Effects of endothelin in portal hypertensive rats

1992 ◽  
Vol 83 (2) ◽  
pp. 165-170 ◽  
Author(s):  
Pi-Chin Yu ◽  
Jon-Son Kuo ◽  
Han-Chieh Lin ◽  
May C. M. Yang
Keyword(s):  
Blood Pressure ◽  
Portal Hypertension ◽  
Portal Vein ◽  
Venous Pressure ◽  
Portal Venous Pressure ◽  
Portal Vein Ligation ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Endothelin 1 ◽  
Sprague Dawley Rats

1. Effects of endothelin-1 on systemic arterial blood pressure, heart rate and portal venous pressure were compared in normal Sprague-Dawley rats and rats with portal hypertension induced by CCl4 and partial portal vein ligation. 2. Endothelin-1 produced biphasic effects on systemic blood pressure and portal venous pressure in all three groups of rats. However, the magnitude of the changes in blood pressure was less in portal hypertensive rats. 3. The ability of endothelin-1 to increase the portal venous pressure was also significantly diminished in portal hypertensive rats. On the other hand, the initial decrease in portal pressure was augmented in rats with partial portal vein ligation, and disappeared at higher dosage in CCl4-treated rats. 4. In accordance with the pressure recording in vivo, the dose-response vasoconstrictive activity of endothelin-1 was significantly attenuated in the intrahepatic vasculature. 5. The plasma immunoreactive endothelin concentration was significantly higher (5.55 ± 0.81 fmol/ml) in Sprague-Dawley rats than in CCl4-treated rats (2.83 ± 0.56 fmol/ml) and rats with partial portal vein ligation (2.68 ± 0.53 fmol/ml). 6. It was concluded that a lower plasma level of endothelin and a reduced vascular responsiveness may contribute, at least in part, to the hyperdynamics of portal hypertension.

Beneficial effects of combined terlipressin and tetramethylpyrazine administration on portal hypertensive rats

1999 ◽  
Vol 77 (8) ◽  
pp. 618-624 ◽  
Author(s):  
Fang-Chi Chang ◽  
Yi-Tsau Huang ◽  
Han-Chieh Lin ◽  
Chuang-Ye Hong ◽  
Jaung-Geng Lin ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Therapeutic Effects ◽  
Portal Vein Ligation ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Beneficial Effects ◽  
Sprague Dawley Rats ◽  
Duct Ligation

The purpose of this study was to investigate the therapeutic effects of terlipressin (TP) alone or in combination with tetramethylpyrazine (TMP) on anesthetized portal hypertensive rats. Portal hypertension was induced by either partial portal vein ligation (PVL, without cirrhosis) or bile duct ligation (BDL, with cirrhosis) in Sprague-Dawley rats. Each PVL or BDL rat received only one of the two regimens: vehicle for 3 min followed by TP (0.017 mg·kg-1·min-1 for 3 min) or TMP (10 mg·kg-1·min-1 for 3 min) followed by TP. In PVL rats, infusion of vehicle followed by TP induced significant reduction of portal venous pressure (PVP, -15.0 ± 1.0%) and prominent elevation of mean arterial pressure (MAP, 57.3 ± 8.1%) as well as total peripheral resistance (TPR, 113 ± 11%) from baseline, and there was a cardiodepressant response (cardiac index, CI, -26.3 ± 1.1%). Infusion of TMP followed by TP induced significant reduction of PVP (-20.3 ± 0.4%) and CI (-9.9 ± 1.2%) and significant elevation of MAP (31.3 ± 2.5%) and TPR (46.0 ± 4.1%) from baseline. In BDL rats, infusion of vehicle followed by TP also induced significant reduction of PVP (-13.8 ± 1.7%) but an increase in MAP (57.1 ± 2.2%) and TPR (101 ± 6%) from baseline, and there also was a cardiodepressant response (CI, -21.4 ± 2.3%). Infusion of TMP followed by TP induced significant reduction of PVP (-18.9 ± 1.4%) and CI (-11.9 ± 2.1%), but an increase in MAP (36.2 ± 2.5%) and TPR (55.0 ± 5.2%). Compared with vehicle followed by TP, TMP not only significantly enhanced portal hypotensive (PVP reduction) effects of TP but also attenuated the systemic pressor (MAP and TPR elevation) and cardiodepressant (CI reduction) effects of TP in both PVL and BDL rats. Our results suggest that TP, alone or in combination with TMP, induced portal hypotensive effects in two models of portal hypertensive rats. Combination of TP and TMP was beneficial in enhancing portal hypotensive effects of TP and ameliorating the systemic pressor and cardiodepressant effects of TP.Key words: terlipressin, tetramethylpyrazine, cirrhosis, portal hypertension, hemodynamics.

