Related Experiment Video
Updated: May 1, 2026
16:31
Fixed Volume or Fixed Pressure: A Murine Model of Hemorrhagic Shock
Published on: June 6, 2011
27.7K
Platelet-activating factor mediates gastric damage induced by hemorrhagic shock
J L Wallace1, C M Hogaboam, G W McKnight
1Gastrointestinal Research Group, University of Calgary, Alberta, Canada.
The American Journal of Physiology
|July 1, 1990
Summary
Platelet-activating factor (PAF) contributes to gastric damage during hemorrhagic shock. PAF antagonists like WEB 2086 and BN 52021 significantly protected the gastric mucosa from shock-induced injury.
Area of Science:
- Gastroenterology
- Pharmacology
- Physiology
Background:
- Hemorrhagic shock can cause significant gastric damage.
- Platelet-activating factor (PAF) is implicated as a mediator in various inflammatory conditions.
Purpose of the Study:
- To investigate the role of PAF in mediating gastric damage induced by hemorrhagic shock in a rat model.
- To evaluate the efficacy of PAF antagonists in preventing this gastric injury.
Main Methods:
- Utilized an ex vivo gastric chamber preparation in rats.
- Induced hemorrhagic shock by reducing systemic arterial blood pressure to 25 mmHg.
- Administered PAF antagonists (WEB 2086, BN 52021) orally prior to shock induction.
- Assessed gastric damage, transmucosal potential difference (PD), protein and hemoglobin (Hb) in gastric lumen, and gastric blood flow using laser-Doppler flowmetry.
Main Results:
- Hemorrhagic shock caused extensive gastric damage (50 +/- 8% of glandular mucosa), decreased PD, and increased luminal protein and Hb.
- Oral pretreatment with PAF antagonists dose-dependently reduced gastric damage, preserved PD, and decreased luminal protein and Hb.
- Both WEB 2086 and BN 52021 demonstrated protective effects against shock-induced gastric injury.
Conclusions:
- PAF plays a significant role in mediating gastric mucosal damage during hemorrhagic shock.
- PAF antagonists offer a promising therapeutic strategy for preventing gastric injury associated with hemorrhagic shock.
Related Concept Videos
01:05Introduction to Hemostasis
14.2K
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,...
14.2K
01:22Formation of the Platelet Plug
6.2K
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...
6.2K
01:09Coagulation
8.4K
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...
8.4K
01:20Extrinsic and Intrinsic Pathways of Hemostasis
10.9K
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...
10.9K
01:16Clot Retraction and Fibrinolysis
6.0K
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.
6.0K
01:22Pathophysiology of Peptic Ulcer Disease: Injurious Factors
1.6K
Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
1.6K