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Related Concept Videos

Inflammation01:38

Inflammation

Overview
Introduction to Hemostasis01:05

Introduction to Hemostasis

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, and...
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...
Acute Inflammation III: Local and Systemic Effects01:25

Acute Inflammation III: Local and Systemic Effects

Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...

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Related Experiment Video

Updated: May 24, 2026

Intravital Widefield Fluorescence Microscopy of Pulmonary Microcirculation in Experimental Acute Lung Injury Using a Vacuum-Stabilized Imaging System
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Intravital Widefield Fluorescence Microscopy of Pulmonary Microcirculation in Experimental Acute Lung Injury Using a Vacuum-Stabilized Imaging System

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Vessel injury and capillary leak.

Rhonda S Fishel1, Chandrakanth Are, Adrian Barbul

  • 1Department of Surgery, Sinai Hospital of Baltimore, MD 21215, USA.

Critical Care Medicine
|August 9, 2003
PubMed
Summary

Pathologic capillary leak in critically ill patients causes edema due to increased permeability. Current understanding is fragmented, and treatments for capillary leak syndrome remain largely ineffective.

Area of Science:

  • Critical care medicine
  • Physiology
  • Pathology

Background:

  • Capillary leak syndrome (CLS) is a critical condition characterized by widespread leakage from capillaries.
  • Edema formation in critically ill patients is often linked to altered microvascular function.

Purpose of the Study:

  • To elucidate the underlying mechanisms of pathologic capillary leak in critically ill patients.
  • To review current understanding of CLS pathogenesis, mediators, and potential interventions.

Main Methods:

  • Comprehensive review of normal and altered microvascular physiology.
  • Systematic literature review of pathogenesis, mediators, and interventions for capillary leak.
  • Inclusion of in vitro, animal, and human in vivo study data.

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Visualization of Neutrophil Extracellular Traps in Mesenteric Venules After Mesenteric Ischemia-Reperfusion Injury via Intravital Microscopy
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Visualization of Neutrophil Extracellular Traps in Mesenteric Venules After Mesenteric Ischemia-Reperfusion Injury via Intravital Microscopy
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Visualization of Neutrophil Extracellular Traps in Mesenteric Venules After Mesenteric Ischemia-Reperfusion Injury via Intravital Microscopy

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Main Results:

  • CLS in critical care arises from Starling's equation imbalances, primarily increased capillary permeability to macromolecules.
  • Inflammatory mediators and mechanical stress are key drivers of capillary leak.
  • Current therapeutic and preventive strategies for CLS show limited success, with resuscitation often being symptomatic.

Conclusions:

  • Understanding of capillary leak syndrome is incomplete, with a focus on specific mediators.
  • The resolution mechanisms of extensive edema in CLS are poorly understood and require further investigation.