Prevention of postoperative bleeding after complex pediatric cardiac surgery by early administration of fibrinogen,prothrombin complex and platelets: a prospective observational study

Some retrospective and in vitro studies suggest that general anesthetics influence breast cancer recurrence and metastasis. We compared the effects of general anesthetics sevoflurane versus propofol on breast cancer cell survival, proliferation and invasion in vitro. The investigation focused on effects in intracellular Ca2+ homeostasis as a mechanism for general anesthetic-mediated effects on breast cancer cell survival and metastasis. Estrogen receptor-positive (MCF7) and estrogen receptor-negative (MDA-MB-436) human breast cancer cell lines along with normal breast tissue (MCF10A) were used. Cells were exposed to sevoflurane or propofol at clinically relevant and extreme doses and durations for dose- and time-dependence studies. Cell survival, proliferation and migration following anesthetic exposure were assessed. Intracellular and extracellular Ca2+ concentrations were modulated using Ca2+ chelation and a TRPV1 Ca2+ channel antagonist to examine the role of Ca2+ in mediating anesthetic effects. Sevoflurane affected breast cancer cell survival in dose-, time- and cell type-dependent manners. Sevoflurane, but not propofol, at equipotent and clinically relevant doses (2% vs. 2 μM) for 6 h significantly promoted breast cell survival in all three types of cells. Paradoxically, extreme exposure to sevoflurane (4%, 24 h) decreased survival in all three cell lines. Chelation of cytosolic Ca2+ dramatically decreased cell survival in both breast cancer lines but not control cells. Inhibition of TRPV1 receptors significantly reduced cell survival in all cell types, an effect that was partially reversed by equipotent sevoflurane but not propofol. Six-hour exposure to sevoflurane or propofol did not affect cell proliferation, metastasis or TRPV1 protein expression in any type of cell. Sevoflurane, but not propofol, at clinically relevant concentrations and durations, increased survival of breast cancer cells in vitro but had no effect on cell proliferation, migration or TRPV1 expression. Breast cancer cells require higher cytoplasmic Ca2+ levels for survival than normal breast tissue. Sevoflurane affects breast cancer cell survival via modulation of intracellular Ca2+ homeostasis.     

Über den Peroxydasetransport im Darmepithel der Ratte

Zusammenfassung Bei Ratten tritt 3 min nach intravenöser Injektion von Peroxydase elektronenmikroskopisch ein entsprechendes Reaktionsprodukt im Kapillarlumen der Lamina propria des Dünndarms und an der Basalmembrangrenze der Saumepithelzellen auf. 5 min nach der Injektion finden sich im basalen Abschnitt des Darmepithels pinozytotische Bläschen mit dem Peroxydase-Reaktionsprodukt. — 10–30 min nach der Injektion erreichen die Partikel die apikalen Teile der Zelle. Sie dringen in den interzellulären Spalten bis zu den Haftplatten vor, erreichen jedoch nie das Darmlumen. Im Dünndarm existiert vermutlich auch ein der Resorption entgegengesetzter Saftstrom, der durch Peroxydase markiert werden kann.

---

The transport of horseradish peroxidase in the epithelium of the small intestine

Summary In rats, 3 minutes after intravenous injection of peroxidase the reaction product can be observed electronmicroscopically in the lumina of the capillaries of the small intestine as well as at the border of the basement membrane of the epithelial border cells. Pinocytotic vesicles containing peroxidase particles occur in the basal portion of the epithelium of the small intestine 5 minutes after injection. 10–30 minutes later, the peroxidase reaches the apical region of the cell. The particles infiltrate into the intercellular spaces as far as the tight junctions but never reach the intestinal lumen. In the small intestine there probably exists a flow of fluid in opposite direction to the resorption, which can be marked by peroxidase.

     

Different modulation of the perioperative stress hormone response under neurolept-anaesthesia or enflurane for cholecystectomy.

Two groups of 13 patients, randomly allocated to receive either enflurane or neurolept anaesthesia for cholecystectomy, were compared in their cardiovascular and neuroendocrine response to surgery and in the postoperative period. There were no significant differences in blood pressure or heart rate. Catecholamine values were higher under neurolept anaesthesia towards the end of surgery and postoperatively. Median values for adrenaline during suture of peritoneum were 342 pg/ml and 88 pg/ml, respectively, P less than 0.05. In contrast, ACTH and cortisol rose to higher levels in enflurane treated patients. At the end of surgery median ACTH values were 75 pg/ml in NLA patients and 322 pg/ml in enflurane patients (P less than 0.01). Vasopressin increments during surgery were similar under both regimens, while prolactin was higher following induction of neurolept anaesthesia. It is discussed whether the differences in stress hormone secretion patterns under either form of anaesthesia reflect different stress protective properties or direct pharmacological effects of certain anaesthetics. We conclude that the hormonal stress response to surgery is critically dependent on the type of anaesthesia and may be discordant in different hormonal systems.