Effects of Hydrogen Sulfide at Normal Body Temperature and in the Cold on Isolated Tail and Carotid Arteries from Rats and TRPA1 Knockout and Wild-Type Mice
2024

Effects of Hydrogen Sulfide on Rat and Mouse Arteries

Sample size: 96 publication Evidence: moderate

Author Information

Author(s): Kelava Leonardo, Pakai Eszter, Ogasawara Kazushi, Fekete Kata, Pozsgai Gabor, Pinter Erika, Garami Andras

Primary Institution: University of Pecs

Hypothesis

The study aims to compare the effects of hydrogen sulfide on isolated carotid and tail arteries from rats and mice at different temperatures.

Conclusion

Hydrogen sulfide causes different vasomotor responses in rat and mouse arteries, influenced by temperature and the presence of TRPA1 channels.

Supporting Evidence

  • Hydrogen sulfide can cause either vasodilation or vasoconstriction depending on the vascular bed and species.
  • The TRPA1 channel mediates some of the vasomotor responses to hydrogen sulfide in mouse carotid arteries.
  • Temperature significantly affects the vasomotor response to acetylcholine in all vessel types studied.
  • Na2S caused different vasomotor responses in rat and mouse arteries.
  • Acetylcholine-induced dilation decreased in the cold across all vessel types.

Takeaway

This study looks at how a gas called hydrogen sulfide affects blood vessels in rats and mice, showing that it can make them either widen or tighten depending on the temperature.

Methodology

The study involved isolating carotid and tail arteries from rats and mice and measuring their responses to sodium sulfide and other vasodilators using wire myography.

Limitations

The study focused on larger arteries rather than arterioles, which may limit the physiological relevance of the findings.

Participant Demographics

32 adult Wistar rats and 64 TRPA1 knockout and wild-type mice of both sexes.

Statistical Information

P-Value

p = 0.009; p = 0.031; p = 0.000463; p = 0.00835; p = 0.00535; p = 0.00821; p = 0.00122

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.3390/biomedicines12122874

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