Researchers used Trpv1-knockout mice to study genetic disruption of the receptor and the agonist resiniferatoxin or the antagonist capsazepine to study pharmacologic disruption of TRPV1. They examined the role of the disruptions in sepsis caused by lipopolysaccharide or cecal ligation and puncture.
Data showed different effects of TRPV1 disruption depending on the type of disruption and cause of sepsis. Genetic disruption after cecal ligation and puncture was associated with higher mortality risk. Disruption with intrathecal resiniferatoxin after cecal ligation and puncture increased mortality risk in wild-type mice, but not Trpv1-knockout mice. This increase was associated with higher blood bacterial count, higher nitrate/nitrite concentrations and down-regulation of tumor necrosis factor α expression. After lipopolysaccharide, TRPV1 disruption with capsazepine also increased mortality risk in WT mice.
Read the Anesthesiology abstract on the role of transient receptor potential vanilloid 1 in sepsis.
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