Decreased vascular contractile and inositol phosphate responses in portal hypertensive rats

1995 ◽  
Vol 73 (3) ◽  
pp. 378-382 ◽  
Author(s):  
Yi-Tsau Huang ◽  
Chuang-Ye Hong ◽  
Pi-Chin Yu ◽  
Ming-Fang Lee ◽  
May C. M. Yang ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Contractile Response ◽  
Inositol Phosphates ◽  
Inositol Phosphate ◽  
Venous Pressure ◽  
Portal Vein Ligation ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Contractile Responses ◽  
Tail Artery

The purpose of this study was to investigate the vascular contractile and inositol phosphate responses in portal hypertensive rats. Portal hypertension was induced by partial portal vein ligation (PVL) in Sprague–Dawley rats. Sham-operated rats served as controls. Pressures, vasoconstrictor responses, and inositol phosphate responses were determined at 14 days after surgery. The portal venous pressure was significantly higher, while systemic arterial pressure and heart rate were lower, in PVL rats. Dose-dependent contractile responses were observed for both norepinephrine (1 × 10−8 – 3 × 10−6 M) and vasopressin (3 × 10−10 – 3 × 10−8 M) in the tail artery of both groups. The contractile response to norepinephrine was significantly decreased in PVL rats compared with controls at all doses. The contractile response to vasopressin was significantly decreased in PVL rats at higher doses. After myo-[3H]inositol incorporation in tail artery, the levels of 3H-labelled phosphatidylinositols (cpm/mg) were similar between the two groups. Norepinephrine (10−7 – 10−5 M) and vasopressin (10−10 – 10−8 M) dose dependently stimulated the 3H-labelled inositol phosphate production in the tail artery of both PVL and sham-operated rats. However, the response was significantly lower in PVL rats. The results suggested that the attenuation of vascular contractile responses in portal hypertension was reflected in the phosphoinositide messenger system.Key words: portal hypertension, inositol phosphates, phosphoinositide, tail artery, contractile response.

Effect of portal hypertension on splenic blood flow, intrasplenic extravasation and systemic blood pressure

2003 ◽  
Vol 284 (6) ◽  
pp. R1580-R1585 ◽  
Author(s):  
Susan Kaufman ◽  
Jody Levasseur
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Portal Hypertension ◽  
Portal Vein ◽  
Venous Pressure ◽  
Splenic Vein ◽  
Systemic Blood Pressure ◽  
Portal Venous Pressure ◽  
Systemic Blood ◽  
Fluid Extravasation

We have previously shown that intrasplenic fluid extravasation is important in controlling blood volume. We proposed that, because the splenic vein flows in the portal vein, portal hypertension would increase splenic venous pressure and thus increase intrasplenic microvascular pressure and fluid extravasation. Given that the rat spleen has no capacity to store/release blood, intrasplenic fluid extravasation can be estimated by measuring the difference between splenic arterial inflow and venous outflow. In anesthetized rats, partial ligation of the portal vein rostral to the junction with the splenic vein caused portal venous pressure to rise from 4.5 ± 0.5 to 12.0 ± 0.9 mmHg ( n = 6); there was no change in portal venous pressure downstream of the ligation, although blood flow in the liver fell. Splenic arterial flow did not change, but the arteriovenous flow differential increased from 0.8 ± 0.3 to 1.2 ± 0.1 ml/min ( n = 6), and splenic venous hematocrit rose. Mean arterial pressure fell (101 ± 5.5 to 95 ± 4 mmHg). Splenic afferent nerve activity increased (5.6 ± 0.9 to 16.2 ± 0.7 spikes/s, n = 5). Contrary to our hypothesis, partial ligation of the portal vein caudal to the junction with the splenic vein (same increase in portal venous pressure but no increase in splenic venous pressure) also caused the splenic arteriovenous flow differential to increase (0.6 ± 0.1 to 1.0 ± 0.2 ml/min; n = 8). The increase in intrasplenic fluid efflux and the fall in mean arterial pressure after rostral portal vein ligation were abolished by splenic denervation. We propose there to be an intestinal/hepatic/splenic reflex pathway, through which is mediated the changes in intrasplenic extravasation and systemic blood pressure observed during portal hypertension.

