Reactive oxygen and nitrogen species in sepsis-induced hepatic microvascular dysfunction

Singer, Georg; Stokes, Karen Y.; Granger, D. Neil

doi:10.1007/s00011-012-0562-3

Cited by 11 publications

(7 citation statements)

References 43 publications

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“…In mice with cecal ligation and puncture (CLP)-induced sepsis and in eNOS KO mice, increased leukocyte and platelet adhesion was detected. In this study, eNOS KO mice or mice treated with L-NAME had an increase in blood cell recruitment in the hepatic microvasculature following CLP 141 . Treatment with pravastatin, a member of the statin class of drugs used to lower high cholesterol and triglycerides, resulted in increased eNOS function and expression in LPS-injected rats, leading to improvement of eNOS-mediated vessel relaxation 23 .…”

Section: Role Of Enos In the Microcirculation During Sepsis—integratimentioning

confidence: 62%

Endothelial nitric oxide synthase in the microcirculation

Shu

Keller

Begandt

et al. 2015

Cell. Mol. Life Sci.

105

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Endothelial nitric oxide synthase (eNOS, NOS3) is responsible for producing nitric oxide (NO) - a key molecule that can directly (or indirectly) act as a vasodilator and anti-inflammatory mediator. In this review, we examine the structural effects of regulation of the eNOS enzyme, including post-translational modifications and subcellular localization. After production, NO diffuses to surrounding cells with a variety of effects. We focus on the physiological role of NO and NO-derived molecules, including microvascular effects on vessel tone and immune response. Regulation of eNOS and NO action is complicated; we address endogenous and exogenous mechanisms of NO regulation with a discussion of pharmacological agents used in clinical and laboratory settings and a proposed role for eNOS in circulating red blood cells.

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Section: Role Of Enos In the Microcirculation During Sepsis—integratimentioning

confidence: 62%

Endothelial nitric oxide synthase in the microcirculation

Shu

Keller

Begandt

et al. 2015

Cell. Mol. Life Sci.

105

View full text Add to dashboard Cite

show abstract

“…Moreover, the isoforms of constitutive NOSs are considered to be parts of two signaling pathways in the cell (Malakhov et al, 2009 ). There are many publications that reveal the involvement of iNOS in physiological synthesis of NO and impact of eNOS and nNOS on extra synthesis of NO in infection, allergic, and autoimmune diseases (Wahl et al, 2003 ; Jarazo-Dietrich et al, 2012 ; Singer et al, 2013 ). Activation of iNOS is a component of many protective-adaptive reactions (Das and Das, 2008 ; Ye et al, 2010 ; Abu-Amara et al, 2012 ).…”

mentioning

confidence: 99%

Platelet hemostasis in patients with metabolic syndrome and type 2 diabetes mellitus: cGMP- and NO-dependent mechanisms in the insulin-mediated platelet aggregation

et al. 2015

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Patients with metabolic syndrome (MetS) and type 2 diabetes mellitus (T2DM) have high risk of microcirculation complications and microangiopathies. An increase in thrombogenic risk is associated with platelet hyperaggregation, hypercoagulation, and hyperfibrinolysis. Factors leading to platelet activation in MetS and T2DM comprise insulin resistance, hyperglycemia, non-enzymatic glycosylation, oxidative stress, and inflammation. This review discusses the role of nitric oxide (NO) in the regulation of platelet adhesion and aggregation processes. NO is synthesized both in endotheliocytes, smooth muscle cells, macrophages, and platelets. Modification of platelet NO-synthase (NOS) activity in MetS patients can play a central role in the manifestation of platelet hyperactivation. Metabolic changes, accompanying T2DM, can lead to an abnormal NOS expression and activity in platelets. Hyperhomocysteinemia, often accompanying T2DM, is a risk factor for cardiovascular accidents. Homocysteine can reduce NO production by platelets. This review provides data on the insulin effects in platelets. Decrease in a number and sensitivity of the insulin receptors on platelets in T2DM can cause platelet hyperactivation. Various intracellular mechanisms of anti-aggregating insulin effects are discussed. Anti-aggregating effects of insulin are mediated by a NO-induced elevation of cGMP and upregulation of cAMP- and cGMP-dependent pathways. The review presents data suggesting an ability of platelets to synthesize humoral factors stimulating thrombogenesis and inflammation. Proinflammatory cytokines are considered as markers of T2DM and cardiovascular complications and are involved in the development of dyslipidemia and insulin resistance. The article provides an evaluation of NO-mediated signaling pathway in the effects of cytokines on platelet aggregation. The effects of the proinflammatory cytokines on functional activity of platelets are demonstrated.

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“…[ 9 ] In an animal study, ROS and reactive nitrogen species were reported to cause hepatic microvascular dysfunction during sepsis. [ 10 ]…”

Section: Discussionmentioning

confidence: 99%

“…Lower ALT concentration can occur in the setting of vitamin B6 deficiency. [ 10 ] Vitamin B6 is an antioxidant and is a strong quencher of ROS. In the ESBL group, vitamin B6 may be consumed largely due to high ROS, resulting in decreased ALT levels.…”

Section: Discussionmentioning

confidence: 99%

Analysis of early-onset bloodstream infection due to Escherichia coli infection in premature babies

Chen

Huang

et al. 2017

Medicine

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In early-onset bacteremia among preterm neonates, Escherichia coli (E. coli) is the main pathogen and can cause a high mortality rate. Thus, the predictive factors of mortality and extended-spectrum β-lactamase (ESBL)-producing E. coli in preterm babies with E. coli early-onset bacteremia were reported.We retrospectively reviewed preterm neonates who had E. coli bacteremia occurring within 3 days after birth between 2004 and 2015. Maternal and perinatal information were collected from their medical records and analyzed by comparing the survival and nonsurvival groups, and also the ESBL-producing and non-ESBL-producing E. coli bacteremia groups. Mann–Whitney U test, Fisher exact test, and multivariate Cox proportional-hazard model were used for statistical analysis.A total of 27 preterm babies had E. coli bacteremia. The overall mortality rate was 55.56% (15 deaths). Five babies had ESBL-producing E. coli. The low systolic blood pressure of <48 mm Hg and low absolute neutrophil count of <2318 cells/mm3 were the most significant factors in predicting mortality. Moreover, the level of serum alanine aminotransferase was significantly lower in the ESBL-producing E. coli group than that in the non-ESBL-producing E. coli group.Therefore, the lower systolic blood pressure and absolute neutrophil count were the risk factors of mortality in preterm babies with early-onset E. coli bacteremia, and alanine aminotransferase could be a significant factor in predicting ESBL-producing E. coli.

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Reactive oxygen and nitrogen species in sepsis-induced hepatic microvascular dysfunction

Cited by 11 publications

References 43 publications

Endothelial nitric oxide synthase in the microcirculation

Endothelial nitric oxide synthase in the microcirculation

Platelet hemostasis in patients with metabolic syndrome and type 2 diabetes mellitus: cGMP- and NO-dependent mechanisms in the insulin-mediated platelet aggregation

Analysis of early-onset bloodstream infection due to Escherichia coli infection in premature babies

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