脑血管畸形血管自动调节功能异常的分子机制探讨

目的：探讨脑血管畸形（AVMs)血管自动调节功能异常的分子机制。方法：14例AVMs及周边脑组织行显微外科手术切除，标本提取总RNA，应用RT－PCR检测脑AVMs中ppET-1和ETA表达变化，并与8例正常脑血标本进行比较。结果：在脑血管畸形血管中，发现ppET-1mRNA和ETA mRNA表达较正常脑血管下降。结论：脑AVMs如ppET-1mRNA表达的下降可能会导致AVMs中ET－1的下降，而脑AVMs中ET－1下降很可能是畸形管自动调节功能异常的主要原因之一；ET1mRNA表达较正常血管下降，可能阻止外源性ET－1，并加强脑AVMs中ET－1的抑制作用，导致脑AVMs血管自动调节功能异常。

The Molecular Mechanism of Dysautoregulation of Malformed Cerebral Vessels

Objective To explore the molecular mechanism of dysautoregulation of malformed cerebral vessels. Methods Total RNA was abstracted from 14 samples of arteriovenous malformations , and adjacent brain tissues and 8 normal cerebral vessels which were removed by microneurosurgery. The expressions of ppET - 1 and ETA receptor in AVMs were detected by RT - PCR. Results The expressions of ppET - 1 and ETA receptor mRNA in AVMs were lower than these in normal cerebral vessels. Conclusion Downregulation of expressions of ppET - 1 mRNA contributed to the lack of ET - 1 secretion in AVMs. Downregulation of ET - 1 has been implicated in a variety of vascular disorders involving both he-modynamic and structural changes in the vasculture. The decrease of ETA mRNA expression on AVM would prevent gene repression from exogenous sources of ET - 1 and reinforce the biological consequences of ET - 1 in AVMs,thus resulting in dysautoregulation of cerebral vessels in AVMs.