TIME-COURSE OF VARIATIONS IN RABBIT CEREBROSPINAL-FLUID LEVELS OF CALCITONIN-GENE-RELATED PEPTIDE AND SUBSTANCE-P-LIKE IMMUNOREACTIVITY IN EXPERIMENTAL SUBARACHNOID HEMORRHAGE

Background and Purpose Cerebral vasospasm after subarachnoid hemorrhag e may result partially from the imbalance between vasodilator and vaso constrictor factors. The vasodilator peptides substance P and calciton in gene-related peptide contained in the trigeminovascular system are involved in the vasomotor phenomenon occurring after subarachnoid hemo rrhage. The delayed arterial narrowing may reflect the time course of the release of these peptides. Therefore, we followed the time course of the changes in cerebrospinal fluid immunoreactivity of substance P and calcitonin gene-related peptide in a model of experimental subarac hnoid hemorrhage. Methods Cerebrospinal fluid samples were taken in th e basal state and at 30 minutes, 24 hours, and 3 days after a single i njection of 1 mL autologous arterial blood into the cisterna magna of rabbits using a percutaneous suboccipital route. Substance P-like and calcitonin gene-related peptide-like immunoreactivities were determine d in centrifuged cerebrospinal fluid and plasma by use of enzyme immun oassay. Results Early (30 minutes) after induced subarachnoid hemorrha ge, there was a large increase in cerebrospinal fluid substance P-like immunoreactivity (P<.01) and calcitonin gene-related peptide-like imm unoreactivity (P<.01). Arterial and hemorrhagic cerebrospinal fluid le vels of substance P-like immunoreactivity were different (P<.03), indi cating that the increased cerebrospinal fluid level did not result onl y from the blood contamination. Twenty-four hours after induced subara chnoid hemorrhage, the immunoreactivities of substance P and calcitoni n gene-related peptide remained significantly higher than the basal le vel (P<.01). At day 3, both immunoreactivities had decreased to a leve l nonsignificantly different from the basal level. Conclusions The ear ly high values of the cerebrospinal fluid immunoreactivities for subst ance P and calcitonin gene-related peptide, apart from the contaminati on by arterial blood, probably resulted from the depletion of neurotra nsmitter peptides from the trigeminovascular fibers.