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

Blood Flow01:29

Blood Flow

Blood is pumped by the heart into the aorta, the largest artery in the body, and then into increasingly smaller arteries, arterioles, and capillaries. The velocity of blood flow decreases with increased cross-sectional blood vessel area. As blood returns to the heart through venules and veins, its velocity increases. The movement of blood is encouraged by smooth muscle in the vessel walls, the movement of skeletal muscle surrounding the vessels, and one-way valves that prevent backflow.
Blood Pressure01:30

Blood Pressure

Blood pressure (BP) is the pressure or force of blood exerted on the artery's walls as it circulates through the body. It is essential for maintaining blood flow throughout the body.
The average BP in an adult is typically around 120/80 mmHg (millimeters of mercury). In this measurement, the numerator (120) indicates the systolic pressure, which is the pressure in the arteries during the contraction of the heart's ventricles as blood is expelled. The denominator (80) represents the diastolic...
Vascular Spasm01:16

Vascular Spasm

The vascular phase, also known as vasospasm, is the initial stage of hemostasis, crucial for preventing excessive bleeding when a blood vessel is injured. After a vessel is cut, nerves in the damaged area trigger pain and other sensory impulses. Simultaneously, the smooth muscles in the vessel wall contract, resulting in a vascular spasm. This contraction reduces the vessel's diameter at the injury site, slowing or stopping blood loss through the vessel wall. Vascular spasms typically last for...
Blood Pressure01:24

Blood Pressure

The movement of blood in a human body, commonly referred to as blood flow, is determined by the volume of blood that traverses a certain section of the bodily system per unit time. It is the rhythmic contraction of the heart's ventricles that primarily instigates this movement. As the ventricles contract, blood is forced into the prominent arteries, which then flow from areas of greater pressure to lower pressure areas. This movement continues into smaller arteries and arterioles and...
Autoregulation of Blood Flow01:17

Autoregulation of Blood Flow

Autoregulation mechanisms are characterized by their inherent capacity for self-regulation without necessitating specific nervous stimulation or endocrine control. These mechanisms facilitate the adjustment of blood flow and, therefore, perfusion specific to each tissue region. This self-regulation encompasses chemical signals and myogenic controls.
Chemical Signaling in Autoregulation
Chemical signaling operates at the precapillary sphincter level, inciting either contraction or relaxation.
Blood Pressure Imbalances and Circulatory Shock01:24

Blood Pressure Imbalances and Circulatory Shock

Disorders affecting blood volume, vascular tone, or vascular function can disrupt vascular homeostasis, including conditions like hypertension, hemorrhage, and shock.
Blood Pressure: Hypertension and Hypotension
Normal blood pressure is 120/80 mm Hg. Elevated blood pressure is 120-129/under 80 mm Hg. Hypertension, warranting treatment at 130/80 mm Hg, is often asymptomatic and can lead to severe cardiovascular events, aneurysms, peripheral arterial disease, chronic renal disease, or cardiac...

You might also read

Related Articles

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

Sort by
Same author

Microbiota-mediated mechanisms of natural products in atherosclerosis: focus on metabolic and inflammatory pathways.

Frontiers in endocrinology·2026
Same author

A novel antibacterial-immunomodulatory injectable hydrogel for periodontitis management: an in vitro study.

BMC oral health·2026
Same author

A DMAHDM-herbal hybrid gargle for orthodontic-associated complications via oral microbiota regulation, inflammation inhibition, and enamel protection.

Materials today. Bio·2026
Same author

KPNA2 Drives Immunosuppression in Ovarian Cancer via CCL2/CCR2-Dependent MDSC Recruitment.

Cancer science·2026
Same author

The 2023 FIGO Stage IA3: shifting the SEOC paradigm from pathogenic debate to clinical precision.

Journal of gynecologic oncology·2026
Same author

Reduced Myocardial Serine Synthesis Impairs Functional, Metabolic, and Redox Adaptations to Cardiac Stress.

bioRxiv : the preprint server for biology·2026

Related Experiment Video

Updated: Jul 7, 2026

Microfluidic Flow Chambers Using Reconstituted Blood to Model Hemostasis and Platelet Transfusion In Vitro
10:25

Microfluidic Flow Chambers Using Reconstituted Blood to Model Hemostasis and Platelet Transfusion In Vitro

Published on: March 19, 2016

Hemodynamic modulation of endocardial thromboresistance.

Navin K Kapur1, Clayton B Deming, Sunil Kapur

  • 1Division of Cardiology, Johns Hopkins School of Medicine, 600 N. Wolfe St, Baltimore, MD 21287, USA.

Circulation
|December 28, 2006
PubMed
Summary

Elevated heart pressure in heart failure reduces thrombomodulin, a key anticoagulant, increasing thrombus risk. Restoring thrombomodulin levels prevents this effect, highlighting its role in preventing blood clots.

More Related Videos

A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time
09:38

A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time

Published on: February 14, 2017

In Vitro Microfluidic Disease Model to Study Whole Blood-Endothelial Interactions and Blood Clot Dynamics in Real-Time
09:19

In Vitro Microfluidic Disease Model to Study Whole Blood-Endothelial Interactions and Blood Clot Dynamics in Real-Time

Published on: May 24, 2020

Related Experiment Videos

Last Updated: Jul 7, 2026

Microfluidic Flow Chambers Using Reconstituted Blood to Model Hemostasis and Platelet Transfusion In Vitro
10:25

Microfluidic Flow Chambers Using Reconstituted Blood to Model Hemostasis and Platelet Transfusion In Vitro

Published on: March 19, 2016

A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time
09:38

A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time

Published on: February 14, 2017

In Vitro Microfluidic Disease Model to Study Whole Blood-Endothelial Interactions and Blood Clot Dynamics in Real-Time
09:19

In Vitro Microfluidic Disease Model to Study Whole Blood-Endothelial Interactions and Blood Clot Dynamics in Real-Time

Published on: May 24, 2020

Area of Science:

  • Cardiovascular Medicine
  • Hematology
  • Molecular Biology

Background:

  • Heart failure patients face higher risks of thromboembolic events like stroke.
  • The role of elevated chamber filling pressure on endocardial function and thrombus formation is not well understood.

Purpose of the Study:

  • To investigate the impact of acute atrial pressure overload on thrombomodulin expression and thrombin generation in rats.
  • To explore the mechanisms underlying thrombomodulin downregulation and its potential therapeutic restoration.

Main Methods:

  • Induction of acute atrial pressure overload via aortic banding in rats.
  • Measurement of atrial endocardial thrombomodulin expression and local thrombin generation.
  • Adenovirus-mediated gene transfer to restore thrombomodulin expression.
  • In vitro co-culture and in vivo antibody administration to investigate transforming growth factor-beta's role.

Main Results:

  • Acute pressure overload significantly inhibited atrial endocardial thrombomodulin expression by 70%.
  • This inhibition led to increased local thrombin generation.
  • Restoration of thrombomodulin expression reduced thrombin generation to baseline.
  • Transforming growth factor-beta, released by stretched cardiac connective tissue, was identified as the cause of thrombomodulin downregulation.

Conclusions:

  • Increased hemodynamic load adversely affects endocardial function.
  • Reduced thrombomodulin expression due to pressure overload is a key factor in thromboembolus formation in heart failure.
  • Targeting thrombomodulin or transforming growth factor-beta may offer therapeutic strategies for heart failure-associated thrombosis.