Portal venous pressure and portasystemic shunting in experimental portal hypertension

1989 ◽  
Vol 257 (1) ◽  
pp. G52-G57 ◽  
Author(s):  
J. G. Geraghty ◽  
W. J. Angerson ◽  
D. C. Carter
Keyword(s):  
Portal Hypertension ◽  
Portal Vein ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Rapid Change ◽  
Quadratic Function ◽  
Portal Venous Pressure ◽  
Portal Vein Ligation ◽  
Strong Positive Correlation ◽  
The Relationship

The relationship between portal venous pressure and the degree of portasystemic shunting was studied in portal vein-ligated and cirrhotic rats anesthetized with halothane. One day after partial portal vein ligation there was a strong positive correlation (r = 0.80, n = 7) between portal pressure and shunting of mesenteric venous blood as measured by injection of radioactive microspheres. The relationship subsequently underwent rapid change but stabilized by 14 days postligation, when higher levels of shunting were again associated with higher portal pressures up to a limit of approximately 70% shunting, above which pressures did not increase further. This relationship was well described by a quadratic function (r = 0.75, n = 17). In cirrhotic rats there was no relationship between portal pressure and shunting (r = -0.01, n = 10). The results suggest that in the prehepatic model there is little inherent variability in capacity to develop shunts, which open to a degree directly related to portal pressure, but that this relationship may be altered in cirrhotic portal hypertension.

scholarly journals The relationship between intrahepatic portal systemic shunts and microsphere induced portal hypertension in the rat liver

Gut ◽  
1998 ◽  
Vol 42 (2) ◽  
pp. 276-282 ◽  
Author(s):  
X Li ◽  
I S Benjamin ◽  
B Alexander
Keyword(s):  
Blood Flow ◽  
Portal Hypertension ◽  
Steady State ◽  
Portal Vein ◽  
Rat Liver ◽  
Venous Pressure ◽  
Portal Venous Pressure ◽  
Portal Vein Ligation ◽  
The Relationship ◽  
Wedged Hepatic Venous Pressure

Background—Portal hypertension is associated with gross haemodynamic disturbances characterised by high cardiac output, low peripheral vascular resistance, increased splanchnic blood flow, and portal systemic shunting.Aims—To study the relationship between intrahepatic portal systemic shunts and microsphere induced portal hypertension in the rat liver.Methods—Different sized microspheres were sequentially injected into the portal vein of male Wistar rats.Results—Steady state portal venous pressure was increased by 102.2 (35.6)% (14.9 (3.6) mm Hg) and 272.3 (78.0)% (24.0 (2.2) mm Hg) above the basal pressure following sequential injections of 15 and 80 μm diameter microspheres, respectively. Sequential injection of 15, 40, and 80 μm diameter microspheres in either ascending or descending order of size did not generate further increases in portal venous pressure. A single injection of 1.8 × 105 80 μm microspheres consistently produced a steady state portal venous pressure of 19.0 (1.3) mm Hg but did not approach the much higher value of 36.6 (43.2) mm Hg measured during clamping of the portal vein. These data indicate that the opening of patent intrahepatic shunts was responsible for the reduced pressures observed during microsphere injections and further evidence for this was provided by the location of microspheres in the pulmonary vascular bed. The elevation in portal venous pressure achieved by microsphere injections was not significantly different to that produced in rats subjected to partial portal vein ligation (20.7 (0.5) mm Hg, p>0.05). Wedged hepatic venous pressure decreased from 6.7 (0.7) to 3.0 (0.6) mm Hg following injection of 80 μm microspheres, suggesting a decrease in total hepatic blood flow. Conversely, injection of 15 μm microspheres induced an increase in wedged hepatic venous pressure from 7.0 (1.0) mm Hg to 12.4 (1.8) mm Hg, indicating a localised redistribution of blood flow at the presinusoidal level of the portal venous vascular network and increased intrahepatic shunt flow.Conclusion—It is suggested that there may be a protective pathophysiological role for these shunts when the liver is subjected to changes which induce acute portal hypertension.

scholarly journals Standardization of experimental microsurgical model of ALPPS (Associating liver portal vein ligation partition and staged for hepatectomy) in Sprague Dawley rats

HPB ◽  
2017 ◽  
Vol 19 ◽  
pp. S114
Author(s):  
C. Mandiola ◽  
M. Zapata ◽  
R. Vargas ◽  
S. Uribe-Echevarraa ◽  
M. Uribe ◽  
...  
Keyword(s):  
Portal Vein ◽  
Portal Vein Ligation ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

