Rie Kitamura

Suppression of acetylcholine-induced relaxation by local anesthetics and vascular NO-cyclic GMP system.

Background: Local anesthetics have been demonstrated to attenuate acetylcholine‐induced relaxation of vascular smooth muscle, but the mechanism responsible has not been elucidated. The present study was undertaken to ascertain whether this effect of local anesthetics is due to suppression of the vascular nitric oxide (NO)‐cyclic GMP (cGMP) system.

Suppression of cyclic guanosine monophosphate formation in rat cerebellar slices by propofol, ketamine and midazolam

PurposeThe nitric oxide (NO)/cyclic guanosine monophosphate (cGMP) system is involved in glutamatergic neurotransmission. The current study determined the effects of propofol, ketamine and midazolam on rat cerebellar cGMP formation, attempting to clarify whether the effect was due to suppression of NO-cGMP system or to direct interaction with glutamatergic receptors.MethodsCerebellar slices, obtained from six-to eight-day-old Wistar rats, were pretreated with propofol (10 μM–1 mM), ketamine (10–100 μM) or midazolam (1–100 μM) for 30 min. and then stimulated with L-glutamate (3 mM), N-methyl-D-aspartate (NMDA, 0.1 mM), kainate (0.1 mM) or sodium nitroprusside (SNP, 0.3 mM) (n = 5–11 for each group). The levels of cGMP were determined by radioimmunoassay.ResultsNone of the anaesthetics studied altered cGMP levels when no stimulant was given. Propofol (10 μM–1 mM) suppressed L-glutamate-, NMDA-, kainate- and SNP stimulated cGMP formation in a concentrationdependent manner, the sensitivity to propofol was in the order of NMDA > kainate > L-glutamate, SNP Ketamine (10–100 μM) suppressed L-glutamate- and NMDA-stimulated cGMP formation, but did not suppress kainate-or SNP-stimulated cGMP formation. Midazolam (10–100 μM) did not affect NMDA-, L-glutamate-or SNP-stimulated cGMP formation, but suppressed kainate-induced formation.ConclusionThe inhibitory effects of propofol, ketamine and midazolam on cGMP formation in rat cerebellar slices are due mainly to interaction with receptors for excitatory amines, and not due to the suppression of nitric oxide synthase or guanylate cyclase activities.RésuméObjectifLe système monoxyde d’azote (NO)/monophosphate de guanosine cyclique (cGMP) participe à la neurotransmission glutamatergique. La présente étude recherchait l’influence du propofol, de la kétamine et du midazolam sur la formation cérébelleuse de cGMP en essayant de préciser si cette influence résultait de la suppression du système NO-cGMP ou d’une interaction directe avec les récepteurs glutamatergiques.MéthodesDes tranches de cerveau prélevées sur des rats Wistar âgés de six à huit jours ont été prétraitées avec du propofol (10 μm–1 mM), de la kétamine (10–100 μM) ou du midazolam (1–100 μM) et ensuite stimulées avec du L-glutamate (3 mM), du N-méthyl-D-aspartate (NMDA, 0,1 mM), du kainate (0,1 mM) ou du nitroprussiate de sodium (SNP 0,3 mM) (n = 5 pour chaque groupe). Le radio-immunodosage a servi à déterminer le niveau de cGMPRésultatsEn absence de stimulus, aucun des anesthésiques n’a modifié les niveaux de cGMP Le propofol (10 μM-mM) supprimait la formation de cGMP stimulée par le L-glutamate, le NMDA, le kainate et le SNP proportionnellement à la concentration. La sensibilité au propofol s’établissait dans l’ordre suivant NMDA > kainate > L-glutamate > SNP La kétamine (10–100 μM) supprimait la formation stimulée par le NMDA de L-glutamate et de cGMP mais ne supprimait pas la formation de cGMP stimulée par le kainate et le SNP Le midazolam (10–100 μM) n’affectait pas la formation de cGMP stimulée par le NMDA, le L-glutamate et le SNP mais supprimait la formation induite par le kainate.ConclusionLinfluence inhibitrice du propofol, de la kétamine et du midazolam sur la formation de cGMP dans les tranches cérébelleuses de rats est principalement causée par l’interaction des récepteurs des amines excitateurs et non par la suppression de la synthase du monoxyde d’azote ou à l’action de la guanylate cyclase.

