Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Acute Pancreatitis II: Pathophysiology01:21

Acute Pancreatitis II: Pathophysiology

The pathophysiology of acute pancreatitis centers on injury to pancreatic acinar cells, which initiates a cascade of harmful intracellular events.This injury leads to premature activation of trypsinogen to trypsin in the pancreas. Trypsin then activates other digestive enzymes, such as chymotrypsin, elastase, and phospholipase A2, which begin breaking down pancreatic tissue. The resulting autodigestion causes local inflammation, tissue swelling, hemorrhage, and fat necrosis.Injured acinar cells...
Acute Pancreatitis II: Clinical Manifestations and Management01:30

Acute Pancreatitis II: Clinical Manifestations and Management

Acute pancreatitis presents a complex medical emergency characterized by rapid onset inflammation of the pancreas, demanding timely diagnosis and management to prevent complications. The condition primarily manifests through severe upper abdominal pain that often radiates to the back. This pain intensifies following the consumption of fatty foods. Accompanying symptoms such as nausea, vomiting, abdominal distention, fever, dyspnea, cyanosis, and jaundice can vary in intensity but significantly...
Acute Pancreatitis I: Introduction01:25

Acute Pancreatitis I: Introduction

Acute pancreatitis is the sudden inflammation of the pancreas caused by the early activation of digestive enzymes, leading to the autodigestion of pancreatic tissue. This results in local inflammation and, in severe cases, systemic complications.EtiologyUnderstanding the underlying causes is crucial, as identifying the etiology guides treatment and anticipates complications. Acute pancreatitis can be triggered by various factors, typically grouped into the following clinical categories.Biliary...
Acute Pancreatitis I: Introduction01:27

Acute Pancreatitis I: Introduction

Pancreatitis is inflammation of the pancreas, an organ located behind the stomach. It can be either acute or chronic.
Acute pancreatitis is characterized by rapid inflammation of the pancreas, often caused by factors like gallstone blockage or excessive alcohol consumption. Chronic pancreatitis, on the other hand, is a slow, progressive inflammation that may result from long-term alcohol abuse, obstructions in the pancreatic duct, or genetic factors.
The causes of acute pancreatitis include:
Chronic Pancreatitis II: Pathophysiology01:21

Chronic Pancreatitis II: Pathophysiology

Chronic pancreatitis is a progressive and irreversible inflammation of the pancreas, most often caused by long-term alcohol abuse, but it can also be related to ductal obstruction, smoking, or genetic factors.Chronic pancreatitis occurs when the pancreas is repeatedly exposed to harmful agents like alcohol, smoking, ductal obstruction, or genetic predisposition. These factors lead to the release of toxic metabolites and inflammatory cytokines, sustaining chronic inflammation in the pancreatic...
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

New Frontiers of Drug Development Through the Use of New Approach Methodologies.

The AAPS journal·2026
Same author

Phase II randomised study of magrolimab combined with bevacizumab-FOLFIRI in patients with previously treated advanced inoperable metastatic colorectal cancer.

ESMO gastrointestinal oncology·2026
Same author

Dietary management of normoalbuminaemic canine chronic enteropathies.

The Journal of small animal practice·2026
Same author

Efficacy of antimicrobial and nutraceutical treatment for canine acute diarrhoea: A systematic review and meta-analysis for European Network for Optimization of Antimicrobial Therapy (ENOVAT) guidelines.

Veterinary journal (London, England : 1997)·2023
Same author

Immune-mediated hematological disease in dogs is associated with alterations of the fecal microbiota: a pilot study.

Animal microbiome·2023
Same author

Avelumab in unresectable/metastatic, progressive, grade 2-3 neuroendocrine neoplasms (NENs): Combined results from NET-001 and NET-002 trials.

European journal of cancer (Oxford, England : 1990)·2022

Related Experiment Video

Updated: Jun 4, 2026

Ferric Chloride-induced Canine Carotid Artery Thrombosis: A Large Animal Model of Vascular Injury
08:39

Ferric Chloride-induced Canine Carotid Artery Thrombosis: A Large Animal Model of Vascular Injury

Published on: September 7, 2018

Hypercoagulability in dogs with protein-losing enteropathy.

L V Goodwin1, R Goggs, D L Chan

  • 1Department of Veterinary Clinical Sciences, Royal Veterinary College, University of London, UK.

Journal of Veterinary Internal Medicine
|February 15, 2011
PubMed
Summary

Dogs with protein-losing enteropathy (PLE) exhibit hypercoagulability, increasing their risk of blood clots. This hypercoagulable state persists even after treatment, suggesting ongoing thromboembolic complications in dogs with PLE.

More Related Videos

Isolation and Culture of Primary Endothelial Cells from Canine Arteries and Veins
08:24

Isolation and Culture of Primary Endothelial Cells from Canine Arteries and Veins

Published on: November 18, 2016

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
04:37

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation

Published on: May 23, 2025

Related Experiment Videos

Last Updated: Jun 4, 2026

Ferric Chloride-induced Canine Carotid Artery Thrombosis: A Large Animal Model of Vascular Injury
08:39

Ferric Chloride-induced Canine Carotid Artery Thrombosis: A Large Animal Model of Vascular Injury

Published on: September 7, 2018

Isolation and Culture of Primary Endothelial Cells from Canine Arteries and Veins
08:24

Isolation and Culture of Primary Endothelial Cells from Canine Arteries and Veins

Published on: November 18, 2016

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
04:37

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation

Published on: May 23, 2025

Area of Science:

  • Veterinary Medicine
  • Hematology
  • Canine Internal Medicine

Background:

  • Protein-losing enteropathy (PLE) in dogs has been anecdotally linked to thromboembolism.
  • The prevalence and underlying causes of hypercoagulability in dogs with PLE remain largely uninvestigated.

Purpose of the Study:

  • To determine if dogs with PLE are hypercoagulable compared to healthy controls.
  • To investigate the coagulation status in dogs with PLE.

Main Methods:

  • A prospective study involving 15 dogs with PLE and 30 healthy controls (HC).
  • Coagulation parameters were assessed using thromboelastography (TEG), including reaction time (R), kinetic time (K), alpha angle (α), and maximum amplitude (M(A)).
  • Nine dogs with PLE were re-evaluated after initiating immunosuppressive treatment.

Main Results:

  • All dogs with PLE demonstrated hypercoagulability, characterized by significantly decreased R and K times, and increased α angles and M(A) values compared to HC (P < .001).
  • Dogs with PLE had borderline low antithrombin (AT) concentrations and severely decreased serum albumin levels.
  • Despite clinical improvement and increased serum albumin after treatment, all re-evaluated dogs with PLE remained hypercoagulable.

Conclusions:

  • The hypercoagulable state in dogs with PLE is not solely due to antithrombin loss.
  • Dogs with PLE remain hypercoagulable despite treatment, indicating a potential predisposition to thromboembolic events.