Role of norepinephrine and excitatory amino acids in edema of the spinal cord after experimental compression injury in rats.

The role of norepinephrine and excitatory amino acids in edema of the spinal cord after an acute experimental compression injury was studied in rats. Control rats received the compression injury only. Intraspinal norepinephrine was depleted in one rat group by injection of 6-hydroxydopamine (6-OHDA) into the subarachnoid space to selectively destroy catecholamine neurons and in a third group MK-801 was administered intravenously to block receptors for N-methyl-d-aspartate (NMDA), an excitatory amino acid. Recovery from motor paralysis and suppression of edema of the spinal cord were then compared in the three groups. Significant recovery from motor paralysis was found 12 h after injury in the 6-OHDA-treated rats, compared with the controls, and 24 h after injury in the MK-801-treated rats. Edema of the spinal cord was significantly suppressed for up to 24 h after injury in the 6-OHDA-treated rats. The MK-801-treated rats showed no significant suppression of the edema until 24 h after the spinal cord injury. It was concluded that norepinephrine is primarily involved in the formation of vasogenic edemas, which develop in the early stages after an injury, whereas excitatory amino acids affect the formation of cytotoxic edemas, which develop at a relatively later stage.