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分离、通气和灌注的大鼠肺对血管活性肠肽的降解作用。

Degradation of vasoactive intestinal peptide by isolated, ventilated, and perfused rat lungs.

作者信息

Bernhard W, Bothe-Sandtfort E, Koop H, Cassel W, Von Wichert P

机构信息

Department of Internal Medicine, Philipps-University of Marburg, FRG.

出版信息

Eur J Clin Invest. 1989 Dec;19(6):506-13. doi: 10.1111/j.1365-2362.1989.tb00267.x.

DOI:10.1111/j.1365-2362.1989.tb00267.x
PMID:2515970
Abstract

The degradation of vasoactive intestinal peptide (VIP) was studied using an isolated perfused rat lung model. 125iodine labelled VIP (125I-VIP) was used as a tracer. VIP was cleared from the perfusate by a single lung passage up to concentrations of 1 nmol l-1. The clearance rate was decreased at higher concentrations of VIP. VIP was taken up by the lung tissue and the cleavage products were re-extruded into the perfusate. The time delay of re-extrusion was increased at starting concentrations of VIP exceeding 1 nmol l-1 and in the presence of the lysosomal inhibitor chloroquine. After a bolus of 9 pmol or 40 nmol 125I-VIP into the pulmonary artery catheter 6.3 pmol or 2920 pmol, respectively, were bound by the lung. Most of the radioactive material was extruded within 25 min and consisted of low molecular weight 125I-labelled degradation products. We conclude that the receptors for VIP in the alveolar capillaries are of high affinity and capacity to extract VIP from the circulation and that lysosomes may be involved in the degradation. The degradation products are of low molecular weight.

摘要

使用离体灌注大鼠肺模型研究了血管活性肠肽(VIP)的降解情况。用125碘标记的VIP(125I-VIP)作为示踪剂。在VIP浓度高达1 nmol l-1时,单肺循环可使灌注液中的VIP清除。在较高浓度的VIP时,清除率降低。肺组织摄取VIP,其裂解产物再排回到灌注液中。当VIP起始浓度超过1 nmol l-1以及存在溶酶体抑制剂氯喹时,再排出的时间延迟增加。向肺动脉导管内一次性注入9 pmol或40 nmol 125I-VIP后,肺分别结合了6.3 pmol或2920 pmol。大多数放射性物质在25分钟内排出,且由低分子量的125I标记的降解产物组成。我们得出结论,肺泡毛细血管中VIP的受体具有从循环中提取VIP的高亲和力和能力,溶酶体可能参与了降解过程。降解产物分子量较低。

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