In order to try to gain a better understanding of the mechanisms of post-operative pain, this study was designed to psychophysically determine physiological and pharmacological characteristics of experimental pain induced by a 4-mm-long incision through the skin, fascia and muscle in the volar forearm of humans. In experiment 1, the subjects (n=8) were administered lidocaine systemically (a bolus injection of 2mg/kg for a period of 5 min followed by an intravenous infusion of 2mg/kg/h for another 40 min), and then the incision was made. In experiment 2, cumulative doses of lidocaine (0.5-2mg/kg) were systemically injected in the subjects (n=8) 30 min after the incision had been made, when primary and secondary hyperalgesia had fully developed. Spontaneous pain was assessed using the visual analog scale (VAS). Primary hyperalgesia was defined as mechanical pain thresholds to von Frey hair stimuli (from 7 to 151 mN) in the injured area. The area of secondary hyperalgesia to punctate mechanical stimuli was assessed using a rigid von Frey hair (151 mN). Flare formation was assessed in the first experiment using a laser doppler imager (LDI). Pain perception was maximal when the incision was made and then rapidly disappeared within 30 min after the incision had been made. Primary hyperalgesia was apparent at 15 min after the incision had been made and remained for 2 days. The incision resulted in a relatively large area of flare formation immediately after the incision had been made. The area of flare began to shrink within 15 min and was limited to a small area around the injured area at 30 min after incision. Secondary hyperalgesia was apparent at 30 min after incision and persisted for 3h after incision and then gradually disappeared over the next 3h. In experiment 1, pre-traumatic treatment with systemic lidocaine suppressed primary hyperalgesia only during the first 1h after the incision had been made. The lidocaine suppressed the development of flare formation without affecting the pain rating when the incision was made. The development of secondary hyperalgesia continued to be suppressed after completion of the lidocaine infusion. In experiment 2, post-traumatic treatment with lidocaine temporarily suppressed primary as well as secondary hyperalgesia that had fully developed; however, the primary and secondary hyperalgesia again became apparent after completion of the lidocaine administration. These findings suggest that pre-traumatic treatment with lidocaine reduces the excessive inputs from the injured peripheral nerves, thus suppressing development of flare formation and secondary hyperalgesia through peripheral and central mechanisms, respectively. Pre-traumatic treatment with lidocaine would temporarily stabilize the sensitized nerves in the injured area, but the nerves would be sensitized after completion of the administration. Post-traumatic treatment with lidocaine reduced primary and secondary hyperalgesia that had fully developed. However, the finding that the suppressive effect of lidocaine on seconda...
Pretraumatic injection of lidocaine reduces primary hyperalgesia more effectively than does posttraumatic injection, but only for a short period after incision. The spread of secondary hyperalgesia is mediated peripheral nerve fibers, but when secondary hyperalgesia has fully developed, it becomes less dependent on or even independent of peripheral neural activity originating from the injured site.
We experienced a case of unanticipated difficult intubation with direct laryngoscopy because of narrowing of the retropharyngeal air space and laryngeal vestibulum. It is suggested that three-dimensional computed tomography is useful for evaluating both the abnormality of an airway and its relationship to surrounding tissue.
Tracheal temperature--the temperature of the tracheal wall--is believed to reflect the core temperature. The trachea reacts quickly to temperature changes because it is surrounded by various large arteries and veins. Using the blood temperature from the cardiopulmonary bypass (CPB) and the jugular vein temperature as standards for core temperature, we evaluated the utility of monitoring the tracheal temperature during cardiac surgery. The tracheal temperature was measured by a thermistor which was attached to the anterior inner surface of the cuff of a tracheal tube. The tracheal temperature had correlation coefficients more than 0.99 with both blood temperature from the CPB (r = 0.993, P < 0.001) and jugular vein temperature (r = 0.993, P < 0.001) during CPB. Because the blood from the CPB draining into the ascending aorta and the jugular vein temperature might reflect the hypothalamic temperature directly, the tracheal temperature, which correlates with both of these quite closely, may reflect the core value directly. The monitoring of the tracheal temperature is not only valuable in monitoring the core value, but is also convenient during general anesthesia.
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