Dirofilaria immitis: heartworm infection alters pulmonary artery endothelial cell behavior.
Dirofilaria immitis: heartworm infection alters pulmonary artery endothelial cell behavior.
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恶丝虫：恶丝虫感染改变肺动脉内皮细胞的行为。
DOI：
10.1152/jappl.1997.82.2.389
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Kaiser,L
中科院分区：
文献类型：
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作者：
Mupanomunda,M;Williams,JF;Mackenzie,CD;Kaiser,L
Mupanomunda, Maria, Jeffrey F. Williams, Charles D. Mackenzie和Lana Kaiser。心丝虫感染可改变肺动脉内皮细胞的行为。达成。生理学报，32(2):389-398,1997。丝虫病的发病机制通常归因于成年寄生虫的物理存在或宿主对寄生虫的免疫反应。然而，丝虫病的谱系不能完全用这些原因来解释，其他机制必须起作用。现在很明显，由丝虫病寄生虫释放的因子可能有助于丝虫病的发病机制。成年心丝虫（Dirofilaria immitis）寄生于右心和肺动脉，因此肺动脉应暴露于丝虫因子浓度最高的地方。我们测试的假设，内皮依赖性松弛是改变体外肺动脉从心丝虫感染的狗。在对照组和心虫感染犬的肺动脉环中测量了内皮依赖性血管扩张剂（甲胆碱、缓激肽、P物质和A-23187）和非内皮依赖性血管扩张剂硝酸甘油的松弛反应和收缩反应。在一氧化氮合酶、环氧化酶和鸟苷酸环化酶抑制剂存在和不存在的情况下，评估内皮依赖性松弛。与对照组相比，心丝虫感染狗的肺动脉对甲胆碱、P物质和A-23187的反应被抑制，但对缓动素、硝化甘油、去甲肾上腺素或KCl的反应没有被抑制，这表明内皮细胞的变化而不是血管平滑肌的行为参与了放松的改变。在甲胆碱的情况下，控制性肺动脉内皮依赖性松弛的机制似乎涉及一氧化氮，而在缓激肽和a -23187的情况下，一氧化氮和环加氧酶产物都涉及。心丝虫感染犬肺动脉内皮依赖性松弛的机制尚不清楚。这些数据没有提供证据表明心丝虫感染会影响内皮细胞受体功能或血管平滑肌鸟苷酸环化酶鸟苷3 ',5 ' -环单磷酸系统，因此细胞内信号的变化可能是观察到的内皮介导的松弛改变的主要原因。由丝虫病寄生虫引起的内皮细胞功能的改变可能是丝虫病相关病理的一个重要组成部分。
Mupanomunda, Maria, Jeffrey F. Williams, Charles D. Mackenzie, and Lana Kaiser.Dirofilaria immitis:heartworm infection alters pulmonary artery endothelial cell behavior.J. Appl. Physiol.82(2): 389–398, 1997.—The pathogenesis of filariasis has generally been attributed to either physical presence of the adult parasites or the host’s immune response to the parasites. However, the spectrum of filariasis cannot be entirely explained by these causes, and other mechanisms must be operative. It is now evident that factors released by filarial parasites likely contribute to the pathogenesis of filarial diseases. Adult heartworms (Dirofilaria immitis) reside in the right heart and pulmonary artery, so the pulmonary artery should be exposed to the highest concentration of filarial factors. We tested the hypothesis that endothelium-dependent relaxation is altered in the in vitro pulmonary artery from heartworm-infected dogs. Relaxation responses to endothelium-dependent vasodilators (methacholine, bradykinin, substance P, and A-23187) and the non-endothelium-dependent vasodilator nitroglycerin and contractile responses were measured in rings of pulmonary artery from control and heartworm-infected dogs. Endothelium-dependent relaxation was assessed in the presence and absence of inhibitors of nitric oxide synthase, cyclooxygenase, and guanylate cyclase. Responses to methacholine, substance P, and A-23187, but not to bradykinin, nitroglycerin, norepinephrine, or KCl, were depressed in pulmonary artery from heartworm-infected dogs when compared with control, suggesting that changes in endothelial cell and not vascular smooth muscle behavior are involved in altered relaxation. The mechanism of endothelium-dependent relaxation in control pulmonary artery appears to involve nitric oxide in the case of methacholine and both nitric oxide and a cyclooxygenase product in the case of bradykinin and A-23187. The mechanism of endothelium-dependent relaxation in pulmonary artery from heartworm-infected dogs was not clearly elucidated. These data provide no evidence that heartworm infection globally influences either endothelial cell receptor function or the vascular smooth muscle guanylate cyclase guanosine 3′,5′-cyclic monophosphate system, making it likely that changes in intracellular signaling are primarily responsible for the observed alteration of endothelium-mediated relaxation. Alteration of endothelial cell function by filarial parasites may be an important component in the pathology associated with filariasis.