Effect of N2O on Sevoflurane Vaporizer Settings during Minimal- and Low-flow Anesthesia

Background: Uptake of a second gas of a delivered gas mixture decreases the amount of carrier gas and potent inhaled anesthetic leaving the circle system through the pop-off valve. The authors hypothesized that the vaporizer settings required to maintain constant end-expired sevoflurane concentration (Etsevo) during minimal-flow anesthesia (MFA, fresh gas flow of 0.5 l/min) or low-flow anesthesia (LFA, fresh gas flow of 1 l/min) would be lower when sevoflurane is used in oxygen-nitrous oxide than in oxygen.

Methods: Fifty-six patients receiving general anesthesia were randomly assigned to one of four groups (n = 14 each), depending on the carrier gas and fresh gas flow used: group Ox.5 l (oxygen, MFA), group NOx.5 l (oxygen-nitrous oxide, MFA after 10 min high fresh gas flow), group Ox1 l (oxygen, LFA), and group NOx1 l (oxygen-nitrous oxide, LFA after 10 min high fresh gas flow). The vaporizer dial settings required to maintain Etsevo at 1.3% were compared between groups.

Results: Vaporizer settings were higher in group Ox.5 l than in groups NOx.5 l, Ox1 l, and NOx1 l; vaporizer settings were higher in group NOx.5 l than in group NOx1 l between 23 and 47 min, and vaporizer settings did not differ between groups Ox1 l and NOx1 l.     

β2-Adrenoceptor Genotype Affects Vasopressor Requirements during Spinal Anesthesia for Cesarean Delivery

Background: Maternal hypotension is common after spinal anesthesia for cesarean delivery. There is wide variability in the incidence and severity of hypotension and in the response to treatment. The [beta]2 adrenoceptor ([beta]2AR) possesses several polymorphic sites. Codons 16 (Arg16Gly) and 27 (Glu27Gln) have been shown to affect desensitization of the receptor. The goal of this study was to determine whether genetic variants of the [beta]2AR alter incidence of hypotension or the amount of vasopressor treatment required during spinal anesthesia for cesarean delivery.

Methods: One hundred seventy healthy women undergoing elective cesarean delivery were studied. Spinal anesthesia was performed with 12 mg hyperbaric bupivacaine, 25 [mu]g fentanyl, and 200 [mu]g morphine. Hypotension was treated with ephedrine and/or phenylephrine intravenously, and [beta]2AR genotype at codons 16 and 27 was determined. Analysis of variance was used to compare variables between genotypes, with data expressed as mean +/- SD.

Results: Ephedrine or phenylephrine was used in more than 90% of patients, with no difference in the incidence of hypotension between [beta]2AR genotypes. However, there was a significant effect of genotype on the amount of vasopressor required. Gly16 homozygotes received significantly less ephedrine (18 +/- 14 mg) than Arg16 homozygotes (28 +/- 13 mg) and Arg16Gly heterozygotes (30 +/- 20 mg; P = 0.0005). Glu27 homozygotes required significantly less ephedrine than Gln 27 homozygotes (14 +/- 13 vs. 30 +/- 19 mg; P = 0.002). Gln27Glu heterozygotes received less ephedrine than Gln27 homozygotes (23 +/- 16 vs. 30 +/- 19 mg; P = 0.03).     

Adenosine A1 but Not A2a Receptor Agonist Reduces Hyperalgesia Caused by a Surgical Incision in Rats: A Pertussis Toxin-sensitive G Protein-dependent Process

Background: Activation of A1 adenosine receptors (A1Rs) causes antinociception after nerve injury and inflammation. However, the role of A2a adenosine receptors (A2aRs) for pain processing is less clear. In the current study, the authors investigated the role of spinal adenosine A1Rs and A2aRs for the maintenance of mechanical hyperalgesia in an animal model for postoperative pain.

Methods: Rats with intrathecal catheters were anesthetized and underwent plantar incision. Spontaneous pain behavior and withdrawal threshold to punctuate stimulation were measured before and after administration of intrathecal R-phenylisopropyl-adenosine (R-PIA; A1R agonist), 2-w p-2-carbonyl-ethyl-phenylethylaminox-5X-N-ethylcarboxami-doadenosine (CGS21680; A2aR agonist), or vehicle. In separate groups of animals, the effects of pertussis toxin, forskolin, glibenclamide, 4-aminopyridine, tetraethylammonium, apamin, charybdotoxin, or margatoxin on R-PIA-induced antinociception were examined.

