Effect of endogenous vasopressin on blood flow to choroid plexus during hypoxia and intracranial hypertension.
Effect of endogenous vasopressin on blood flow to choroid plexus during hypoxia and intracranial hypertension.
复制标题
缺氧和颅内高压期间内源性加压素对脉络丛血流的影响。
DOI：
10.1152/ajpheart.1994.266.2.h393
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Heistad,DD
中科院分区：
文献类型：
--
作者：
Faraci,FM;Kinzenbaw,D;Heistad,DD
外源性加压素可减少脉络丛的血流量和脑脊液的产生。一些研究表明，缺氧和颅内压 (ICP) 增加会导致循环加压素增加。我们检验了这样的假设：在缺氧和ICP增加期间，内源性加压素的释放会减少脉络丛的血流量。使用微球测量麻醉兔子的脉络丛血流量。缺氧使脑血流量增加两倍以上，但对脉络丛的血流量几乎没有影响。相反，在存在加压素 V1 拮抗剂 [d(CH2)5Tyr(Me)]AVP 的情况下，缺氧会导致流向脉络丛的血流量显着增加。颅内高压期间，当 ICP 从 1 增加到 40 mmHg 时，脉络丛的血流量从 409 +/- 42 减少到 295 +/- 25 ml.min-1 x 100 g-1（平均值 +/- SE；与对照相比，P < 0.05）。加压素拮抗剂可抑制因 ICP 增加而导致的脉络丛血流减少。因此，缺氧和ICP增加期间加压素的释放对脉络丛的血管具有收缩作用。在缺氧和 ICP 增加期间，加压素的血浆水平略有增加，这表明血浆以外的加压素来源会影响脉络丛的血管。我们认为，内源性加压素可能通过负反馈机制减少脉络丛血流量，在缺氧和颅内高压期间发挥保护作用。
Exogenous vasopressin decreases blood flow to the choroid plexus and production of cerebrospinal fluid. Some studies indicate that hypoxia and increases in intracranial pressure (ICP) produce increases in circulating vasopressin. We examined the hypothesis that endogenous release of vasopressin decreases blood flow to the choroid plexus during hypoxia and increased ICP. Blood flow to the choroid plexus was measured in anesthetized rabbits using microspheres. Hypoxia increased cerebral blood flow more than twofold but had little effect on blood flow to the choroid plexus. In contrast, hypoxia produced a marked increase in blood flow to the choroid plexus in the presence of a vasopressin V1-antagonist, [d(CH2)5Tyr(Me)]AVP. During intracranial hypertension, blood flow to the choroid plexus decreased from 409 +/- 42 to 295 +/- 25 ml.min-1 x 100 g-1 (means +/- SE; P < 0.05 vs. control) when ICP was increased from 1 to 40 mmHg. The vasopressin antagonist inhibited the decrease in blood flow to the choroid plexus in response to increased ICP. Thus release of vasopressin during hypoxia and increased ICP have a constrictor effect on blood vessels of the choroid plexus. Plasma levels of vasopressin increased minimally during hypoxia and increased ICP, which suggests that sources of vasopressin other than plasma affect blood vessels of the choroid plexus. We propose that endogenous vasopressin may play a protective role during hypoxia and intracranial hypertension by a negative feedback mechanism to reduce blood flow to the choroid plexus.