2005
DOI: 10.1001/archsurg.140.8.801
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Role of Thromboxane in Producing Hepatic Injury During Hepatic Stress

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Cited by 45 publications
(40 citation statements)
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References 108 publications
(139 reference statements)
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“…TXA 2 is produced by Kuppfer cells in response to stress and promotes hepatic inflammation, portal vasoconstriction, and leukocyte adhesion in the sinusoids (6,15,21). Inhibition of TX is hepatoprotective in models of endotoxemia, ischemiareperfusion, cirrhosis, and alcoholic liver disease (41). Dietary fish oil has previously been shown to lower plasma TXB 2 in septic rats.…”
Section: Discussionmentioning
confidence: 99%
“…TXA 2 is produced by Kuppfer cells in response to stress and promotes hepatic inflammation, portal vasoconstriction, and leukocyte adhesion in the sinusoids (6,15,21). Inhibition of TX is hepatoprotective in models of endotoxemia, ischemiareperfusion, cirrhosis, and alcoholic liver disease (41). Dietary fish oil has previously been shown to lower plasma TXB 2 in septic rats.…”
Section: Discussionmentioning
confidence: 99%
“…Measurement of these products was done using the Colorimetric Non-enzymatic Assay for Nitric Oxide kit (Oxford Biomedical; Oxford, Michigan). Briefly, 50 μL of serum was deproteinated using ZnSO 4 and subsequently incubated with cadmium to convert the nitrate to nitrite. The quantitation of total nitrite using the Griess Reagent is then accurate for total nitric oxide in the samples.…”
Section: Nitric Oxide Assaymentioning
confidence: 99%
“…Transient episodes of hepatic ischemia occur during solid organ transplantation, trauma, hypovolemic shock, and elective liver resection, when inflow occlusion or total vascular exclusion is used to minimize blood loss. The pathophysiology of liver I/R injury includes both direct cellular damage as the result of the ischemic insult as well as delayed dysfunction and damage resulting from activation of inflammatory pathways [1][2][3][4]. There is evidence that the L-arginine-nitric oxide pathway plays an important role in mediating this injury [5][6][7].…”
Section: Introductionmentioning
confidence: 99%
“…[25][26][27][28][29] The elevated levels of TXB 2 have been found in liver and systemic circulation after hepatic injury was induced by different agents, such are endotoxemia, hepatic ischemia-reperfusion, hepatectomy, liver transplantation, hepatic cirrhosis, ethanol and CCl 4 . 21,23,[31][32][33] Due to the unstabile nature and very short half-life of TXA 2 , its stabile metabolite, TXB 2 , was used in our investigations. Although TXB 2 is considered to be a biologically inactive metabolite of TXA 2 , it has been shown that TXB 2 has several biological activities such as increasing pulmonary airway, pulmonary arterial and systemic arterial pressure in dogs, increasing or decreasing myocardial contractility on isolated rat heart and increasing the rate of apoptosis in cultured rat hepatocytes.…”
Section: Discussionmentioning
confidence: 99%
“…In the present experiments, treatment of mice with daltroban, a selective antagonist of TPR, alleviated the liver damage induced by APAP as shown by the decrease in mortality of animals and plasma ALT level. Numerous animal studies have shown that other specific TPR antagonists protected the liver from injury after toxic dose of ethanol and CCl 4 , 21,37 endotoxemia, 22,32 warm ischemia, 33 ischemia-reperfusion, 31 etc. On the other hand, the administration of the well-known stabile analog of TXA 2 , U-46619, to normal mice or animals which received APAP did not produce or aggravate liver injury.…”
Section: Discussionmentioning
confidence: 99%