Abstract:
:Sepsis is a life-threatening clinical syndrome defined as a deregulated host response to infection associated with organ dysfunction. Mechanisms underlying the pathophysiology of septic liver dysfunction are incompletely understood. Among others, the iron containing tetrapyrrole heme inflicts hepatic damage when released into the circulation during systemic inflammation and sepsis. Accordingly, hemolysis and decreased concentrations of heme-scavenging proteins coincide with an unfavorable outcome of critically ill patients. As the liver is a key organ in heme metabolism and host response to infection, we investigated the impact of labile heme on sinusoidal microcirculation and hepatocellular integrity. We here provide experimental evidence that heme increases portal pressure via a mechanism that involves hepatic stellate cell-mediated sinusoidal constriction, a hallmark of microcirculatory failure under stress conditions. Moreover, heme exerts direct cytotoxicity in vitro and aggravates tissue damage in a model of polymicrobial sepsis. Heme binding by albumin, a low-affinity but high-capacity heme scavenger, attenuates heme-mediated vasoconstriction in vivo and prevents heme-mediated cytotoxicity in vitro. We demonstrate that fractions of serum albumin-bound labile heme are increased in septic patients. We propose that heme scavenging might be used therapeutically to maintain hepatic microcirculation and organ function in sepsis.
journal_name
Arch Biochem Biophysjournal_title
Archives of biochemistry and biophysicsauthors
Englert FA,Seidel RA,Galler K,Gouveia Z,Soares MP,Neugebauer U,Clemens MG,Sponholz C,Heinemann SH,Pohnert G,Bauer M,Weis Sdoi
10.1016/j.abb.2019.108075subject
Has Abstractpub_date
2019-09-15 00:00:00pages
108075eissn
0003-9861issn
1096-0384pii
S0003-9861(19)30251-6journal_volume
672pub_type
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journal_title:Archives of biochemistry and biophysics
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更新日期:1995-01-10 00:00:00
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