1990
DOI: 10.1097/00007890-199003000-00002
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Prostanoid Release in Experimental Liver Transplantation

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Cited by 33 publications
(14 citation statements)
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“…Vasoactive agents liberated from the liver after initiation of reperfusion have been proposed as the responsible factors underlying the pathophysiology of transplantation-related liver failure. The levels of prostanoids in the hepatic vein immediately after liver grafting are markedly increased, 57 and this is significantly associated with poor early graft function. 58 Thus, pretreatment with TXA 2 synthase inhibitor not only significantly reduced the serum levels of TXA 2 but also provided a better graft function and survival rate after liver transplantation.…”
Section: Ischemia-reperfusion-induced Hepatic Injurymentioning
confidence: 99%
“…Vasoactive agents liberated from the liver after initiation of reperfusion have been proposed as the responsible factors underlying the pathophysiology of transplantation-related liver failure. The levels of prostanoids in the hepatic vein immediately after liver grafting are markedly increased, 57 and this is significantly associated with poor early graft function. 58 Thus, pretreatment with TXA 2 synthase inhibitor not only significantly reduced the serum levels of TXA 2 but also provided a better graft function and survival rate after liver transplantation.…”
Section: Ischemia-reperfusion-induced Hepatic Injurymentioning
confidence: 99%
“…Experimental models suggest a role for initiating mediator of reperfusion injury. In this study, OKY046 decreased TXA synthesis during preservation prostanoid immediately after reprefusion [17][18][19][20]. Post et al [17,18] demonstrated a massive intrahepatic re-and perfusion, but OKY046 did not increase PGI synthesis during preservation.…”
Section: Figmentioning
confidence: 74%
“…In this study, OKY046 decreased TXA synthesis during preservation prostanoid immediately after reprefusion [17][18][19][20]. Post et al [17,18] demonstrated a massive intrahepatic re-and perfusion, but OKY046 did not increase PGI synthesis during preservation. Histologically, OKY046 reduced lease of prostanoids during the first minutes after reperfusion in porcine hepatic allografts but they were unable the amount of reperfusion damage of the sinusoidal endothelial cells and the hepatocytes.…”
Section: Figmentioning
confidence: 74%
“…These data have been confirmed in clinical liver transplantation. One explanation for the beneficial effect of a protein flushout after cold ischemia may be the removal of cytotoxic end products of metabolism such as free fatty acids, thromboxane or leukotrienes which can cause reperfusion injury [19,20]. The same effect might be true for a protein flushout after hyperthermic isolated liver perfusion.…”
Section: Discussionmentioning
confidence: 99%