfused at 37 degrees C and radio-labeled with [3H]-leucine from 0.5 to 2.5 h of perfusion. Following 0.5 h of 4 degrees C or 0.2 h of 20 degrees C ischemia, minimal or no effect was seen by fluorography on the patterns of protein synthesis and there was no apparent synthesis of the stress-induced (heat shock) protein with Mr = 71,000 (SP71). After 4.0 h of 4 degrees C or 0.5 h of 20 degrees C ischemia, SP71 was detectable on fluorograms. After 17 h of 4 degrees C or 1 h of 20 degrees C or 30 degrees C ischemia, SP71 was a prominent spot on fluorograms; the percentage incorporation of precursor into SP71 was significantly increased and overall incorporation of precursor into protein appeared depressed. Following 17 h at 4 degrees C, during which time the buffer was continuously oxygenated, percentage incorporation of precursor into SP71 was only moderately increased, suggesting that hypoxia was responsible for the high level of SP71 synthesis. The effect of perfusion temperature was initially examined using a perfusion method which results in a moderate synthesis of SP71 at 37 degrees C between 2.5 and 4.5 h of perfusion. Fluorograms revealed synthesis of some normal proteins at all temperatures, with little or no synthesis of SP71 at 31 degrees and 34 degrees C, moderate synthesis at 37 degrees C, and intense synthesis at 40 degrees C. The percentage incorporation of precursor into SP71 and total incorporation of precursor appeared depressed at 31 degrees C and 34 degrees C, from that at 37 degrees C, while at 40 degrees C, percentage incorporation of precursor into SP71 was significantly increased but overall incorporation of precursor into protein appeared depressed. When SP71 synthesis was induced by 17 h of 4 degrees C ischemia, hearts were sensitive to a lower perfusion temperature (34 degrees C); the percent incorporation of precursor into SP71 was significantly reduced from that seen at 37 degrees C. Interestingly, the effect of prolonged ischemia on protein synthesis (increased synthesis of SP71; suppression of overall synthesis) is the same as the heat shock response seen after perfusion at 40 degrees C.