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Effect of Nitric Oxide Pathway Inhibition on the Evolution of Anaphylactic Shock in Animal Models: A Systematic

Maryam Alfalasi1, Sarah Alzaabi1, Linda Östlundh2

  • 1College of Medicine and Health Sciences, UAE University, Al Ain, United Arab Emirates.

Biology
|June 24, 2022
PubMed

Insights

Inhibiting nitric oxide (NO) pathways may not be sufficient to treat or prevent anaphylactic shock (AS). Further research is needed to explore combination therapies for effective AS management.

Area of Science:

  • Pharmacology
  • Immunology
  • Critical Care Medicine

Background:

  • Nitric oxide (NO) is known to cause vasodilation in various shock states.
  • The role of modulating the NO pathway in anaphylactic shock (AS) is not well understood.
  • Anaphylaxis is a severe, life-threatening allergic reaction.

Purpose of the Study:

  • To systematically review the literature on the efficacy of inhibiting NO pathways (INOP) for preventing or treating AS.
  • To evaluate the impact of blocking NO synthase or guanylate cyclase on AS outcomes.

Main Methods:

  • A systematic literature search was performed across major databases (PubMed, EMBASE, Scopus, Cochrane, Web of Science) until March 2022.
  • Seventeen studies were included after screening 135 full-text articles from 990 unique identified studies.
  • Included studies investigated six different NO pathway inhibitors, with varying pre-treatment and post-treatment models.

Main Results:

  • Seven of fourteen pre-treatment studies suggested improved survival and/or arterial blood pressure.
  • Four of eight post-treatment studies indicated positive outcomes.
  • Heterogeneity among studies precluded meta-analysis.

Conclusions:

  • There is currently insufficient strong evidence to support the sole blockade of the NO/cGMP pathway for preventing or reversing anaphylactic hypotension.
  • Further investigation into combination drug therapies is warranted for effective AS treatment.
Keywords:
anaphylactic shockcyclic guanosine monophosphateguanylate cyclasenitric oxidenitric oxide synthase

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