Bacterial translocation in cirrhotic rats stimulates eNOS-derived NO production and impairs mesenteric vascular contractility
Summary
This summary is machine-generated.Bacterial translocation to mesenteric lymph nodes in cirrhotic rats increases tumor necrosis factor-alpha and tetrahydrobiopterin. This enhances nitric oxide overproduction, impairing vascular function.
Area Of Science
- Vascular Biology
- Gastroenterology
- Immunology
Background
- Liver cirrhosis is associated with arterial vasodilation and hyporesponsiveness to vasoconstrictors.
- Bacteria in mesenteric lymph nodes (MLNs) can activate nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha) synthesis.
Purpose Of The Study
- To investigate the impact of bacterial translocation (BT) to MLNs on TNF-alpha production, NO release, and mesenteric vascular contractility in cirrhotic rats.
Main Methods
- Assessed vascular response to methoxamine in cirrhotic rats with and without BT.
- Measured NO release, blocked by N(omega)-nitro-L-arginine, and examined endothelial NO synthase (eNOS) expression.
- Quantified TNF-alpha and tetrahydrobiopterin (BH(4)) levels in MLNs and serum.
Main Results
- BT further blunted vascular response to methoxamine in cirrhotic rats.
- BT promoted shear stress-dependent NO release, involving enhanced eNOS expression.
- BT induced TNF-alpha production and elevated BH(4) levels, linked to increased eNOS activity.
Conclusions
- Bacterial translocation to MLNs contributes to increased TNF-alpha and BH(4) in cirrhosis.
- This process enhances eNOS-derived NO overproduction, exacerbating impaired mesenteric vascular contractility.
View abstract on PubMed