Spinal trauma: pharmacological evidence for vasoconstrictor activity in cerebrospinal fluid.

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Abstract
Cerebrospinal fluid from six cases of acute spinal trauma collected 0--6 days after injury was examined for vasoconstrictor activity using both human isolated cerebral arteries and animal tissues. The cerebrospinal fluid of four out of six patients was vasoactive. The identities of the vasoconstrictor substances were not established, but experiments with pharmacological antagonists showed that arterial contractions were not due to serotonin, histamine, noradrenaline, acetylcholine or angiotensin II, substances which are known potent spastic agents on cerebral arteries. Our findings would explain by the mechanism of arterial spasm, principally in the anterior spinal artery, the neuropathological appearance of central haemorrhagic necrosis in spinal cord injury. The infarction of the core of the spinal cord could be caused by vasoconstrictor substances, reported here, in the cerebrospinal fluid after spinal injury. If the identities of the substances could be established, drug therapy to prevent or relieve the spasm would be possible.
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