Changes in blood flow, oxygen tension, action potentials, and vascular permeability induced by arterial ischemia or venous congestion on the lumbar dorsal root ganglia in dogs.

It is generally believed that radiculopathy associated with the degenerative conditions of the spine may result from both mechanical compression and circulatory disturbance. However, the basic pathophysiology of circulatory disturbance induced by ischemia and congestion is not fully understood. This study investigated the effect of ischemia and congestion on the dorsal root ganglion (DRG) using an in vivo model. The sixth and seventh lumbar laminae were removed and the seventh lumbar DRG was exposed using adult dogs. The aorta was clamped as an ischemic model in the DRG, and the inferior vena cava was clamped as a congestion model at the sixth costal level for 30 min using forceps transpleurally. Measurements of blood flow, partial oxygen pressure, and action potentials in the DRG were recorded over a period of 1 h after clamp release. Finally, we examined the status of intraganglionic blood permeability under a fluorescence microscope following injection of Evans blue albumin into the cephalic vein to determine the type of circulatory disturbance occurring in the DRG. Immediately after inferior vena cava clamping, the central venous pressure increased approximately four times and marked extravasation of protein tracers was induced in the lumbar DRG. Blood flow, partial oxygen pressures, and action potentials within the DRG were more severely affected by the aorta clamping; however, this ischemic model did not reveal any permeability changes in the DRG. The permeability change in the DRG was more easily increased via venous congestion than by arterial ischemia. The intraganglionic venous flow was stopped with compression at much lower pressures than that needed to impact arterial flow. From a clinical perspective, intraganglionic edema formation, rather than arterial ischemia, may be an earlier phenomenon inducing DRG dysfunction.