Effect of phosphoramidon on brain tissue angiogenesis in the chronic phase of vasospasm after subarachnoid hemorrhage in the rat.
Effect of phosphoramidon on brain tissue angiogenesis in the chronic phase of vasospasm after subarachnoid hemorrhage in the rat.
复制标题
磷酰胺对大鼠蛛网膜下腔出血后血管痉挛慢性期脑组织血管生成的影响。
DOI:
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发表时间:
2001
期刊:
影响因子:
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通讯作者:
J. Jochem
中科院分区:
文献类型:
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作者:
J. Jośko;S. Hendryk;H. Jędrzejowska‐Szypułka;J. Słowiński;B. Gwóźdź;D. Lange;M. Śnietura;K. Żwirska;J. Jochem
BACKGROUND
Subarachnoid hemorrhage (SAH) frequently leads to prolonged cerebral vasospasm resulting in vascular pathology due to endothelial cell ischemia and neuronal hypoxia. Posthemorrhagic vasospasm can be counteracted by the administration of phosphoramidon, which blocks the endothelin converting enzyme (ECE) responsible for the conversion of big endothelin into a fully active ET1 peptide. The aim of the study was to determine the effect of chronic vasospasm after SAH on angiogenesis and the effect on this process of endothelin-1, the main causative factor in vasospasm.
MATERIAL AND METHODS
Male Wistar rats were examined. Seven days after cannulation of the cisterna magna, blood was administered to induce SAH. The ECE inhibitor phosphoramidon was administered in a dose of 40 nmol in 50 microl of cerebrospinal fluid three times: 20 min before SAH, 60 min after SAH, and 24 hours after SAH. The brains were removed 48 hours later for histological evaluation. The vascular surface density was measured in cerebral hemisphere sections (at the level of the dorsal part of the hippocampus) and brainstem sections (1/2 of the pons).
CONCLUSION
Increased angiogenesis was observed in the cerebral hemispheres after SAH. The administration of phosphoramidon inhibits angiogenesis in cerebral hemispheres after SAH.