Venous endothelium reactivity to Angiotensin II: A study in primary endothelial cultures of rat vena cava and portal vein

Cholangiocarcinoma (CCA) is an aggressive malignancy of the biliary tract. To date, surgical treatment remains the only hope for definitive cure of CCA patients. Involvement of major vascular structures was traditionally considered a contraindication for resection. Nowadays, selected cases of CCA with vascular involvement can be successfully approached. Intrahepatic CCA often involves the major hepatic veins or the inferior vena cava and might necessitate complete vascular exclusion, in situ hypothermic perfusion, ex situ surgery and reconstruction with autologous, heterologous or synthetic grafts. Hilar CCA more frequently involves the portal vein and hepatic artery. Resection and reconstruction of the portal vein is now considered a relatively safe and beneficial technique, and it is accepted as a standard option either with direct anastomosis or jump grafts. However, hepatic artery resection remains controversial; despite accumulating positive reports, the procedure remains technically challenging with increased rates of morbidity. When arterial reconstruction is not possible, arterio-portal shunting may offer salvage, while sometimes an efficient collateral system could bypass the need for arterial reconstructions. Keys to achieve success are represented by accurate selection of patients in high-volume referral centres, adequate technical skills and eclectic knowledge of the various possibilities for vascular reconstruction.

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In situ quantification of endothelial cell damage caused by iodinated contrast media using a rat vena cava model

European Journal of Radiology ◽

10.1016/j.ejrad.2011.02.035 ◽

2012 ◽

Vol 81 (5) ◽

pp. 879-884 ◽

Cited By ~ 4

Author(s):

Natsuko Tsuda

Keyword(s):

Endothelial Cell ◽

Contrast Media ◽

Cell Damage ◽

Vena Cava ◽

Iodinated Contrast Media ◽

Endothelial Cell Damage ◽

Iodinated Contrast ◽

Rat Vena Cava

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5-HT causes splanchnic venodilation

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00165.2017 ◽

2017 ◽

Vol 313 (3) ◽

pp. H676-H686 ◽

Cited By ~ 12

Author(s):

Bridget M. Seitz ◽

Hakan S. Orer ◽

Teresa Krieger-Burke ◽

Emma S. Darios ◽

Janice M. Thompson ◽

...

Keyword(s):

Blood Pressure ◽

Inferior Vena Cava ◽

Portal Vein ◽

Superior Mesenteric Vein ◽

Inferior Vena ◽

Vena Cava ◽

Receptor Protein ◽

Mesenteric Vein

Serotonin [5-hydroxytryptamine (5-HT)] causes relaxation of the isolated superior mesenteric vein, a splanchnic blood vessel, through activation of the 5-HT7 receptor. As part of studies designed to identify the mechanism(s) through which chronic (≥24 h) infusion of 5-HT lowers blood pressure, we tested the hypothesis that 5-HT causes in vitro and in vivo splanchnic venodilation that is 5-HT7 receptor dependent. In tissue baths for measurement of isometric contraction, the portal vein and abdominal inferior vena cava relaxed to 5-HT and the 5-HT1/7 receptor agonist 5-carboxamidotryptamine; relaxation was abolished by the 5-HT7 receptor antagonist SB-269970. Western blot analyses showed that the abdominal inferior vena cava and portal vein express 5-HT7 receptor protein. In contrast, the thoracic vena cava, outside the splanchnic circulation, did not relax to serotonergic agonists and exhibited minimal expression of the 5-HT7 receptor. Male Sprague-Dawley rats with chronically implanted radiotelemetry transmitters underwent repeated ultrasound imaging of abdominal vessels. After baseline imaging, minipumps containing vehicle (saline) or 5-HT (25 μg·kg−1·min−1) were implanted. Twenty-four hours later, venous diameters were increased in rats with 5-HT-infusion (percent increase from baseline: superior mesenteric vein, 17.5 ± 1.9; portal vein, 17.7 ± 1.8; and abdominal inferior vena cava, 46.9 ± 8.0) while arterial pressure was decreased (~13 mmHg). Measures returned to baseline after infusion termination. In a separate group of animals, treatment with SB-269970 (3 mg/kg iv) prevented the splanchnic venodilation and fall in blood pressure during 24 h of 5-HT infusion. Thus, 5-HT causes 5-HT7 receptor-dependent splanchnic venous dilation associated with a fall in blood pressure. NEW & NOTEWORTHY This research is noteworthy because it combines and links, through the 5-HT7 receptor, an in vitro observation (venorelaxation) with in vivo events (venodilation and fall in blood pressure). This supports the idea that splanchnic venodilation plays a role in blood pressure regulation.

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Hepatic encephalopathy due to a large intrahepatic communication between the portal vein and inferior vena cava

Journal of Gastroenterology and Hepatology ◽

10.1111/j.1440-1746.1990.tb01133.x ◽

1990 ◽

Vol 5 (6) ◽

pp. 718-721

Author(s):

SHOZO IWAMOTO ◽

KUNIO OKUDA

Keyword(s):

Hepatic Encephalopathy ◽

Inferior Vena Cava ◽

Portal Vein ◽

Inferior Vena ◽

Vena Cava

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Tumoural portal vein thrombosis

Acta Radiologica ◽

10.1080/02841859709172397 ◽

1997 ◽

Vol 38 (5) ◽

pp. 655-659

Author(s):

L. Marti-Bonmati ◽

E. Lonjedo ◽

D. Mathieu ◽

C. Coffin ◽

C. Poyatos ◽

...

Keyword(s):

Mr Imaging ◽

Portal Vein ◽

Imaging Techniques ◽

Vena Cava ◽

Tumour Thrombus ◽

Vein Thrombosis ◽

Significant Difference ◽

Before And After ◽

Portal Veins ◽

Cellular Carcinoma

Purpose: Intrahepatic thrombus is usually associated with either cirrhosis or hepato-cellular carcinoma (HCC). Most HCCs enhance after the administration of MnDPDP (Teslascan). Our objective was to analyze the enhancement characteristics of tumour portal vein thrombi. Material and Methods: Thrombi affecting the main or segmental portal veins (17 cases) and the suprahepatic inferior vena cava (1 case) were retrospectively selected from a series of 128 patients studied with MR imaging before and after the administration of MnDPDP. Enhancement was assessed qualitatively and quantitatively. Results: All tumour thrombi enhanced after MnDPDP administration. The enhancement was more conspicuous in the GRE images. On the quantitative evaluation, the portal thrombus enhancement was greater for GRE images than SE images. Portal thrombi enhanced more than the liver and the HCCs. There was a significant difference between the enhancement of the HCCs and the thrombi with both MR imaging techniques. Conclusion: The greater enhancement of the tumour thrombus associated with the liver and HCC may suggest that other mechanisms, apart from accumulation of the contrast medium within the hepatocytes inside the thrombi, are involved in thrombus enhancement.

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