Cortical injury without ischemia produced by topical monoamines.
Responses to monoamines perfused over the cortical surface through modified pial windows were monitored in 106 cats. Norepinephrine (NE) and serotonin (5-HT) were diluted in mock CSF to concentrations of 50 and 500 ng/ml respectively, levels at or near the maximum concentrations to which the cortical surface might be exposed in subarachnoid hemorrhage or damage to nearby neurons. Each cat had simultaneous one-hour perfusions of monoamine solution over one hemisphere and a control solution over the other hemisphere thus serving as its own control. The perfusion solutions were observed to be restricted to the area of the pial window, and minimal histological damage was seen with the perfusion technique. The 5-HT perfusions were associated with an almost 20% narrowing of small pial arteries and arterioles but no significant effect on regional cerebral blood flow (rCBF), cortical water content or cortical function as monitored by EEG and somatosensory evoked potentials (SEP). In contrast, NE caused cortical edema and changes in the EEG and SEP's without significant vascular effect. These results suggest a non-ischemic toxicity of NE released by subarachnoid hemorrhage or cerebral damage.[1]References
- Cortical injury without ischemia produced by topical monoamines. Stein, S.C., Cracco, R.Q. Stroke (1982) [Pubmed]
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