LYSOPHOSPHATIDIC ACID ALTERS CEREBROVASCULAR REACTIVITY IN PIGLETS
LYSOPHOSPHATIDIC ACID ALTERS CEREBROVASCULAR REACTIVITY IN PIGLETS
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DOI：
10.1152/ajpheart.1995.268.5.h2048
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发表时间：
1995-05-01
影响因子：
4.8
通讯作者：
LEFFLER, CW
中科院分区：
文献类型：
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作者：
TIGYI, G;HONG, LL;LEFFLER, CW
本实验采用闭合式脑窗观察了脂质介质溶血磷脂酸（LPA）对新生猪脑循环的影响。局部应用合成LPA引起剂量依赖性血管收缩，并抑制高碳酸血症和异丙肾上腺素的血管舒张。这些血管扩张剂引起脑脊液中腺苷3 '，5'-环一磷酸（cAMP）含量的升高，LPA呈剂量依赖性地抑制。百日咳毒素（1 μ g/ml）完全取消LPA诱导的血管收缩和血管反应性的改变，LPA不再降低cAMP。非洲爪蟾卵母细胞中LPA样脂质诱发的电流的电生理记录表明，脑脊液通常是缺乏LPA样因子。相反，鞘内注射自体血后4天产生的LPA样因子的量在1-10 μ M LPA当量的范围内。这些数据表明，LPA样的生物活性介质中产生的颅内血肿模型，这些磷脂可能发挥作用的病理生理学改变血管反应性经常发现在出血后的条件，也可能有助于出血后血管收缩的发展。
Effects of the lipid mediator lysophosphatidic acid (LPA) were studied on the cerebral circulation of newborn pigs using closed cranial windows. Topical application of synthetic LPA caused dose-dependent vasoconstriction and inhibited vasodilation to hypercapnia and isoproterenol. These vasodilators elicited a rise in the adenosine 3',5'-cyclic monophosphate (cAMP) content of the cerebrospinal fluid, which was inhibited dose dependently by LPA. Pertussis toxin (1 mu g/ml) completely abolished LPA-induced vasoconstriction and the altered vascular reactivity, and LPA no longer decreased cAMP. Electrophysiological recording of currents evoked by LPA-like lipids in Xenopus oocytes showed that cerebrospinal fluid is normally devoid of LPA-like factors. In contrast, the amount of LPA-like factors generated 4 days after intrathecal injection of autologous blood was in the range of 1-10 mu M LPA equivalents. The data indicate that LPA-like bioactive mediators were generated in an intracranial hematoma model and that these phospholipids might play a role in the pathophysiology of altered vascular reactivity often found in posthemorrhagic conditions and could also contribute to the development of posthemorrhagic vasoconstriction.