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Hyperdynamic circulatory syndrome in a mouse model transgenic for SerpinB3
Gianmarco Villano1, Alberto Verardo2, Andrea Martini2
1Dept. of Surgery, Oncology and Gastroenterology, University of Padova, Padova, Italy.
Annals of Hepatology
|October 15, 2019
Summary
SerpinB3, a liver disease protein, increases blood flow and vascular reactivity in mice. This effect is linked to angiotensin II receptors, suggesting a role in circulatory changes.
Area of Science:
- Cardiovascular Physiology
- Hepatology
- Protease Inhibition
Background:
- SerpinB3 is a cysteine protease inhibitor.
- Its expression increases in chronic liver disease but not in normal liver.
- The role of SerpinB3 in vascular reactivity is unknown.
Purpose of the Study:
- To evaluate the in vivo and in vitro effects of SerpinB3 on systemic and splanchnic hemodynamics.
- To investigate the potential involvement of angiotensin II pathways.
Main Methods:
- Hemodynamic parameters were assessed using ultrasonography in SerpinB3 transgenic mice and controls.
- In vitro studies analyzed SerpinB3's effect on rat mesenteric microvessels.
- Angiotensin II type 1 receptor inhibition was used to assess pathway involvement.
Main Results:
- SerpinB3 transgenic mice showed significantly increased cardiac output, hepatic artery pulsatility index, and portal vein blood flow.
- In vitro, SerpinB3 enhanced phenylephrine-induced vasoconstriction in mesenteric arteries.
- This enhanced vasoconstriction was blocked by inhibiting angiotensin II type 1 receptors.
Conclusions:
- SerpinB3 is associated with a hyperdynamic circulatory syndrome-like pattern in transgenic mice.
- This effect appears to be mediated by angiotensin II receptors.
- SerpinB3 may play a role in regulating vascular tone and systemic hemodynamics.
