Neuronophagia by leukocytes in experimental spinal cord injury.

Experimental spinal cord injury was produced in cats by compression trauma. The major histologic features in the first 24 hours following injury included hemorrhagic necrosis, edema, and acute inflammation of gray and white matter. Neutrophilic leukocytes (NL) were apparent in the walls of and adjacent to veins and venules within four hours of injury, but large numbers of NL were not observed in tissue until eight to 24 hours. Acute inflammation was especially prominent in gray matter, and NL frequently surrounded and phagocytized neuronal somata. Large numbers of NL and neuronophagia by leukocytes were evident only in areas of hemorrhage. The role of blood in producing the acute inflammatory response and in generating chemotactic factors responsible for neuronophagia is incompletely understood. Neutrophilic leukocytes, in addition to their response as phagocytes, release histolytic enzymes, reactive species of oxygen, and proinflammatory factors which lead to further tissue necrosis and inflammation.