Inhibition of glucagon improves splanchnic hyporesponse to terlipressin in cirrhotic rats with blood retention in the gastric lumen

Concomitant inhibition of oxidative stress and angiogenesis by chronic hydrogen‐rich saline and N‐acetylcysteine treatments improves systemic, splanchnic and hepatic hemodynamics of cirrhotic rats

“…In the first set of rats, mean arterial pressure, heart rate and superior mesenteric arterial blood flow (SMA BF ) were measured. Additionally, superior mesenteric arterial resistance (SMA R ) was calculated using the formula of (SMA R = [mean arterial pressure – portal perfusion pressure] / SMA BF ) . Finally, plasma concentrations of interleukin (IL)‐1β, tumor necrosis factor (TNF)‐α, IL‐6, IL‐8 and IL‐17 were measured by commercially available enzyme‐linked immunoassay (ELISA) kits (R&D Systems, Minneapolis, MN, USA).…”

“…Additionally, superior mesenteric arterial resistance (SMAR) was calculated using the formula Hydrogen-rich saline for cirrhotic circulation of (SMAR = [mean arterial pressure -portal perfusion pressure] / SMABF). 5,22 Finally, plasma concentrations of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, IL-6, IL-8 and IL-17 were measured by commercially available enzyme-linked immunoassay (ELISA) kits (R&D Systems, Minneapolis, MN, USA). For analysis of relative fibrotic area, Masson-trichrome blue stained area in 10-field high-power (×20) field was calculated in five slides in each animal.…”

The relationship between endotoxemia and hepatic endocannabinoids in cirrhotic rats with portal hypertension

“…Mean arterial pressure (MAP), cardiac index (CI), systemic vascular resistance, superior mesenteric arterial blood flow and resistance, and portal venous pressure (PVP) were measured [15,16]. Plasma TNF-a and endotoxin levels were quantified by ELISA kits.…”

Hyperdynamic mesenteric circulation in cirrhosis: humoral or neural mechanism?

“…There are currently two theories to explain this phenomenon; one is the humoral factor hypothesis. This theory contends that in cirrhosis, portosystemic collaterals allow gut‐derived humoral substances, such as glucagon , bile acid and calcitonin gene‐related peptide (CGRP) to directly enter the systemic circulation without detoxification by the liver. Moreover, portosystemic shunts also allow gut‐derived endotoxemia which stimulate local vasodilators such as prostaglandins, nitric oxide (NO) and carbon monoxide.…”