A double-blind investigation of the effect of adrenaline on conduction blockade was undertaken in six groups of rats (n = 12 or more) using a standardized injection of 0.4 ml of solution into the left infraorbital nerve. All six solutions contained lignocaine 0.25 g dl-1. In groups 1-3, the solutions were isotonic, in groups 4-6 the osmolarity was 0.6 isotonic. Solutions 1 and 4 contained potassium chloride 4 mmol litre-1 but no adrenaline; solutions 2 and 5 potassium chloride and adrenaline 5 micrograms ml-1 (1:200 000); solutions 3 and 6 adrenaline but no potassium chloride. The presence and duration of sensory blockade was determined from the reflex submandibular electromyographic response to periodic electrical stimulation of the homolateral and contralateral upper lips. In groups 1 and 4 (adrenaline absent) the mean durations of blockade (+/- SD) were 45 +/- 24 and 43 +/- 19 min. In groups 2, 3, 5 and 6 (adrenaline present) the durations of block averaged 97 +/- 4, 97 +/- 38, 105 +/- 21 and 92 +/- 16 min, respectively. Thus adrenaline approximately doubled the duration of blockade irrespective of osmolarity or potassium chloride concentration of the local anaesthetic solution (P less than 0.001).

John Barsa Constantino Benedetti John A. Bokan Monte S. Buchsbaum Stephen H. Butler Donald A. Calsyn William H. Calvin Amiram Carmon C. Richard Chapman Andrew C.N. Chen Willie K. Dong Samuel F. Dworkin Steven G. Fey B. Raymond Fink Wilbert E. Fordyce Gerald F. Gebhart Lawrence M. Halpern John F. Howe Bernard Kenton John C. Liebeskind John D. Loeser Richard F. Martin Harold Merskey Terence Murphy L. Brian Ready Ronald R. Tasker Arnold L. Towe Judith A. Turner Donald C. Tyler

One hundred and seventy-four rats received a standardized 0.4-ml injection into the left infraorbital nerve and all solutions contained lignocaine 0.25 g dl-1. In groups 1-4, the solutions were isoosmotic and contained, besides sodium chloride, potassium chloride 0 or 4 mmol litre-1 and glucose 0 or 20 mmol litre-1 (0 or 360 g dl-1). For groups 5-8, the solutions were hypoosmotic, containing sodium chloride to 0.6 of normal tonicity but were otherwise identical to solutions 1-4. Presence and duration of sensory block were determined from the reflex sublingual electromyographic response to periodic homolateral and contralateral electrical stimulation of the upper lip. In groups 1-4, the presence of potassium chloride 4 mmol litre-1 approximately doubled the duration of blockade (P less than 0.001). Groups 5-8 showed that hypoosmolarity also doubled the duration of block (P less than 0.001), but hypoosmolarity and potassium chloride did not have additive effects. It is concluded that addition of potassium- chloride 4 mmol litre-1 to isotonic solutions of lignocaine is likely to enhance their clinical effectiveness.

When a standard hypodermic needle is used to perform a stellate ganglion block, it is necessary to withdraw it 2 to 3 mm after bony contact with the transverse process of C6 or C7 so that the injectate is deposited superficial to the longus colli muscle into the fascial plane that contains the stellate ganglion. This study evaluates a 22-gauge side-port needle to perform a stellate ganglion block. Since this needle has a side-port 2 to 4 mm proximal to the needle tip, it was found that, with the needle resting on the C6 transverse process, the local anesthetic solution was discharged superficial to the longus colli muscle into the correct fascial plane to produce stellate ganglion block. Using criteria established by the authors, the success rate with a side-port needle was 95% in 58 blocks performed on patients where diagnostic stellate blocks were clinically indicated. Observations included the presence of Horner's syndrome, change in skin temperature on the ipsilateral upper extremity, and, in some subjects, the effect of block on the ipsilateral and contralateral psychogalvanic skin reflex. The authors feel this needle has advantages over standard hypodermic needles for performing stellate ganglion block.

