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SNS AND LUNG VASCULAR PERMEABILITY

SNS AND LUNG VASCULAR PERMEABILITY
SNS 和肺血管通透性
批准号:
3448562
负责人:
MICHAEL B MARON
金额:
$5.14万
依托单位国家:
美国
项目类别:
财政年份:
1983
资助国家:
美国
项目状态:
已结题
起止时间:
1983-07-01 至 1986-06-30

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中文摘要
翻译
我们将检验这一假设,即交感神经的强烈激活 神经系统(SNS)可导致肺微血管增多 对液体和蛋白质的渗透性。这个问题很有意思,因为 最近的研究表明,渗透性的增加可能会 促进神经源性肺水肿的发展,这是一种 常发生在中枢神经系统损伤后的浮肿,引起 大量的中央调节的SNS的释放。我们的基本方法将是 以确定肺微血管系统是否有能力 血管外液体滤过过程中筛子蛋白与水的关系 在这些情况下会受到损害。这一能力的变化 将通过分析淋巴流量和淋巴蛋白的变化进行评估 在原位犬肺制剂中可能出现的浓度,其中 将收集纯净的结前肺淋巴。的正常能力。 筛选蛋白质的微血管系统将在对照组中进行评估 通过抬高左房增加液体滤过率的动物 机械地施压。淋巴流量和淋巴蛋白的变化 在这些条件下发生的浓度将与在这些条件下发生的 在刺激了SNS的动物群体中观察到的 中心的或外围的。中枢刺激将由 颅内给药(藜芦碱和毒素)和 颅内压升高。星状神经节和内脏神经 刺激将用于激活SNS的外周成分。 肾上腺素能受体和肾上腺在脑出血中的特殊作用 介导肺血管通透液和蛋白质流量的变化 对这些刺激的反应将通过评估进一步去除 在阿尔法肾上腺素能受体阻滞剂或 肾上腺切除术。
英文摘要
We will test the hypothesis that intense activation of the sympathetic nervous system (SNS) may cause an increase in pulmonary microvascular permeability to fluid and proteins. This question is of interest, because recent studies have suggested that an increased permeability might contribute to the development of neurogenic pulmonary edema, a form of edema which often occurs after central nervous system injury which evokes a massive centrally-mediated discharge of the SNS. Our basic approach will be to determine if the capability of the pulmonary microvasculature to sieve proteins relative to water during extravascular fluid filtration becomes impaired under these conditions. Alterations in this capability will be evaluated by analyzing changes in lymph flow and lymph protein concentration that may occur in an in situ canine lung preparation in which pure pre-nodal lung lymph will be collected. The normal capability of the microvasculature to sieve proteins will be evaluated in a control group of animals in which fluid filtration has been increased by raising left atrial pressure mechanically. Changes in lymph flow and lymph protein concentration occurring under these conditions will be compared with those observed in groups of animals in which the SNS has been stimulated either centrally or peripherally. Central stimulation will be evoked by intracranial drug administration (veratrine and tityustoxin) and by intracranial pressure elevation. Stellate ganglion and splanchnic nerve stimulation will be used to activate components of the SNS peripherally. The specific role of adrenergic receptors and the adrenal gland in mediating the changes in lung transvascular fluid and protein flux that occur in response to these stimuli will be further delinated by evaluating additional groups of animals following either Alpha-adrenergic blockade or adrenalectomy.
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