This study was done to determine the dose-responsiveness during the development of acute pressure-induced median neuropathy in rabbits and to develop a new animal model of acute carpal tunnel syndrome. Twenty-three rabbits were used. Carpal tunnel syndrome was induced by infusing a controlled saline solution into the carpal tunnel of rabbits using a 21-gauge needle under general anesthesia to elevate the carpal tunnel pressure. The changes in the amplitude and latency of the compound muscle action potential obtained by abductor pollicis recording were observed after a complete conduction block, and after the release of pressure at various pressure levels. Pressures greater than 30 mm Hg applied to the carpal tunnel caused a remarkable electrophysiologic change. A higher pressure level resulted in a shorter time required for a complete conduction block and also for recovery after the release of pressure. Complete conduction block occurred between 40 and 50 minutes at a pressure of 100 mm Hg. The degree of recovery after a conduction block was related inversely to the pressure-time integrals. Our animal model reflects the pathophysiology of acute carpal tunnel syndrome and shows a regular dose-responsiveness during the development of acute pressure-induced neuropathy.