This study was undertaken because of several recent reports of adverse neurologic reactions following the use of 2-chloroprocaine. Carotid sheaths containing undisturbed vagus nerve were surgically exposed in rabbits and bathed in situ for up to 1 hour in one of the following isotonic solutions: physiologic salt solution, lidocaine 2%, bupivacaine 0.75%, 2-chloroprocaine 3%, or a mixture of 2-chloroprocaine 1.5% and bupivacaine 0.375%. Each solution contained epinephrine, 5 μ/ml, (1:200,000). In other animals the carotid sheaths were bathed in physiologic salt solution, or 2-chloroprocaine 3% without epinephrine. The nerves were excised 10 to 12 days later. C-fiber impulse conduction was normal in nerves that had been exposed to physiologic salt solution with or without epinephrine, to lidocaine, or to bupivacaine. Conduction was absent or markedly impaired in several nerve specimens following exposure to 2-chloroprocaine. Histologie sections revealed the presence of epineurial cellular infiltration and fibrosis, perineurial fibrosis, and axonal degeneration in nerves that had been exposed to 2-chloroprocaine or the mixture of 2-chloroprocaine and bupivacaine. Histologic abnormalities were minor or absent following exposure to lidocaine, to bupivacaine, or to physiologic salt solution. These findings suggest that, under the conditions of the experiments, 2-chloroprocaine is more neurotoxic than lidocaine or bupivacaine.

aDepartment of Anesthesiology, University of Washington, Seattle, WA 98195, USA bDepartment of Psychiatry and Behavioral Sciences, University of Washington, Seattle, WA 98195, USA

Departments of Anaesthesiology, Rehabilitation Medicine & Surgery, University of Washington, Seattle, Washington, 98195 USA

Local anesthetics administered intrathecally seen more effective when in hypobaric solution than when in hyperbaric solution. To test whether an unrecognized osmotic effect might be playing a part in this, sheathed vagus nerves of rabbit were incubated in electrolyte-deficient or electrolyte-free media of various degrees of hypo-osmolarity. The nerves gained weight over a period of 15 min. They lost nearly half their sodium, but very little potassium, within 5 min. Electrolyte depletion by incubation in sucrose solutions depressed the amplitude of the C-fiber component of the compound action potential more rapidly in hypo-osmotic than in iso-osmotic solutions. In iso-osmotic sucrose, 50 per cent depression developed in 61 +/- 12 min (mean +/- SD, n = 5), but in 0.6 iso-osmotic sucrose, 50 per cent depression was reached in 17 +/- 3 min (n = 5). Lidocaine, 100 microM (approximately 0.003 g/100 ml) in iso-osmotic sucrose was without observed effect; lidocaine, 100 microM in 0.6 iso-osmotic sucrose produced 50 per cent depression in 7 +/- 2 min (n = 4). Thus, osmotic swelling plus electrolyte depletion, but not electrolyte depletion alone, markedly intensified inhibition of conduction by lidocaine. All effects were reversible by returning the nerves to isotonic physiologic incubation medium. The results suggest that intrathecal osmotic swelling of neural tissue may contribute to the conduction block in hypobaric spinal anesthesia.

A possible means of rapid cooling in the emergency treatment of malignant hyperpyrexia, peritoneal dialysis using a cold dialysate, is described. Experimental observations in a young man on a regular peritoneal dialysis regime showed that significant heat extraction can be obtained when either a cool (20 degrees C) or cold (9 degrees C) dialysis fluid is used. The maximum heat exchange observed was 17.5 kJ/min when 2 litre of cold dialysis was instilled for a mean time of 10 min. This rate of heat exchange is within the 10--40 kJ/min range of excess heat production that occurs in malignant hyperpyrexia. Since peritoneal dialysis is, technically, a very quick and simple procedure, it is suggested that it might play a very useful role in the emergency treatment of malignant hyperpyrexia. The dialysis treatment would also correct some of the biochemical disturbances that occur in this condition.