[Experimental study on compression neuropathy--determination of blood flow by a hydrogen washout technic].

The role of ischemia in the pathophysiology of compression neuropathy is still a subject of debate. Nor is the effect on blood supply induced by neurolysis for this lesion so clearly elucidated. In order to shed some light on these problems, two series of experiments were undertaken. In the first series of experiments, the changes in intrafascicular blood flow and nerve function when acute, graded compression was applied to a dog's sciatic nerve by a specially designed compression device were investigated by means of the hydrogen washout technique, electrophysiological study and histological observation. In the second series, Type II injury according to the classification of Sunderland was experimentally caused by embedding a compression device for three weeks, and the intrafascicular blood flow of this model was measured by using the embedded electrode for the hydrogen clearance method. Furthermore, the blood flow before and after neurolysis for this lesion was compared, and cases in which internal neurolysis had been performed were observed after one and three weeks. The intrafascicular blood flow was decreased at 47.2 +/- 3.7 (mean +/- S.D.) mmHg, with increasing pressure, blood flow gradually declined and a statistically significant correlation was shown between the values (r=-0.77, p less than 0.01). This completely stopped at 118.6 +/- 5.9 mmHg (p less than 0.001). The effect of compression on intrafascicular blood flow was immediately observed and disappeared at once after release of the compression. An actual pressure of 118.6 mmHg maintained for 75 minutes produced complete conduction block, which was immediately recovered after release of the compression, though more slowly than the blood flow. When the compression device was applied, the intrafascicular blood flow was reduced to about 80% of the precompression level (p less than 0.05) and this reduction remained unchanged after three weeks (p less than 0.01), at which time the nerve had sustained the Type II injury. After the removal of the device, the blood flow was restored to more than the precompression level (p less than 0.01). Following this, when external neurolysis was performed, a slight reduction of blood flow was observed. After internal neurolysis, however, a remarkable reduction was noticed, the blood flow decreasing to about 20% of the precompression value (p less than 0.01). The blood flow after internal neurolysis was restored to about 70% of the precompression level after one week and, three weeks later, remained about the same.