Development of portacaval shunts in portal-stenotic cats

1993 ◽  
Vol 71 (9) ◽  
pp. 671-674 ◽  
Author(s):  
Andres C. Inglés ◽  
Dallas J. Légaré ◽  
W. Wayne Lautt

The goal of the present study was to investigate the formation of portacaval shunts in a new experimental model of chronic portal hypertension, portal vein stenosis in the cat. The procedure gradually occluded the portal vein by use of an Ameroid constrictor around the portal vein. After 4 weeks, the portal vein was completely occluded and portal venous pressure was elevated to 15.6 ± 0.3 mmHg (1 mmHg = 133.3 Pa) (n = 8). The hemodynamic changes did not affect the functional capacity of the liver. Latex injection was used to study the shunts. This revealed the spontaneous development of porta-systemic collaterals in all hypertensive cats, mainly between the gastrosplenic and right gastroepiploic veins and the left renal vein. Fine small branches also drained directly into the cava. The left renal vein was markedly dilated in all cats. Collateral circulation also developed between the inferior vena cava and the inferior mesenteric vein through both left internal testicular and iliolumbar veins. Some branches of the inferior mesenteric vein were connected directly to the cava. Esophageal varices in the mucosa or submucosa were not demonstrated. However, the presence of latex in the pulmonary veins and the visualization of periesophageal collaterals suggest the opening of porta-pulmonary shunts. A constant feature in all cats was the presence of a dilated azygos vein, which drained collaterals retroperitoneally and from the abdominal wall. In conclusion, an experimental model of prehepatic portal hypertension of gradual onset has been developed in cats. The formation of the porta-systemic shunts mimics other animal models and the human form of the disease. It is a homogeneous model and easily reproducible.Key words: portal hypertension, porta-systemic shunts, portal stenosis, Ameroid constrictor, cat.

2009 ◽  
Vol 22 (12) ◽  
pp. 1189-1192 ◽  
Author(s):  
Hiroyuki Kanazawa ◽  
Yasutsugu Takada ◽  
Yasuhiro Ogura ◽  
Fumitaka Oike ◽  
Hiroto Egawa ◽  
...  

Author(s):  
F. M. Andrade ◽  
R. P. Rocha ◽  
H. M. Pereira ◽  
R. M. P. Fernandes ◽  
M. A. Babinski

2003 ◽  
Vol 284 (6) ◽  
pp. R1580-R1585 ◽  
Author(s):  
Susan Kaufman ◽  
Jody Levasseur

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.


1992 ◽  
Vol 83 (2) ◽  
pp. 165-170 ◽  
Author(s):  
Pi-Chin Yu ◽  
Jon-Son Kuo ◽  
Han-Chieh Lin ◽  
May C. M. Yang

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.


2010 ◽  
Vol 41 (3) ◽  
pp. 322-326 ◽  
Author(s):  
Vikash SrinivasaiahSetty Chennur ◽  
Raju Sharma ◽  
Shivanand Gamanagatti ◽  
Veereshwar Bhatnagar ◽  
Arun Kumar Gupta ◽  
...  

2013 ◽  
Vol 12 (4) ◽  
pp. 335-338 ◽  
Author(s):  
Marcus Vinicius Martins Cury ◽  
Fernanda Mesquita de Brito Castro ◽  
Lister Arruda Modesto Santos ◽  
Sandra Lucia Lodi Peres ◽  
Roberto Sacilotto

Right portal vein embolization is often performed to prevent liver insufficiency after major hepatic resection. The procedure usually involves direct puncture of the portal vein, which requires hepatic hilum manipulation, and may be associated with liver injury, pneumothorax, and hemoperitoneum. This report describes a technique of laparoscopic insertion of a sheath into the inferior mesenteric vein followed by right portal vein embolization.


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