Compression injuries of spinal nerve roots are very common. However, the basic pathophysiology of these conditions is not fully understood. In this study a model is presented for experimental graded compression of the nerve roots of the pig cauda equina, including a technique for vital microscopic studies on the microcirculation flow of the intrinsic vessels of the nerve roots during compression. With this model critical pressure levels for compression-induced occlusion of the arterioles, capillaries, and venules of the intrinsic vasculature of the nerve roots were determined. The study showed that the average minimum pressure in the inflated balloon required to stop the flow in the arterioles was 127 mm Hg (SD = 18, n = 11), in the capillaries 40 mm Hg (SD = 6, n = 12), and in the venules 30 mm Hg (SD = 10, n = 12). The average mean arterial pressure (MAP) was 150 mm Hg (SD = 14, n = 12). There was a statistically significant correlation (p greater than 0.001) between the MAP and the pressure required to stop the flow in the arterioles (r = 0.83, n = 14), but no correlation between MAP and capillary (r = 0.09 NS, n = 20) or venular (r = -0.28 NS, n = 34) occlusion pressure. After the nerve roots had been compressed at 50 or 200 mm Hg for 10 min or 2 h, the recirculation started immediately. There was a hyperemia during the first 10 min, with a dilatation of the vessels, particularly the venules. In nerve roots exposed to compression for 2 h at either 50 or 200 mm Hg, an intraneural edema developed.(ABSTRACT TRUNCATED AT 250 WORDS)