Life-threatening hemobilia caused by hepatic artery pseudoaneurysm: A rare complication of chronic cholangitis

Hemobilia is one of the causes of obscure gastrointestinal haemorrhage. Most cases of hemobilia are of iatrogenic or traumatic origin. Hemobilia caused by a hepatic artery pseudoaneurysm due to ascending cholangitis is very rare and its mechanism is undear. We report a 74-year-old woman with a history of surgery for choledocholithiasis 30 years ago, suffering from a protracted course of life-threatening gastrointestinal bleeding. A small intestines series and endoscopic retrograde cholangiopancreatography revealed a chronic cholangitis with marked contrast reflux into the biliary tree. Angiography confirmed the bleeding from a pseudoaneurysm of the middle hepatic artery. Coil embolization achieved successful hemostasis. We discussed the mechanism and reviewed the literature.

Vascular contractile response and signal transduction in endothelium-denuded aorta from cirrhotic rats

AIM: The mechanism of decreased vascular reactivity to vasoconstrictors in portal hypertension is still unclear. In addition to nitric oxide, defects in post-receptor signal transduction pathway have been suggested to play a role.However, substantial evidences observed equivocal changes of vascular reactivity following different agonists that challenged the hypothesis of the post-receptor defect. The current study was to evaluate the vascular reactivity to different agonists and the inositol trisphosphate (IP3)changes in signal transduction cascade from cirrhotic rats with portal hypertension.METHODS: The endothelial denuded aortic rings from cirrhotic and sham-operated rats were obtained for ex vivo tension study and measurement of the corresponding [3H] IP3 formation following different receptor and nonreceptor-mediated agonists' stimulation. Additionally,iNOS protein expression was measured in thoracic aorta.The contractile response curves to phenylephrine were performed in endothelial denuded aortic rings with and without preincubation with a specific iNOS inhibitor (L-N (6)-(1-iminoethyl)-lysine, L-NIL).RESULTS: In endothelial denuded aortic rings of cirrhotic rats, the vascular responses were reduced with phenylephrine and arginine vasopressin (AVP) stimulation but were normal with U-46619, NaF/AlCl3, and phorbol esterdibutyrate (PdBU) stimulation. Compared to the corresponding control groups, the degree of the increment of [3H] IP3 formation from basal level was also decreased with phenylephrine and AVP stimulation, but was normal with U-46619 and NaF/AlCl3 stimulation. The preincubation with L-NIL did not modify the hyporesponsiveness to phenylephrine. Additionally, the iNOS protein expression in thoracic aorta was not different in cirrhotic and shamoperated rats.CONCLUSION: Without the influence of nitric oxide, vascular hyporeactivity to vasoconstrictors persisted in cirrhotic rats with portal hypertension. However, the decreased vascular reactivity is an agonist-specific phenomenon. In addition,G-protein and phospholipase C pathway associated with the IP3 productions may be intact in cirrhotic rats with portal hypertension.