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MULTIPLE MECHANISMS INVOLVED IN INTRAVENOUS REGIONAL ANESTHESIA (IVRA). P.H. Rosenbergl*, J. Kyttal*, J. Haasio' and J.E. Heavner2 (SPON: P. Chandra), lAnesthesiology, Helsinki U School of Medicine, 00130 Helsinki, Finland, 2Anesthesiology and Physiology, TTUHSC, Lubbock, TX 79430, USA

Aim of Investigation: Investigations of how IVRA works have yielded con- flicting results and conclusions. Multiple and complimentary mechanisms probably are involved (e.g. temperature, asphyxia, cuff pressure and local anesthetic block of nerves).

Methods: Five healthy adult male volunteers ages 31-42 years, partici- pated in a crossover study. Each was given the following treatment: limb exsanguination and tourniquet plus (a) arm and hand maintained at 35C, (b) same as (a) except warm lidocaine solution was injected, (c) arm and hand cooled (22C) and (d) same as (c) except cold lidocaine solution was in- jected. Psychophysical, radiographical and electrophysiological techniques were used in the study.

Results: During ischemia sensory loss progressed from distal to proximal portions of the extremity. When the hand was insensitive, median nerve stimulation at the elbow produced sensations which radiated only to the mid forearm. When lidocaine was injected , sensation in the musculocutaneous n. distribution was generally lost before sensation in other parts of the limb. Stimulation of the median N. at the elbow when the hand and forearm were in.sensitive did not produce radiating sensations. Cooling delayed washout of local anesthetic from the arm and recovery of nerve action potentials. Marked extravasation of contrast material was observed at the elbow.

Conclusions: Nerve block in the core of nerve bundles under the tourniquet is the major cause of sensory loss during ischemia alone. The effects of the cuff and the local anesthetic at the elbow are prominent determinants of the quality and quantity of anesthesia produced during IVRA.

EFFECTS OF LIDOCAINE ON ISCHEMIC PAIN AND SOMATO- SENSORY EVOKED POTENTIALS. F.Schimek', U.W.Buett- ner'*, D.Friess" and 'Anesthesiology, 'Neurology and 'Pharmacy,

"ni_ WI R.Schorer'*, Departments of

versity of Eberhard Karl, D-7400 Tiibingen, F.R.G. Ai Lidocaine (0.1 mH1 preserves conduction by impeding loss of K' from energy lacking nerves in vitro. We investigated effects of lidocaine on preservation of conductionin sensory and motor fibers of ischemic nerves in vivo. Methods: A tourniquet was ap- plied sequentially on both arms of five volunteers. Prior to in- flation blood was drawn from basilar vein to determine baseline values of serum K'. Median nerve was stimulated at wrist (II-15 mA, 5 Hz) and SEP recorded over sensory cortex, at Et-b's point and 3-5 cm proximal of medial epicondyle. SEP amplitudes and la- tencies for each recording site and conduction velocities distal and across tourniquet were calculated. Tactile discrimination and pain were assessed with a tuning fork and rating scale (O- 10). After tourniquet inflation i.v. lidocaine (50 ml, 0. 4 mH) was administered to one arm, the other serving as control. After deflation blood was drawn at l/3-4 min intervals and serum K'and lidocaine were determined. Data collected during and after isch- emia at 5-10 min intervals were expressed as % of baseline valu- es and compared. Results: SEP recorded at Erb's point were affe- cted more without than with lidocaine at 10 min of ischemia and recovery (p<O.O51. There was a tendency for higher pain ratings and K' increase and faster loss of sensation without than with lidocaine. Conclusions: Low concentrations of lidocaine seem to preserve conduction in sensory and motor fibers of ischemic ner- ves in vivo. Neural loss of K* may be one of the factors contri- buting to acute ischemic pain.