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Related Experiment Video

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Cecal Ligation Puncture Procedure
11:53

Cecal Ligation Puncture Procedure

Published on: May 7, 2011

Vitamin C in sepsis.

John X Wilson1, F Wu

  • 1Department of Exercise and Nutrition Sciences, University at Buffalo, Buffalo, NY, 14214-8028, USA, jxwilson@buffalo.edu.

Sub-Cellular Biochemistry
|November 26, 2011
PubMed
Summary
This summary is machine-generated.

Intravenous vitamin C (ascorbate) may improve microvascular function and survival in sepsis. This therapy addresses low ascorbate levels in critically ill patients by restoring capillary blood flow and arteriolar responsiveness, potentially reducing organ failure.

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Evaluation of a Reliable Biomarker in a Cecal Ligation and Puncture-Induced Mouse Model of Sepsis

Published on: December 9, 2022

Area of Science:

  • Critical Care Medicine
  • Biochemistry
  • Vascular Biology

Background:

  • Bacterial bloodstream infections cause sepsis, leading to systemic inflammatory response syndrome (SIRS), encephalopathy, severe sepsis, and septic shock.
  • Microvascular dysfunction, characterized by impaired capillary blood flow and arteriolar responsiveness, is a key factor preceding multiple organ failure in sepsis.
  • Critically ill patients often exhibit low vitamin C (ascorbate) levels, impacting disease progression.

Purpose of the Study:

  • To investigate the potential of intravenous ascorbate administration to improve microvascular function and survival in sepsis.
  • To explore the mechanisms by which ascorbate may exert protective effects in sepsis models.

Main Methods:

  • Utilized animal models of polymicrobial sepsis to assess the effects of intravenous ascorbate injection.
  • Measured microvascular function, including capillary blood flow and arteriolar responsiveness.
  • Investigated the biochemical pathways potentially modulated by ascorbate, such as oxidative stress and nitric oxide homeostasis.

Main Results:

  • Intravenous ascorbate administration restored microvascular function and increased survival rates in animal models of polymicrobial sepsis.
  • Ascorbate demonstrated potential to inhibit oxidative stress by scavenging reactive oxygen species (ROS) and inhibiting NADPH oxidase.
  • Ascorbate may modulate intracellular signaling pathways and maintain nitric oxide homeostasis, influencing endothelial function.

Conclusions:

  • Intravenous vitamin C (ascorbate) shows promise as an adjunctive therapy for improving microvascular function in sepsis.
  • Ascorbate's protective effects may stem from its antioxidant properties and its ability to modulate nitric oxide pathways.
  • Further research into intravenous ascorbate therapy could lead to improved clinical outcomes for sepsis patients.