Comparison of a combination of fentanyl and alfentanil with propofol in brief surgery

We studied 96 patients undergoing short gynecological procedures. Anaesthesia has been induced with fentanyl 1.5 micrograms/kg (45 patients) or alfentanil micrograms /kg (51 patients) and a hypnotic dose of propofol, and maintained with 70% N2O via facial mask. We observed a better and more rapid control of surgical analgesia with alfentanil, and an earlier recovery of postoperative psychophysical functions. Post-induction apnea has been more frequent and prolonged in the alfentanil group, but no difference in the time necessary to recover an adequate ventilation has been observed between the two groups. Alfentanil anaesthesia determined a more marked intraoperative bradycardia. By virtue of the speed of onset and the short duration of action, alfentanil is a suitable anaesthetic agent for short surgical procedures, particularly in day-stay patients.     

Reactive oxygen intermediates induce regulated secretion of von Willebrand factor from cultured human vascular endothelial cells

Exocytosis from Weibel-Palade bodies, the secretory granules of vascular endothelial cells, causes the rapid release of von Willebrand factor (vWF), an adhesive glycoprotein involved in primary hemostasis, and cell surface expression of P-selectin, a membrane protein involved in neutrophil binding. Thus, exocytosis may represent a link between hemostasis and inflammation. We investigated the effect of reactive oxygen intermediates (ROIs) on vWF secretion. Incubation of cultured endothelial cells with xanthine oxidase (XO), which generates superoxide anions (O2-), induces a potent, rapid secretory response. However, vWF release was not observed in response to H2O2. Extracellular, subendothelial vWF deposits typically seen after exocytosis from Weibel-Palade bodies were observed after exposure to XO. XO caused a rapid, sustained increase in intracellular free calcium concentration ([Ca2+]i). vWF secretion was markedly inhibited by BAPTA- AM, a cell-permeant calcium chelator. Removal of extracellular calcium did not inhibit vWF release, although the sustained phase of the [Ca2+]i increase was suppressed. These results suggest that XO-induced vWF release is mediated by the initial increase in [Ca2+]i which is caused by calcium mobilization from intracellular stores rather than by calcium influx. Exocytosis from Weibel-Palade bodies may contribute to the pathogenic effect of ROIs in atherosclerosis and inflammation.