Maki Matsumoto

Intrathecal buprenorphine in the treatment of phantom limb pain.

I? hantom limb pain is a chronic pain perceived in an absent part of the body. It can totally consume a patient’s life. Suggested treatments for this complaint are many, but none have proved to have lasting efficacy. We have treated two patients suffering from phantom limb pain. Intrathecal buprenorphine provided not only immediate and long-lasting pain relief, but also increased the temperature of the lower part of the body. These cases are described and possible mechanisms for the analgesic and hyperthermic actions of intrathecal buprenorphine are discussed.

Ca2+ channel modulation alters halothane-induced depression of ventricular myocytes

PurposeThis study examined the direct myocardial depressant effect of halothane and determined whether an L-type Ca2+ channel agonist and antagonists altered the myocardial depression induced by halothane in cultured rat ventricular myocytes.MethodsVentricular myocytes were obtained from neonatal rats by enzymatic digestion with collagenase and then cultured for 6 to 7 days. The myocytes were stabilized in a serum-free medium, and the spontaneous beating rate and amplitude were measured. To assess the halothane-induced conformational changes in L-type Ca2+ channel, receptor binding study was performed using a dihydropyridine derivative, [3H] PN 200-110, in cardiac membrane preparation.ResultsHalothane (1%, 2%, 3%, 4%) decreased the beating rate and amplitude in a concentration-dependent manner (P < 0.05). The myocardial depressant effects of halothane were potentiated by nifedipine or verapamil (P < 0.05). Bay K 8644, an L-type Ca2+ channel agonist, completely prevented the halothane-induced depression in amplitude (P < 0.05), but affected the beating rate less. Adding halothane (2%) decreased (P < 0.05) the maximum binding site density for [3H] PN 200-110 (from 198.6 ± 23.7 fmol·mg−1 protein to 115.3 ± 21.6 fmol·mg−1 protein) but did not affect binding affinity (from 0.461 ± 0.077 nM to 0.307 ± 0.055 nM).ConclusionThe reduction of Ca2+ current via sarcolemmal L-type Ca2+ channel, probably due to conformational changes in dihydropyridine binding sites, plays an important role in halothane-induced myocardial depression in living heart cells.RésuméObjectifLétude actuelle a examiné l’effet dépresseur myocardique direct de l’halothane et déterminé si un agoniste ou un antagoniste des canaux calciques de type L modifie la dépression myocardique induite par l’halothane sur des myocytes ventriculaires de rats, en culture.MéthodesLes myocytes ventriculaires ont été obtenus à partir de rats nouveau-nés, par digestion enzymatique avec collagénase, et puis mis en culture pendant 6 ou 7 jours. Les myocytes ont été stabilisés dans un milieu sans sérum et le rythme et l’amplitude des battements spontanés ont été mesurés. Pour évaluer les changements de conformation induits par l’halothane dans le canal calcique de type L, l’étude de la liaison aux récepteurs a été réalisée en utilisant un dérivé dihydropyridine, [3H] PN 200-110, d’une préparation de membranes cardiaques.RésultatsL’halothane (1 %, 2 %, 3 %, 4%) a diminué le rythme des battements et leur amplitude en fonction de la concentration (P < 0,05). Les effets dépresseurs myocardiques de l’halothane ont été accentués par la nifédipine ou le vérapamil. Le Bay K 8644, un agoniste des canaux calciques de type L, a complètement empêché la dépression d’amplitude induite par l’halothane (P < 0,05), mais a eu moins d’effet sur le rythme des battements. L’accroissement de l’halothane (2 %) a diminué (P < 0,05) la densité maximale au site de liaison pour le [3H] PN 200-110 (de 198,6 ± 23,7 fmol·mg−1 de protéine à 115,3 ± 21,6 fmol·mg−1 de protéine), mais n’a pas affecté l’affinité de la liaison (de 0,461 ± 0,077 nM à 0,307 ± 0,055 nM).ConclusionLa réduction de l’entrée de calcium dans le canal calcique sarcolemmique de type L joue un rôle important dans la dépression myocardique induite par l’halothane dans des cellules cardiaques en culture à cause, probablement, des changements de conformation des sites de liaison de la dihydropyridine.

Evaluation of alkalinized lidocaine solution in brachial plexus blockade.

The effect of alkalinization of lidocaine solution in brachial plexus blockade was evaluated in a double blind study. Commercial 1.5% lidocaine with epinephrine 1∶200,000 (pH 5.72) was compared with an alkalinized solution of lidocaine (pH 7.12). 10 mg·kg−1 of each solution was administrated by the axillary perivascular technique in 34 adult patients scheduled for elective surgery. The onset and spread of sensory blockade and the intensity of motor blockade were determined. An alkalinized lidocaine solution produced more complete sensory blockade in all of four main nerves of the upper extremity as compared with the control lidocaine solution. The onset of sensory blockade in the musculocutaneous, radial, ulnar and median nerves was shortened 58%, 40%, 30% and 28%, respectively, by employing the alkalinized lidocaine solution. Also the analgesic onset in the radial and musculocutaneous nerves was significantly faster than the other two nerves (P<0.05 andP<0.01). Furthermore, the intensity of motor blockade was greatly potentiated when alkalinized lidocaine solution was employed. There was no significant increase in plasma concentration of lidocaine in patients who were given alkalinized solution.