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脑脊液压力升高所致肺动脉高压中的肾上腺因素。

Adrenal component to pulmonary hypertension induced by elevated cerebrospinal fluid pressure.

作者信息

Maron M B, Dawson C A

出版信息

J Appl Physiol Respir Environ Exerc Physiol. 1979 Jul;47(1):153-60. doi: 10.1152/jappl.1979.47.1.153.

Abstract

In this study we investigated the possibility that a circulating vasoactive agent contributes to the pulmonary hypertension elicited by elevated cerebrospinal fluid pressure (PCSF) using a denervated canine left lower lung lobe (LLL) preparation that was pump perfused with mixed venous blood at constant flow and venous pressure. Raising the PCSF to an average 190 Torr resulted in a 34.3% increase in LLL inflow pressure. This response was eliminated by adrenal venous occlusion and also by alpha-blockade of the LLL. The results indicated that adrenal catecholamines were responsible for the LLL response. The passively induced elevation of left atrial pressure (Pla) that occurs in the intact animal during elevated PCSF was stimulated in the LLL by raising the outflow pressure. This maneuver attenuated the increase in LLL vascular resistance and suggested that the elevation in Pla seen in the intact animal could mask humorally mediated responses of the magnitude we observed.

摘要

在本研究中,我们使用去神经支配的犬左下肺叶(LLL)制备物,以恒定流量和静脉压用混合静脉血进行泵灌注,研究了循环血管活性物质是否导致脑脊液压力升高(PCSF)引起的肺动脉高压。将PCSF升高至平均190托导致LLL流入压力增加34.3%。这种反应通过肾上腺静脉闭塞以及LLL的α受体阻滞而消除。结果表明,肾上腺儿茶酚胺是导致LLL反应的原因。在完整动物中,PCSF升高时出现的被动诱导的左心房压力(Pla)升高,在LLL中通过升高流出压力而被刺激。该操作减弱了LLL血管阻力的增加,提示在完整动物中观察到的Pla升高可能掩盖了我们所观察到的这种程度的体液介导反应。

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