Portal Vein Aneurysm Treated With Trans-Jugular Intrahepatic Porto-Systemic Shunt

2021 ◽  
pp. 153857442110232
Author(s):  
Robert Dunlap ◽  
Sean Golden ◽  
Gray R. Lyons
Keyword(s):  
Portal Hypertension ◽  
Portal Vein ◽  
Standard Treatment ◽  
Venous Pressure ◽  
Portal Venous Pressure ◽  
Rare Entity ◽  
Cryptogenic Cirrhosis ◽  
Portal Vein Aneurysm

Portal vein aneurysm (PVA) is a rare entity that can lead to hemorrhage or thrombosis. Although there is no standard treatment, most cases can be managed conservatively; intervention is reserved for symptomatic or enlarging aneurysms. For patients who are not surgical candidates due to cirrhosis and portal hypertension, endovascular creation of a trans-jugular intrahepatic porto-systemic shunt (TIPS) is an option to reduce portal venous pressure. This report describes a case of an enlarging PVA successfully treated with TIPS in a patient with cryptogenic cirrhosis.

Antibiotics attenuate experimental hypertension in rats

1985 ◽  
Vol 105 (3) ◽  
pp. 347-350 ◽  
Author(s):  
J. W. Honour ◽  
S. P. Borriello ◽  
U. Ganten ◽  
P. Honour
Keyword(s):  
Blood Pressure ◽  
Oral Administration ◽  
High Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Experimental Hypertension ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Intramuscular Injections ◽  
Sprague Dawley Rats

ABSTRACT Hypertension was produced in Sprague–Dawley rats by intramuscular injections of either corticosterone or ACTH. Lower increases in blood pressure to these challenges were observed in Sprague–Dawley rats pretreated with neomycin or vancomycin which alone had no effect on blood pressure or growth. The development of high blood pressure in spontaneously hypertensive rats of a stroke-prone substrain was also attenuated by oral administration of neomycin. These results suggest that experimental hypertension can be modulated by the administration of antibiotics. J. Endocr. (1985) 105, 347–350

Up-regulation of vascular and renal mitogen-activated protein kinases in hypertensive rats is normalized by inhibitors of the Na+/Mg2+ exchanger

2003 ◽  
Vol 105 (2) ◽  
pp. 235-242 ◽  
Author(s):  
Rhian M. TOUYZ ◽  
Guoying YAO
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Map Kinase ◽  
Map Kinases ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Blood Pressure Elevation ◽  
Sprague Dawley Rats ◽  
Mitogen Activated Protein

In the present in vivo study, we have investigated whether inhibitors of the Na+/Mg2+ exchanger quinidine and imipramine influence the development of hypertension and whether this is associated with modulation of mitogen-activated protein (MAP) kinase activation in arteries and kidneys of hypertensive rats. Sprague—Dawley rats were divided into four groups (n=6/group): control (vehicle), angiotensin II (Ang II; 150 ng/kg of body weight per min subcutaneously), quinidine [Ang II (150 ng/kg of body weight per min)+quinidine (5 mg/kg of body weight per day in food)] and imipramine groups [Ang II (150 ng/kg of body weight per min)+imipramine (5 mg/kg/day in food)]. Rats were studied for 3 weeks. Phosphorylation of vascular and renal extracellular-signal-regulated protein kinase 1/2 (ERK1/2), p38MAP kinase and c-Jun N-terminal kinase (JNK) were assessed using phospho-specific antibodies. Ang II increased systolic blood pressure from 112±5 mmHg to 215±9 mmHg (P<0.01). Development of hypertension was attenuated in Ang II-infused rats treated with quinidine (173±6 mmHg) and imipramine (152±6 mmHg) (P<0.01). Phosphorylation of ERK1/2, p38MAP kinase and JNK, which were increased 2–3-fold in arteries of the Ang II group, were reduced by quinidine and imipramine (P<0.05). Activation of renal MAP kinases was also increased in the Ang II group (P<0.05). Quinidine and imipramine reduced the phosphorylation of renal ERK1/2, but did not modify renal p38MAP kinase or JNK. Our data demonstrate that Ang II induces severe hypertension in Sprague—Dawley rats and this is associated with increased phosphorylation of vascular and renal MAP kinases. Quinidine and imipramine attenuated the development of hypertension and normalized MAP kinase activity. The findings from this study suggest a possible role for the Na+/Mg2+ exchanger in vascular signalling events associated with blood pressure elevation in Ang II-dependent hypertension.

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