Effect of U-50488h, a selective opioid kappa receptor agonist, on vascular injury after spinal cord trauma
| Autor: | Chung Y. Hsu, Jian Xu, Edward L. Hogan, Zhi Xiang Qu |
|---|---|
| Rok vydání: | 1993 |
| Předmět: |
Pyrrolidines
Neutrophils Central nervous system Vascular permeability Pharmacology Neuroprotection Capillary Permeability Rats Sprague-Dawley Edema medicine Animals Molecular Biology Spinal cord injury Spinal Cord Injuries biology business.industry General Neuroscience Receptors Opioid kappa 3 4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide (trans)-Isomer medicine.disease Spinal cord Extravasation Rats Disease Models Animal medicine.anatomical_structure Myeloperoxidase Anesthesia biology.protein Blood Vessels Female Neurology (clinical) medicine.symptom business Developmental Biology |
| Zdroj: | Brain research. 626(1-2) |
| ISSN: | 0006-8993 |
| Popis: | U-50488H, a selective opioid kappa receptor agonist has been shown to be a neuroprotective agent in animal models of spinal cord injury. The mechanism of action of U-50488H is not known. Methylprednisolone, the only neuroprotective drug proven in patients with acute spinal cord injury may prevent the secondary injury after an initial trauma. Secondary vascular injury develops after experimental spinal cord trauma. In this study we examined the effects of U-50488H on post-traumatic vascular injury based on the measurement of vascular permeability, edema and neutrophil infiltration in a rat spinal cord injury model. Vascular permeability was assessed by vascular extravasation of fluorescein isothiocyanate conjugated dextran (FITC-D), a macromolecular tracer. Tissue edema was determined by percentage water content and neutrophil infiltration by myeloperoxidase (MPO) activity, a marker enzyme for neutrophils. U-50488H at doses of 5, 10, 20 and 40 mg/kg i.p. administered twice (0.5 h before and 0.5 h after trauma) reduced vascular permeability in a dose-dependent manner. More frequent dosing (10 mg/kg, 0.5 h before and 0.5, 2, 8 and 22 h after injury) reduced vascular permeability 24 h after injury. U-50488H also reduced edema formation but did not affect neutrophil infiltration. Results from this study raise the possibility that the neuroprotective effect of U-50488H involves a secondary vascular event. |
| Databáze: | OpenAIRE |
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