We have compared the efficacy of two non-invasive methods of transdermal anaesthesia: application of EMLA cream and iontophoresis of 5% lignocaine with adrenaline 1:50,000 in six healthy subjects. We tested depth of tissue penetration (pinprick) and effect on pain evoked by i.v. injection. After iontophoresis, pain on i.v. injection was abolished in five of six volunteers, whereas EMLA had no effect. We conclude that local anaesthetics penetrate deeply enough to numb both veins and skin with iontophoresis only.
Hyperalgesia on intradermal capsaicin application can be attenuated by systemic application of local anesthetics. We tested whether low doses of local anesthetics applied pre- or post-traumatically can reduce heat trauma-induced primary and secondary hyperalgesia in humans. Six healthy volunteers consented to the randomized, double-blind, and cross-over designed study. In each subject, a first-degree burn injury was induced three times (corresponding to a pre-traumatic, post-traumatic and control group) at an interval of at least 3 weeks. Heat was applied by a computer-controlled Peltier thermode (47 degrees C, 5 min). In the pre-traumatic group, lidocaine infusion was commenced 30 min prior to heat trauma, and in the post-traumatic group immediately after heat trauma for a total infusion time of 60 min each. Volunteers rated pain on a visual analogue scale (VAS) between threshold and tolerance maximum (0-100% VAS). Primary hyperalgesia was quantified by determining mechanical (von Frey hairs) and thermal (Peltier thermode) pain thresholds. Secondary hyperalgesia was quantified by determining the area in which normally unpleasant von Frey hairs evoked pain or tenderness. Baseline thermal and mechanical pain thresholds did not differ between groups. Heat application always resulted in a first-degree burn injury including both primary and secondary hyperalgesia. The former remained by and large stable for about 4 h whereas the latter continuously increased within the first 2 h. Lidocaine did not affect primary hyperalgesia, irrespective of pre- or post-traumatic application, but substantially reduced the development of secondary hyperalgesia on pre-traumatic, and for tendency on post-traumatic infusion (treatment groups did not differ significantly). Burn injury-induced erythema was smallest in the pre-traumatic group and largest in the control group; however, the level of significance was not reached. Plasma concentrations of lidocaine were always higher than 1.5 microg/ml 30 min after bolus application of lidocaine and reached a peak of 2-3 microg/ml after about 1 h. Thus, local anesthetics at concentrations that do not block nerve conduction substantially affect ongoing central changes in pain processing that are induced by a real tissue trauma. A significant preemptive effect could not be demonstrated. The anti-hyperalgesic effect of lidocaine is likely based on action of central (spinal) sites, but peripheral sites may also be addressed.
In awake humans, intravenous lidocaine and bupivacaine both dose-dependently attenuated the hyperreactive response to a nonspecific inhalational challenge with acetylcholine.
Whether or not neural blockade of pulmonary sympathetic innervation is of relevance for airway resistance in patients with chronic obstructive pulmonary disease (COPD) is unknown. Accordingly we evaluated airway resistance during sympathetic blockade by high thoracic epidural anaesthesia in patients with COPD. Before and 45 min after thoracic epidural injection of bupivacaine 0.75% (6-8 ml; n = 10) total respiratory resistance (oscillometry, ROS), vital capacity (VC), forced expiratory vital capacity in 1 s (FEV1, [%VC]), functional residual capacity (FRC; helium dilution method), and arterial blood gases were measured. Three additional patients received bupivacaine intravenously (1.2 mg.min-1 for 45 min), another three received saline epidurally. Sensory blockade covered segment C5 through T8. As an indicator of widespread sympathetic blockade including the lungs, skin temperature increased significantly on thumb and little toe. Despite pulmonary sympathetic denervation ROS, FEV1, and FRC remained unchanged, while VC decreased slightly, probably due to intercostal muscle blockade. Blood gases remained constant. Neither intravenous bupivacaine nor epidural saline evoked directional changes. Since, in contrast to beta-adrenoceptor blockade, pulmonary sympathetic denervation did not increase airway resistance in patients with COPD, neural sympathetic blockade seems to be of no relevance for airway resistance in these patients.
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