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 Respiratory Failure-III01:30

Acute Respiratory Failure-III

Hypercapnic respiratory failure, also known as Type 2 or ventilatory respiratory failure, is a severe condition characterized by the body's inability to effectively remove carbon dioxide (CO2) from the bloodstream. It leads to an arterial CO2 pressure (PaCO2) exceeding 45 mmHg and a blood pH above 7.35. This situation indicates that the body's ventilatory demand, or the ventilation needed to maintain normal PaCO2 levels, surpasses its supply or the maximum gas flow achievable without causing...
Mechanical Ventilation III: Noninvasive Ventilation01:23

Mechanical Ventilation III: Noninvasive Ventilation

Noninvasive positive-pressure ventilation (NIPPV), continuous positive airway pressure (CPAP), and bilevel positive airway pressure (BiPAP) are essential methods in respiratory care. These ventilation techniques offer unique benefits for patients with various respiratory conditions, providing adequate support without requiring intubation. Let's explore how each method is crucial in improving patient outcomes and enhancing respiratory therapy.
Noninvasive Positive-Pressure Ventilation (NIPPV)
Complement System01:27

Complement System

The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a membrane...
Pneumonia III: Complications and Assessment01:30

Pneumonia III: Complications and Assessment

Pneumonia poses the potential for numerous complications that warrant consideration. These complications include the following:
Acute Respiratory Failure-II01:21

Acute Respiratory Failure-II

Type I Respiratory Failure, or hypoxemic respiratory failure, occurs when the partial pressure of oxygen (PaO2) in arterial blood falls below 60 mmHg while breathing room air without a corresponding increase in arterial carbon dioxide levels (PaCO2). This condition highlights a significant impairment in the lungs' capacity to oxygenate the blood.
The underlying physiological abnormalities that contribute to hypoxemic respiratory failure include:
Acute Respiratory Failure-I01:21

Acute Respiratory Failure-I

Acute respiratory failure is a condition characterized by the inability of the lungs to perform their primary function: gas exchange. This failure leads to insufficient oxygen levels (hypoxemia) in the blood, elevated carbon dioxide levels (hypercapnia), or both, causing critical impairment in organ function.
Definition: It is defined by specific criteria based on blood gas measurements. Hypoxemia happens when the partial pressure of oxygen (PaO2) falls below 60 mmHg. At the same time,...

You might also read

Related Articles

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

Sort by
Same author

Deconstructing the Role of Mechanical Power in Lung Injury and Respiratory Failure.

Anesthesiology·2026
Same author

Simultaneous Pi2 pulsation detected by CSES-01, Swarm, RBSP and Arase satellites.

Scientific reports·2026
Same author

Antibodies to mannose-binding lectin and factor XI Inhibit Shiga toxin-induced kidney injury additively in a murine model.

Pediatric research·2026
Same author

Imaging Traumatic Brain Injuries in Mice with Potassium Channel PET Tracer [<sup>18</sup>F]3F4AP.

Journal of neurotrauma·2026
Same author

Dietary sugars inhibit biologic functions of the pattern recognition molecule, mannose-binding lectin.

Open journal of immunology·2026
Same author

Pulmonary complications following urological, gastrointestinal and gynaecological abdominal Surgery--A post-hoc analysis of an observational study in 29 countries.

Anaesthesia, critical care & pain medicine·2025

Related Experiment Video

Updated: May 28, 2026

Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury
14:48

Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury

Published on: March 21, 2021

Complement 3 is involved with ventilator-induced lung injury.

Kazue Takahashi1, Dalia Saha, Ivany Shattino

  • 1Program of Developmental Immunology, Department of Pediatrics, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. ktakahashi1@partners.org

International Immunopharmacology
|October 8, 2011
PubMed
Summary

Complement 3 (C3) plays a role in ventilator-induced lung injury (VILI). Inhibiting complement activation may offer a therapeutic strategy for VILI by reducing lung damage.

More Related Videos

Surfactant Depletion Combined with Injurious Ventilation Results in a Reproducible Model of the Acute Respiratory Distress Syndrome (ARDS)
06:22

Surfactant Depletion Combined with Injurious Ventilation Results in a Reproducible Model of the Acute Respiratory Distress Syndrome (ARDS)

Published on: April 7, 2021

Monitoring Lung Function with Electrical Impedance Tomography in the Intensive Care Unit
05:56

Monitoring Lung Function with Electrical Impedance Tomography in the Intensive Care Unit

Published on: September 6, 2024

Related Experiment Videos

Last Updated: May 28, 2026

Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury
14:48

Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury

Published on: March 21, 2021

Surfactant Depletion Combined with Injurious Ventilation Results in a Reproducible Model of the Acute Respiratory Distress Syndrome (ARDS)
06:22

Surfactant Depletion Combined with Injurious Ventilation Results in a Reproducible Model of the Acute Respiratory Distress Syndrome (ARDS)

Published on: April 7, 2021

Monitoring Lung Function with Electrical Impedance Tomography in the Intensive Care Unit
05:56

Monitoring Lung Function with Electrical Impedance Tomography in the Intensive Care Unit

Published on: September 6, 2024

Area of Science:

  • Immunology
  • Pulmonology
  • Biochemistry

Background:

  • Mechanical ventilation can cause lung injury.
  • Humoral factors contribute to tissue damage.
  • The role of complement 3 (C3) in ventilator-induced lung injury (VILI) is not fully understood.

Purpose of the Study:

  • To investigate the role of complement 3 (C3) in a mouse model of ventilator-induced lung injury (VILI).
  • To explore the relationship between C3 activation, matrix metalloproteinases (MMPs), and bronchoalveolar lavage (BAL) cells in VILI.

Main Methods:

  • Utilized a mouse model of ventilator-induced lung injury (VILI).
  • Compared wild-type (WT) mice with C3 null mice under mechanical ventilation.
  • Assessed bronchoalveolar lavage (BAL) cells, thrombin activity, and matrix metalloproteinase (MMP) levels.
  • Used humanized cobra venom factor to inactivate C3 in WT mice.

Main Results:

  • Ventilated WT mice showed reduced BAL cells and elevated thrombin and MMP activities compared to sham-treated mice.
  • C3 null mice exhibited significantly different parameters compared to sham-treated mice.
  • Mechanical ventilation led to lower thrombin activity and MMPs in C3 null mice, inversely correlated with BAL cells.
  • In vitro studies showed C3 activation is linked to MMP activation.
  • Inactivating C3 reduced lung deposition and increased BAL cells in VILI.

Conclusions:

  • Complement 3 (C3) is implicated in the pathogenesis of ventilator-induced lung injury (VILI).
  • C3 activation is associated with increased thrombin and MMP activity in VILI.
  • Inhibition of complement activation presents a potential therapeutic avenue for VILI.