Abstract
Experimental studies have suggested what the primary role is of free radical products
in the development of vasospasm. It has been suggested that the degradation products
of hemolysis trigger free radical reactions leading to lipid peroxidation is subarachnoid
hemorrhage (SAH). Therefore, Fe2+, a degradation product of hemoglobin, seems to be the most important substance in
the pathogenesis of vasospasm. Cobaltous ion was shown to be a powerful inhibitor
of lipid peroxidation in biological membrane. Eleven rabbits were anesthetized and
received 5 ml of autologous arterial blood into the cisterna magna. Group 1 (n = 6)
received 0.1 mg/kg cobalt solution intratecally via the cisterna magna simultaneously
with blood. Group 2 (n = 5) underwent sham operation as a control group. Forty-eight
hours later the rabbits were deeply anesthetized and the brainstem was quickly removed
and put under the operating microscope to measure the basilar artery diameter. Afterwards,
the upper part of the brainstem was used for lipid peroxidation measurement and the
lower part for the histopathological examination. Significant vasospasm was observed
in four and moderate vasospasm in one rabbit of group 2; mild vasospasm was seen in
five rabbits and moderate vasospasm was seen in one rabbit of group 1. There was no
vasospasm in the control group. A statistically significant increase in the levels
of lipid peroxide was found in the brainstem of group 2. These data demonstrate that
cobaltous ion represents a promising therapeutic tool in vasospasm after SAH.
