Effect and mechanism of salvianolic acid B in attenuating elevated portal pressure in a rat model of portal hypertension induced by endothelin-1

2007 ◽  
pp. 61-64 ◽  
Author(s):  
Yang Zhou
Keyword(s):  
Portal Hypertension ◽  
Rat Model ◽  
Portal Pressure ◽  
Salvianolic Acid B ◽  
Salvianolic Acid ◽  
Endothelin 1

scholarly journals Salvianolic Acid B Suppresses Inflammatory Mediator Levels by Downregulating NF-κB in a Rat Model of Rheumatoid Arthritis

2018 ◽  
Vol 24 ◽  
pp. 2524-2532 ◽  
Author(s):  
Zeng-Bing Xia ◽  
Yong-Jian Yuan ◽  
Qiang-Hua Zhang ◽  
Heng Li ◽  
Ji-Lin Dai ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Rat Model ◽  
Inflammatory Mediator ◽  
Salvianolic Acid B ◽  
Salvianolic Acid

Evolution of portal hypertension and mechanisms involved in its maintenance in a rat model

1985 ◽  
Vol 248 (6) ◽  
pp. G618-G625 ◽  
Author(s):  
E. Sikuler ◽  
D. Kravetz ◽  
R. J. Groszmann
Keyword(s):  
Blood Flow ◽  
Portal Hypertension ◽  
Portal Vein ◽  
Rat Model ◽  
Portal Pressure ◽  
Portal System ◽  
Hypertensive Rats ◽  
Hemodynamic Changes ◽  
Sequence Of Events ◽  
Radioactive Microsphere

In rats with portal hypertension induced by partial ligation of the portal vein, we have recently demonstrated an increased portal venous inflow that becomes an important factor in the maintenance of portal hypertension. The sequence of events that leads into this circulatory disarray is unknown. We evaluated chronologically the chain of hemodynamic changes that occurred after portal hypertension was induced by partial ligation of the portal vein. In this model it is possible to follow, from the initiation of the portal-hypertensive state, the interaction between blood flow and resistance in the portal system as well as the relation between the development of portal-systemic shunting and the elevated portal venous inflow. The study was performed in 45 portal-hypertensive rats and in 29 sham-operated rats. Blood flow and portal-systemic shunting were measured by radioactive microsphere techniques. The constriction of the portal vein was immediately followed by a resistance-induced portal hypertension characterized by increased portal resistance (9.78 +/- 0.89 vs. 4.18 +/- 0.71 dyn X s X cm-5 X 10(4), mean +/- SE, P less than 0.01), increased portal pressure (17.7 +/- 0.9 vs. 9.5 +/- 0.6 mmHg, P less than 0.001), and decreased portal venous inflow (3.93 +/- 0.26 vs. 6.82 +/- 0.49 ml X min-1 X 100 g body wt-1, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Interaction of flow and resistance in maintenance of portal hypertension in a rat model

1986 ◽  
Vol 250 (2) ◽  
pp. G205-G212 ◽  
Author(s):  
E. Sikuler ◽  
R. J. Groszmann
Keyword(s):  
Portal Hypertension ◽  
Portal Vein ◽  
Rat Model ◽  
Portal Pressure ◽  
Flow Theory ◽  
Sham Operation ◽  
Portal Flow ◽  
Hemodynamic Changes ◽  
Forward Flow ◽  
Arteriolar Resistance

To clarify the roles that portocollateral resistance ("backward-flow" theory) and portal flow ("forward-flow" theory) play in maintaining chronic portal hypertension, we studied, in a rat model with prehepatic portal hypertension, the hemodynamic changes that occur when portocollateral resistance is reduced and high portal venous inflow is maintained. In 30 portal-hypertensive rats the constriction around the portal vein was removed 4 days after induction of portal hypertension, 30 rats were used as portal vein-constricted controls, and 30 additional rats were subjected to a sham operation. The removal of the ligature constricting the portal vein was followed by an immediate decrease in portal pressure (from 16.3 +/- 0.8 to 9.6 +/- 0.8 mmHg, P less than 0.001). Two days after the ligature removal, hyperdynamic circulation was still evident and was characterized by a decreased splanchnic arteriolar resistance and an increased portal venous inflow. The coexistence of high portal venous inflow and normal portal pressure indicates that high portal venous inflow per se is not sufficient to produce an increase in portal pressure when it faces a low-resistance vascular bed. We conclude that portal hypertension is induced by the interaction of an abnormally high portal venous inflow and high resistance offered to the flow by the portocollateral vessels. Neither the forward-flow theory nor the backward-flow theory can be applied solely to explain the increased portal pressure.

