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Thalidomide ameliorates portal hypertension via nitric oxide synthase independent reduced systolic blood pressure

World Journal of gastroenterology 2015年第14期21卷 4126-4135页

作者： nicholas g theodorakis Yining N Wang Vyacheslav A Korshunov Mary A Maluccio nicholas J Skill Division of Transplant Surgery Department of SurgerySchool of MedicineIndiana University School of Medicine University of Rochester

AIM: Portal hypertension is a common complication of liver cirrhosis and significantly increases mortality and *** reports have suggested that the compound thalidomide attenuates portal hypertension(PHT).However, the mechanism for this action is not fully *** hypothesis is that thalidomide destabilizes tumor necrosis factor α(TNFα) mR NA and therefore diminishes TNFα induction of nitric oxide synthase(NOS) and the production of nitric oxide(NO).To examine this hypothesis, we utilized the murine partial portal vein ligation(PVL) PHT model in combination with endothelial or inducible NOS isoform gene knockout ***: Wild type, inducible nitric oxide synthase(i NOS)-/- and endothelial nitric oxide synthase(e NOS)-/-mice received either PVL or sham surgery and were given either thalidomide or *** nitrate(total nitrate, NOx) was measured daily for 7 d as a surrogate of NO *** TNFα level was quantified by enzyme-linked immunosorbent ***α m RNA was quantified in liver and aorta tissue by reverse transcription-polymerase chain *** was determined by recording splenic pulp pressure(SPP) and abdominal aortic flow after 0-7 *** to thalidomide was determined by measurement of SPP and mean arterial pressure(MAP).RESULTS: SPP, abdominal aortic flow(Qao) and plasma NOx were increased in wild type and i NOS-/-PVL mice when compared to sham operated control *** contrast, SPP, Qao and plasma NOx were not increased in e NOS-/- PVL mice when compared to sham *** TNFα level in both sham and PVL mice was below the detection limit of the commercial ELISA ***, the effect of thalidomide on serum TNFα levels was undetermined in wild type, e NOS-/-or i NOS-/- *** acutely increased plasma NOx in wild type and e NOS-/- mice but not i NOS-/-***, thalidomide temporarily(0-90 min) decreased mean arterial pressure, SPP and Qao in wild type, e NOS-/- and i NOS-/- PVL mice, aft

关键词： Portal hypertension Thalidomide Nitric oxide Knock

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Murine study of portal hypertension associated endothelin-1 hypo-response

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World Journal of gastroenterology 2015年第16期21卷 4817-4828页

作者： nicholas theodorakis Mary Maluccio nicholas Skill Department of Surgery Division of Transplant SurgeryIndiana School of MedicineIndiana University

AIM:To investigate endothelin-1 hypo-responsive associated with portal hypertension in order to improve patient treatment ***:Wild type,e NOS-/-and i NOS-/-mice receivedpartial portal vein ligation surgery to induce portal hypertension or sham *** of portal hypertension was determined by measuring the splenic pulp pressure,abdominal aortic flow and portal systemic *** measure splenic pulp pressure,a microtip pressure transducer was inserted into the spleen *** aortic flow was measured by placing an ultrasonic Doppler flow probe around the abdominal aorta between the diaphragm and celiac *** systemic shunting was calculated by injection of fluorescent microspheres in to the splenic vein and determining the percentage accumulation of spheres in liver and pulmonary ***-1 hypo-response was evaluated by measuring the change in abdominal aortic flow in response to endothelin-1 intravenous *** addition,thoracic aorta endothelin-1contraction was measured in 5 mm isolated thoracic aorta rings ex-vivo using an ADI small vessel ***:In wild type and i NOS-/-mice splenic pulp pressure increased from 7.5±1.1 mm Hg and 7.2±1 mm Hg to 25.4±3.1 mm Hg and 22±4 mm Hg *** e NOS-/-mice splenic pulp pressure was increased after 1 d(P=NS),after which it decreased and by 7 d was not significantly elevated when compared to 7 d sham operated controls(6.9±0.6 mm Hg and 7.3±0.8 mm Hg respectively,P=0.3).Abdominal aortic flow was increased by 80%and 73%in 7 d portal vein ligated wild type and i NOS when compared to shams,whereas there was no significant difference in 7 d portal vein ligated e NOS-/-mice when compared to ***-1 induced a rapid reduction in abdominal aortic blood flow in wild type,e NOS-/-and i NOS-/-sham mice(50%±8%,73%±9%and 47%±9%respectively).Following portal vein ligation endothelin-1 reduction in blood flow was significantly diminished in each mouse group

关键词： Liver disease Portal hypertension Hyperdynamiccirculation Endothelin-1 Nitric oxide synthaseisoforms

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