Propofol suppresses prostaglandin E(2) production in human peripheral monocytes.

Prostaglandin E(2) secreted from monocytes/macrophages plays important roles in immunity and in inflammation. Currently, propofol, an intravenous anesthetic, is the most widely used drug for the anesthesia and sedation of patients, including those who are vulnerable to infection and/or immunosuppression. Here we report that propofol suppressed prostaglandin E(2) production in lipopolysaccharide-activated human peripheral monocytes.

[Combined use of the airway scope and fiberoptic bronchoscopy for tracheal intubation in a patient with a large epiglottic cyst].

A 26-year-old man was scheduled for surgical extraction of a large epiglottic cyst. Mask ventilation was possible under propofol anesthesia without muscle relaxant. It was difficult to see the glottis using either a Macintosh laryngoscope or by fiberoptic bronchoscopy.

Propofol inhibits cyclo-oxygenase activity in human monocytic THP-1 cells.

Purpose: Monocytes/macrophages are key players in innate and adaptive immunity. Upon stimulation, they secrete prostanoids, which are produced by cyclooxygenase from arachidonic acid. Prostanoids influence inflammation and immune responses.

[Use of the laryngeal mask airway prevents gas leak around a tracheal tube].

A 59-year-old man with cervical spondylosis was scheduled for a posterior spine surgery. After induction of anaesthesia with propofol and fentanyl, and neuromuscular blockade with vecuronium, the trachea was intubated using an 8.0-mm ID refinforced tube, without difficulty.

Effect of subhypnotic doses of dexmedetomidine on antitumor immunity in mice.

Dexmedetomidine, a selective alpha2 adrenergic receptor agonist, is a drug often used for sedation. Despite the high prevalence of sedating patients with tumors in intensive care settings, little is known about the effect of sedative drugs on tumor growth. We studied the effect of dexmedetomidine on antitumor immunity in mice.

Ketamine-induced c-Fos expression in the mouse posterior cingulate and retrosplenial cortices is mediated not only via NMDA receptors but also via sigma receptors.

Ketamine induces marked c-fos expression in the posterior cingulate and retrosplenial cortices (PC/RS). We investigated whether NMDA and/or sigma receptors were involved in the c-Fos expression. The number of Fos-LI positive boutons in NMDA receptor knockout mice was significantly lower than that in wild-type mice.