Turn Up the Hydroxyeicosatetraenoic on Septic Shock

Kirby Thomas, Luke Strong, Fan Fan, Richard J. Roman

Research output: Contribution to journalArticlepeer-review

Abstract

Abstract:Septic shock is life-threatening organ dysfunction due to a dysregulated response to infection. It is a leading cause of death caused by the excessive release of cytokines and inflammatory mediators in response to bacterial endotoxins. It produces hypotension refractory to vasoconstrictors leading to tissue hypoperfusion and multiple organ failure. Despite intensive investigation, there still are no specific pharmacologic treatments. Current therapy relies on supportive care, including antibiotics, fluid resuscitation, corticosteroids, and pressor agents. This commentary summarizes little-known previous observations that inhibition of vascular 20-hydroxyeicosatetraenoic acid (20-HETE) by nitric oxide plays a key role in sepsis. It also highlights the new and exciting current report by Tunctan et al (2022) in this issue of Journal of Cardiovascular Pharmacology that administration of a 20-HETE mimetic can prevent lipopolysaccharide-induced vascular hyporeactivity, hypotension, and tachycardia in rats by activating the recently discovered GPR75/20-HETE receptor. Overall, these results provide a compelling case for initiating 20-HETE clinical trials to prevent hypotension, multiple organ failure, and death in septic shock.

Original languageEnglish (US)
Pages (from-to)206-209
Number of pages4
JournalJournal of Cardiovascular Pharmacology
Volume80
Issue number2
DOIs
StatePublished - Aug 1 2022
Externally publishedYes

Keywords

  • 20-HETE
  • arachidonic acid
  • cytochrome P450
  • LPS
  • nitric oxide
  • septic shock

ASJC Scopus subject areas

  • Pharmacology
  • Cardiology and Cardiovascular Medicine

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