| Platelet-derived growth factor-induced severe and chronic vasoconstriction of cerebral arteries: proposed growth factor explanation of cerebral vasospasm. | |
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MedLine Citation:
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PMID: 20305494 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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OBJECTIVE: After subarachnoid hemorrhage (SAH), platelet-derived growth factor-BB (PDGF-BB) is secreted in and around the cerebral arteries. To clarify the role of PDGF-BB in the development of vasospasm after SAH, we determined whether PDGF-BB alone can cause long-lasting vasoconstriction of a severity similar to that of vasospasm. In addition, the anti-vasospastic effect of trapidil, an antagonist of PDGF-BB function, was investigated. METHODS: We infused recombinant PDGF-BB (10 microg/mL saline as the vehicle) (n = 14) into the subarachnoid space of rabbits and analyzed alterations in the caliber of the basilar artery using repeated angiography. To study the role of PDGF-BB on the development of vasospasm, trapidil was administered continuously starting 1 hour after SAH, on day 0 (0.63-1.25 mg/kg /h or vehicle) for 47 hours (n = 24), or after the full development of cerebral vasospasm on day 2 (3.0 mg/kg/h or vehicle) for 0.5 hours (n = 17), and alterations in the caliber of the basilar artery were monitored. RESULTS: PDGF-BB caused long-lasting vasoconstriction, with maximum constriction of 56% (P < .001) of the control value (= 100%) on day 2, resembling vasospasm seen after SAH. Prolonged administration of intravenous trapidil, starting soon after SAH, prevented the development of vasospasm in a dose-dependent manner (P < .05, .01, or .001). Intravenous or intra-arterial administration of trapidil significantly dilated vasospasm (P < .01) on day 2, at least transiently. CONCLUSION: PDGF-BB, a growth factor synthesized in the subarachnoid space after SAH, can cause severe and long-lasting vasoconstriction. Significant prevention and resolution of vasospasm can be achieved by the PDGF-BB antagonist trapidil. We propose that excessive production of PDGF-BB, essentially aiming to repair injured arteries, causes cerebral vasospasm. Although the half-life of trapidil in serum may be shorter than that of PDGFG-BB-derived spasmogenic signaling, trapidil is a candidate drug for constructing a new therapeutic modality for preventing and resolving vasospasm. |
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Authors:
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Zhi-Wen Zhang; Hiroji Yanamoto; Izumi Nagata; Susumu Miyamoto; Yukako Nakajo; Jing-Hui Xue; Koji Iihara; Haruhiko Kikuchi |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Neurosurgery Volume: 66 ISSN: 1524-4040 ISO Abbreviation: Neurosurgery Publication Date: 2010 Apr |
Date Detail:
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Created Date: 2010-03-22 Completed Date: 2010-06-22 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 7802914 Medline TA: Neurosurgery Country: United States |
Other Details:
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Languages: eng Pagination: 728-35; discussion 735 Citation Subset: IM |
Affiliation:
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Laboratory for Cerebrovascular Disorders, Research Institute of National Cardiovascular Center, Suita, Osaka, Japan. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Cerebral Angiography / methods Cerebral Arteries / drug effects* Disease Models, Animal Dose-Response Relationship, Drug Male Platelet-Derived Growth Factor / adverse effects*, metabolism* Rabbits Subarachnoid Hemorrhage / chemically induced, physiopathology* Time Factors Trapidil / adverse effects Vasoconstriction / drug effects* Vasodilator Agents / adverse effects Vasospasm, Intracranial / etiology* |
| Chemical | |
Reg. No./Substance:
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0/Platelet-Derived Growth Factor; 0/Vasodilator Agents; 15421-84-8/Trapidil |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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