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SNX-111, a novel, presynaptic N-type calcium channel antagonist, is neuroprotective against focal cerebral ischemia in rabbits.
- Source :
-
Journal of the neurological sciences [J Neurol Sci] 1997 Dec 09; Vol. 153 (1), pp. 25-31. - Publication Year :
- 1997
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Abstract
- Cytosolic Ca2+ overload has been proposed as a main cause of neuronal injury during cerebral ischemia. SNX-111, a synthetic product of the naturally occurring omega-conotoxin MVIIA, is a novel, presynaptic N-type Ca2+ channel antagonist and has been reported to be neuroprotective against cerebral ischemia. We studied the neuroprotective effects of SNX-111 in a rabbit model of focal cerebral ischemia. New Zealand white male rabbits (2.5-3.5 kg) were given 1 mg/kg/h i.v. SNX-111 (n=8) or normal saline (n=8) 10 min after onset of a 2-h period of transient focal cerebral ischemia induced by occlusion of the left middle cerebral, anterior cerebral and internal carotid arteries followed by 4 h reperfusion. SNX-111 significantly attenuated overall cortical ischemic neuronal damage by 44% (saline, 38.7+/-3.0%; SNX-111, 21.5+/-6.0%, P<0.05) and regions of hyperintensity on T2-weighted MRI by 30% (saline, 70.6+/-4.0%; SNX-111, 49.3+/-11.0%, P<0.05). No significant difference in (regional cerebral blood flow) rCBF or MAP (mean arterial blood pressure) was found between SNX-111- and saline-treated rabbits suggesting that neuroprotection is due to a cellular effect. We conclude that SNX-111 reduces ischemic injury in this model. Its use as a clinical neuroprotective agent for cerebrovascular surgery or stroke should be investigated further.
- Subjects :
- Animals
Blood Pressure drug effects
Cerebrovascular Circulation drug effects
Cerebrovascular Circulation physiology
Evoked Potentials, Somatosensory physiology
Magnetic Resonance Imaging
Male
Rabbits
Brain Ischemia pathology
Calcium Channel Blockers pharmacology
Neuroprotective Agents pharmacology
Peptides pharmacology
omega-Conotoxins
Subjects
Details
- Language :
- English
- ISSN :
- 0022-510X
- Volume :
- 153
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Journal of the neurological sciences
- Publication Type :
- Academic Journal
- Accession number :
- 9455974
- Full Text :
- https://doi.org/10.1016/s0022-510x(97)00196-2