Diabetes mellitus, internal thoracic artery grafting, and risk of an elevated hemidiaphragm after coronary artery bypass surgery

The elevated hemidiaphragm after coronary artery bypass grafting (CABG) that occurs in some patients is associated with internal thoracic artery (ITA) grafting as well as with the use of topical cardiac hypothermia. An increased incidence of elevated hemidiaphragm after CABG surgery in diabetic patients was observed. To determine the incidence and risk factors of elevated hemidiaphragm after CABG surgery and the relationship to preoperative diabetes, 200 consecutive patients undergoing CABG were studied; 29 (14.5%) had hemidiaphragm elevation postoperatively (25 on the left, 1 on the right, 3 bilateral). In the remaining 171 there was no hemidiaphragm elevation. Factors analyzed were age, gender, preoperative diabetes, duration of cardiopulmonary bypass (CPB) and aortic cross-clamping, minimum esophageal temperature during CPB, and use of the ITA graft. Univariate analysis showed a significant association between elevated hemidiaphragm and diabetes (P < 0.05), left ITA grafting (P < 0.01), and age (P < 0.05). Right ITA was not used for any patient. Multivariate analysis ruled out age, whereas preoperative diabetes and the use of the ITA remained the independent factors associated with elevated hemidiaphragm (odds ratio, 3.41; 95% confidence interval 1.41 to 8.18, and 2.86; 1.01 to 8.06, respectively). The relative risk of an elevated hemidiaphragm was 9.75 in diabetic patients with the ITA graft, as compared with nondiabetic patients without this graft. All 3 patients with bilateral diaphragm paralysis and a patient with a right hemidiaphragm elevation were diabetic. In conclusion, both diabetes and use of the ITA graft appear to be important risk factors for the development of elevated hemidiaphragm following CABG.(ABSTRACT TRUNCATED AT 250 WORDS)

Comparison of postoperative liver dysfunction following halothane and sevoflurane anesthesia in women undergoing mastectomy for cancer

The incidence of an abnormal increase in the serum levels of glutamic oxaloacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) following anesthesia with halothane and 65% nitrous oxide in oxygen (halothane group) or with sevoflurane and 65% nitrous oxide in oxygen (sevoflurane group) was compared in women undergoing surgery for breast cancer. An abnormal increase in GOT and GPT, both defined as higher than 50 IU, occurred postoperatively in 2 of the 150 patients (1.7%) in the sevoflurane group, and in 37 of the 200 (18.5%) in the halothane group (P<0.001). The elevated levels of serum transaminases after sevoflurane ranged from 50 to 65 IU whereas those after halothane ranged from 50 to 1000 IU, except for a value greater than 5000 IU in 1 patient. In the halothane group, there was a significant association between postoperative increases in serum transaminases and previous exposure to inhalation anesthetics, postoperative mitomycin therapy, and radiation therapy (all P<0.001). The results of multivariate analysis, when data from all patients were taken together, showed that the type of anesthetic (halothane) was the highest factor related to postoperative increases in GOT and GPT (odds ratio 35.85; 95% confidence interval 5.92–217.37), followed next by prior exposure to inhalation anesthetics (8.65; 2.96–25.27), postoperative radiation therapy (4.37; 1.70–11.19), and postoperative mitomycin therapy (3.56; 1.23–10.35). These data suggest that sevoflurane is less likely to cause anesthesia-related liver dysfunction than halothane.

Erythemas caused by electrodes while monitoring neuromuscular blockade: three cases

Skin erythemas formed in three patients during surgery at the sites where negative electrodes had been attached to stimulate the ulnar nerve for a neuromuscular transmission monitor (Relaxograph). The patients were all women, aged 52, 62, and 74 years, and general anesthesia lasted 8 h 20 min, 4 h 50 min, and 8 h 45 min, respectively. The electrodes used were disposable ECG electrodes in the first two patients and one designed for a neuromuscular monitor in the third; all were carbon-coated and then covered with gel. However, when the electrodes were detached from the lesion, they all showed loss or damage of the carbon coating under the gel. We recommend balancing the merit of monitoring with the risk of complications, even when applying an apparently safe, noninvasive monitor.