Tourniquet-Induced Limb Ischemia

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Abstract
A rat model of tourniquet ischemia was created to observe the changes in sciatic afferent neuronal activity associated with prolonged tourniquet inflation on the hind leg. The sciatic nerve was divided in the proximal thigh and a two-electrode microfilament recording technique and signal averaging computer were used to survey afferent neuronal activity prior to and after tourniquet inflation. This method was able to determine both firing rate and conduction velocity of spontaneously active or mechanically sensitive nerve fibers. In 14 rats observed prior to tourniquet inflation there was much spontaneous activity. These fibers all had rapid conduction velocities (30 .+-. 6.9 m/s) (mean .+-. SD) and firing rates (16.3 .+-. 1.9 H). All fibers could be stimulated by movement of distal joints or by probing the skin of the leg. After tourniquet inflation, a pressure-induced conduction block occurred stopping all spontaneous and mechanically induced activity. After a short interval, (55 .+-. 16 min) a different group of spontaneously active fibers were observed that had both slow conduction (2.04 .+-. 0.77 m/s) and firing rates (0.54 .+-. 0.9 H). These fibers did not respond to mechanical stimulation of the limb distal to the tourniquet, or local anesthetic or cold block of the nerve distal to the tourniquet. Blockade of the sciatic nerve just proximal to the tourniquet and deflation of the tourniquet did abolish activity in these fibers. In ten separate rats in which tourniquets were placed but no surgical incision made, mean arterial blood pressure rose significantly after tourniquet inflation. With tourniquet deflation, blood pressure fell significantly from levels observed during tourniquet inflation. This study showed the presence of a group of spontaneously active fibers with velocities in the C-fiber range that were not observed prior to tourniquet inflation. The receptive fields of these fibers were most likely in the ischemic tissue or axons directly under or just proximal to the tourniquet. The neurophysiologic changes noted in this experimental model could represent the physiologic basis of tourniquet pain.