Aminoguanidine ameliorates splanchnic hyposensitivity to glypressin in a haemorrhage-transfused rat model of portal hypertension

1998 ◽  
Vol 95 (5) ◽  
pp. 629-636 ◽  
Author(s):  
Chi-Jen CHU ◽  
Fa-Yauh LEE ◽  
Sun-Sang WANG ◽  
Full-Young CHANG ◽  
Han-Chieh LIN ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Portal Hypertension ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Portal Vein ◽  
Rat Model ◽  
Portal Pressure ◽  
Hypotensive Effect ◽  
Portal Vein Ligation ◽  
Nitric Oxide Synthase Inhibitor

1.Hyposensitivity to vasopressin is a well-documented phenomenon in animals with portal hypertension and patients with cirrhosis subjected to haemorrhage. Excessive formation of nitric oxide is at least partly responsible for the vascular hyporesponsiveness to vasoconstrictors observed in experimental portal hypertension or in rats with haemorrhagic shock. This study investigated whether addition of aminoguanidine, a preferential inducible nitric oxide synthase inhibitor, to glypressin (a long-acting vasopressin analogue) could enhance its portal hypotensive effect in portal-hypertensive rats with bleeding. 2.Portal hypertension was induced by partial portal vein ligation. Fourteen days after operation, systemic and portal haemodynamics were measured in stable or bleeding portal vein-ligated rats receiving intravenous glypressin (0.07 ;mg/kg) or aminoguanidine (70 ;mg/kg) followed by glypressin infusion. In rats with a hypotensive haemorrhage, 4.5 ;ml of blood was withdrawn and 50% of the withdrawn blood was reinfused before the administration of glypressin or aminoguanidine. 3.Glypressin resulted in a significantly greater decrease in portal pressure in portal vein-ligated rats without bleeding than in those with bleeding (P< 0.001). In contrast, glypressin induced similar changes in mean arterial pressure between the two groups (P> 0.05). The addition of aminoguanidine significantly potentiated the portal-hypotensive effect of glypressin in bleeding portal vein-ligated rats (P< 0.005) without an effect on the changes in mean arterial pressure induced by glypressin infusion (P> 0.05). 4.Splanchnic hyposensitivity to glypressin exists in a haemorrhage-transfused rat model of portal hypertension. This hyposensitivity can be ameliorated by the administration of aminoguanidine.

scholarly journals Salvianolic acid B inhalation solution enhances antifibrotic and anticoagulant effects in a rat model of pulmonary fibrosis

2021 ◽  
Vol 138 ◽  
pp. 111475
Author(s):  
Tianyi Zhang ◽  
Mengjiao Liu ◽  
Yunhang Gao ◽  
Han Li ◽  
Ling Song ◽  
...  
Keyword(s):  
Pulmonary Fibrosis ◽  
Rat Model ◽  
Salvianolic Acid B ◽  
Salvianolic Acid

scholarly journals Salvianolic acid B reduced the formation of epidural fibrosis in an experimental rat model

2016 ◽  
Vol 11 (1) ◽  
Author(s):  
Feng Chen ◽  
Changyao Wang ◽  
Jintang Sun ◽  
Jin Wang ◽  
Lanfeng Wang ◽  
...  
Keyword(s):  
Rat Model ◽  
Salvianolic Acid B ◽  
Epidural Fibrosis ◽  
Salvianolic Acid ◽  
Experimental Rat Model
Sign in / Sign up

Export Citation Format

Share Document