在败血症中的毛细血管泄漏综合征:内在凝血通路激活的作用
Li Shu1,2, Jin-Lian Jiang2, Yun-Fen Chen2
1Department of Infectious Diseases, Suining Central Hospital, Suining, Sichuan Province, 629000, China.
BMC infectious diseases
|November 25, 2025
概括
激活的部分血栓形成时间 (APTT) 是预测败血症相关毛细血管泄漏综合征 (SACLS) 的敏感指标. APTT延长可能是由于XII因子的丰富,激活素和补充系统,导致毛细血管泄漏.
科学领域:
- 凝血和血栓形成的原因
- 败血症病理生理学病理生理学
- 补充系统 补充系统
背景情况:
- 败血症涉及到凝血,炎症和金因系统之间的复杂相互作用.
- 凝血在败血症相关毛细血管泄漏综合征 (SACLS) 的确切作用需要进一步阐明.
- 了解这些联系对于管理败血症并发症至关重要.
研究的目的:
- 调查凝血指标对血症中的毛细血管泄漏的预测值.
- 探索SACLS中的凝血系统的机制.
- 在具有SACLS的条件下验证凝血标记物,例如HFRS和 scrub typhus.
主要方法:
- 招募了败血症患者来评估凝血指标,以预测毛细血管泄漏.
- 包括患有HFRS和擦伤风的患者,以验证SACLS中的标志物.
- 分析了败血症患者的凝血因子水平,并使用了由脂多糖诱导的老鼠SACLS模型.
主要成果:
- 输血红素时间 (PT) 和激活的部分血栓塑时间 (APTT) 显示出了在败血症中毛细血管泄漏综合征的预测潜力.
- APTT在早期SACLS检测方面表现出比PT更高的灵敏度.
- 在大鼠模型中,APTT延长与血FXI和FXII活动和血清补充水平的降低以及肺FXII,补充和布拉迪基宁水平的升高相关.
结论:
- APTT作为一个敏感的生物标志物用于预测SACLS.
- 血中APTT延长可能是由于微循环中的XII因子 (FXII) 丰富.
- 微循环FXII丰富可能会触发素和补充系统,导致SACLS中的毛细血管泄漏.
相关概念视频
Extrinsic and Intrinsic Pathways of Hemostasis
11.9K
Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...
11.9K
Coagulation
9.5K
The coagulation phase is a critical part of the body's process to prevent blood loss following injury to blood vessels. It involves chemical reactions that form a clot to seal the injured area. The clotting process begins shortly after injury, within 15-20 seconds for severe damage and 1-2 minutes for minor injuries.
During the coagulation phase, clotting factors, or procoagulants, play a vital role in initiating and progressing the coagulation cascade. This cascade is a series of reactions...
During the coagulation phase, clotting factors, or procoagulants, play a vital role in initiating and progressing the coagulation cascade. This cascade is a series of reactions...
9.5K
Introduction to Hemostasis
13.1K
Hemostasis is a complex physiological process that prevents excessive bleeding when a blood vessel is injured. It's crucial for maintaining the integrity of the circulatory system, as it ensures that our blood remains fluid while still within the vascular network and yet clots to prevent blood loss upon vessel injury.
The three phases of hemostasis involve many clotting factors present in plasma and several substances released by platelets and injured tissue cells. It is a fast, localized,...
The three phases of hemostasis involve many clotting factors present in plasma and several substances released by platelets and injured tissue cells. It is a fast, localized,...
13.1K
Formation of the Platelet Plug
8.6K
The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
8.6K
Inflammation
61.5K
Overview
61.5K
Clot Retraction and Fibrinolysis
8.3K
After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
8.3K


