Advances in Vascular Hyporeactivity After Shock: The Mechanisms and Managements

Shock. 2015 Dec;44(6):524-34. doi: 10.1097/SHK.0000000000000457.

Abstract

Vascular reactivity to vasoconstrictors and vasodilators is greatly reduced after severe trauma, shock, and sepsis or multiple organ dysfunction syndrome. This reduced vascular reactivity severely interferes with the treatment of shock and other critical conditions. In particular, it interferes with the efficacy of vasoactive agents. Consequently, it is very important to elucidate the mechanisms and search for the effective treatment measures. In recent years, a lot of studies focused on the characteristics and the change rules of vascular hyporeactivity and mechanisms following shock. Also, the treatment approaches based on various mechanisms have been a hot pot these years.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Acidosis
  • Adult
  • Age Factors
  • Aged
  • Analgesics, Opioid / chemistry
  • Blood Vessels / drug effects
  • Blood Vessels / physiopathology*
  • Burns / therapy
  • Calcium / chemistry
  • Carbon Monoxide / chemistry
  • Cell Membrane / metabolism
  • Critical Illness
  • Endothelins / chemistry
  • Female
  • Humans
  • Male
  • Middle Aged
  • Nitric Oxide / chemistry
  • Peptides / chemistry
  • Protein Kinase C / chemistry
  • Sex Factors
  • Shock, Hemorrhagic / physiopathology*
  • Shock, Hemorrhagic / therapy*
  • Shock, Septic / therapy
  • Tetradecanoylphorbol Acetate / chemistry
  • Vasoconstrictor Agents / therapeutic use*
  • Vasodilator Agents / therapeutic use*
  • rho-Associated Kinases / metabolism

Substances

  • Analgesics, Opioid
  • Endothelins
  • Peptides
  • Vasoconstrictor Agents
  • Vasodilator Agents
  • Nitric Oxide
  • Carbon Monoxide
  • rho-Associated Kinases
  • Protein Kinase C
  • Tetradecanoylphorbol Acetate
  • Calcium