Results: Intrathecal administration of 5 nmol R-PIA but not 10 nmol CGS21680 decreased nonevoked spontaneous pain behavior. Furthermore, intrathecal administration of R-PIA but not of CGS21680 increased withdrawal thresholds after incision. Pretreatment with pertussis toxin and administration of forskolin, glibenclamide, 4-aminopyridine, and tetraethylammonium inhibited R-PIA-induced antinociception. In addition, intrathecal administration of apamin, charybdotoxin, or margatoxin did not modify mechanical hypoalgesia mediated by R-PIA.     

Effect of Propofol on Arachidonate Cascade by Vasopressin in Aortic Smooth Muscle Cells: Inhibition of PGI2 Synthesis

Background: The mechanisms underlying the vascular effects of propofol are not fully understood. Vasopressin, a potent vasoactive peptide, stimulates the arachidonate cascade and the synthesis of prostacyclin (PGI (2); the main metabolite of the cascade in vascular smooth muscle cells). Arachidonic acid (AA) release by phospholipases is the rate-limiting step in the cascade. We investigated the mechanisms underlying vasopressin-induced AA release and the effect of propofol on PGI2 synthesis in a rat aortic smooth muscle cell line: A10 cells.

Methods: In cultured A10 cells pretreated with propofol, the stimulation by vasopressin of AA release and PGI2 synthesis was evaluated by measuring [(3) H]AA and 6-keto PGF1 [small alpha, Greek], respectively, in the culture medium. The effects of propofol on vasopressin-induced activation of phosphoinositide-hydrolyzing phospholipase C and phosphatidylcholine-hydrolyzing phospholipase D were evaluated by measuring inositol phosphate formation and choline formation, respectively.

Results: A phospholipase C inhibitor and a phosphatidic acid phosphohydrolase inhibitor both attenuated vasopressin-induced AA release and PGI2 synthesis, as did a phospholipase A2 inhibitor. Propofol inhibited vasopressin-induced activation of phosphoinositide-hydrolyzing phospholipase C and phosphatidylcholine-hydrolyzing phospholipase D, but this effect of propofol was significant only at supraclinical concentration (0.1 mM). Propofol reduced vasopressin-induced PGI2 synthesis. The inhibitory effect was observed at concentrations (10 [micro sign]M-0.1 mM) higher than those used clinically.     

Titration of Propofol for Anesthetic Induction and Maintenance Guided by the Bispectral Index: Closed-loop versus Manual Control: A Prospective, Randomized, Multicenter Study

Background: This report describes a closed-loop titration of propofol target control infusion based on a proportional-differential algorithm guided by the Bispectral Index (BIS) allowing induction and maintenance of general anesthesia and compares this to manual propofol target control infusion.

Methods: One hundred sixty-four patients scheduled to undergo elective minor or major surgery were prospectively randomized in a multicenter study into the closed-loop (n = 83) or manual target control infusion group (n = 81). The goal was to reach a BIS target of 50 during induction and to maintain it between 40 and 60 during maintenance. For both groups, remifentanil target control infusion was adjusted manually, and ventilation was without nitrous oxide.

Results: Closed-loop control was able to provide anesthesia induction and maintenance for all patients. During induction, propofol consumption was lower in the closed-loop group (1.4 +/- 0.5 vs. 1.8 +/- 0.6 mg/kg; P < 0.0001), but the duration was longer (320 +/- 125 vs. 271 +/- 120 s; P < 0.0002). Adequate anesthesia maintenance, defined as the BIS in the range of 40-60, was significantly higher in the closed-loop group (89 +/- 9 vs. 70 +/- 21%; P < 0.0001), with a decrease of the occurrence of BIS less than 40 (8 +/- 8 vs. 26 +/- 22%; P < 0.0001). Time from discontinuation of propofol infusion to tracheal extubation was shorter in the closed-loop group (7 +/- 4 vs. 10 +/- 7 min; P < 0.017). Unwanted somatic events and hemodynamic instability were similar.