Early adverse changes in liver microvascular circulation during experimental septic shock are not linked to an absolute nitric oxide deficit

Morel, J.; Li, Jacques Yuan; Eyenga, Pierre; Meiller, Anne; Gustin, Marie Paule; Bricca, Giampiero; Molliex, Serge; Viale, J. P.

doi:10.1016/j.mvr.2013.07.005

Cited by 6 publications

(5 citation statements)

References 24 publications

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“…In this study, we used a hypotensive CLP model of severe sepsis that is widely used to investigate the physiologic derangement at the early phase of septic disease in spontaneously breathing [7,17,19] or mechanically ventilated animals [13,15,16]. In accordance with previous studies using the same severe model of sepsis [7,13,15,16,17,18,19], we observed an early arterial hypotension within the rst 3 h (Fig. 1A).…”

Section: Discussionsupporting

confidence: 78%

“…The experiments were carried out in a rat model of sepsis, as previously described [7,13,17]. In both sham-operated (n = 12) and cecal ligation and puncture (CLP) (n = 12) groups, anesthesia was induced by intraperitoneal injection of sodium pentobarbital (56 mg.kg − 1 ) and fentanyl (20 µg.kg − 1 ) and further maintained by continuous infusion of sodium pentobarbital (56 mg.kg − 1 .h − 1 ) and fentanyl (20 µg.kg − 1 .h − 1 ) administered in saline 0.9%.…”

Section: Animal Proceduresmentioning

confidence: 99%

“…The protocol of CLP was performed to induce sepsis as described previously [7,13,17]. After a stabilization period of 30 min, under an aseptic condition, a 3-cm-long abdominal midline incision was made to expose the cecum at the adjoining intestine in 12 rats of the CLP groups.…”

Section: Animal Proceduresmentioning

confidence: 99%

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Mechanical Ventilation Preserves Diaphragm Mitochondrial Function in a Rat Sepsis Model

Eyenga

Roussel

Rey

et al. 2020

Preprint

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Background: To describe the effect of mechanical ventilation on diaphragm mitochondrial oxygen consumption, ATP production, reactive oxygen species (ROS) generation, and cytochrome-c oxidase activity and content, and their relationship to diaphragm strength in an experimental model of sepsis.Methods: A cecal ligation and puncture (CLP) protocol was performed in 12 rats while 12 controls underwent sham-operation. Half of the rats in each group were paralyzed and mechanically ventilated. We performed blood gas analysis and lactic acid assays 6 hours after surgery. Afterwards, we measured diaphragm strength and mitochondrial oxygen consumption, ATP and ROS generation, and cytochrome-c oxidase activity. We also measured malondialdehyde (MDA) content as an index of lipid peroxidation, and mRNA expression of the pro-inflammatory interleukin-1β (IL-1β) in diaphragms.Results: CLP rats showed severe hypotension, metabolic acidosis, and upregulation of diaphragm IL-1β mRNA expression. Compared to sham controls, spontaneously breathing CLP rats showed lower diaphragm force and increased susceptibility to fatigue, along with depressed mitochondrial oxygen consumption and ATP production and cytochrome-c oxidase activity. These rats also showed increased mitochondrial ROS generation and MDA content. Mechanical ventilation markedly restored mitochondrial oxygen consumption and ATP production in CLP rats; lowered mitochondrial ROS production by the complex 3; and preserved cytochrome-c oxidase activity.Conclusion: In an experimental model of sepsis, early initiation of mechanical ventilation restores diaphragm mitochondrial function.

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Section: Discussionsupporting

confidence: 78%

Section: Animal Proceduresmentioning

confidence: 99%

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Mechanical Ventilation Preserves Diaphragm Mitochondrial Function in a Rat Sepsis Model

Eyenga

Roussel

Rey

et al. 2020

Preprint

Self Cite

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“…The novelty of our approach-which allowed the establishment of a cause/effect relationship between a bacterial toxin and microcirculation impairment-is that mice were inoculated with a single bacterial strain (either an ExoU-producing strain or its mutant with deletion of the exoU gene). In contrast, most of the other experimental studies were carried out with animals infected with mixed bacterial population, as the result of the cecal ligation and puncture sepsis model (Vachharajani et al 2010;Araújo et al 2012;Wang et al 2012;Morel et al 2013), or the intraperitoneal injection of fecal suspensions (Taccone et al 2010;Kao et al 2011;Salgado et al 2011).…”

Section: Pafr/mice Infection Assaysmentioning

confidence: 99%

Contribution of the platelet activating factor signaling pathway to cerebral microcirculatory dysfunction during experimental sepsis by ExoU producingPseudomonas aeruginosa

Plotkowski

Estato

Santos

et al. 2015

Pathogens and Disease

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Intravital microscopy was used to assess the involvement of ExoU, a Pseudomonas aeruginosa cytotoxin with phospholipase A2 activity, in dysfunction of cerebral microcirculation during experimental pneumosepsis. Cortical vessels from mice intratracheally infected with low density of the ExoU-producing PA103 P. aeruginosa strain exhibited increased leukocyte rolling and adhesion to venule endothelium, decreased capillar density and impaired arteriolar response to vasoactive acetylcholine. These phenomena were mediated by the platelet activating factor receptor (PAFR) pathway because they were reversed in mice treated with a PAFR antagonist prior to infection. Brains from PA103-infected animals exhibited a perivascular inflammatory infiltration that was not detected in animals infected with an exoU deficient mutant or in mice treated with the PAFR antagonist and infected with the wild type bacteria. No effect on brain capillary density was detected in mice infected with the PAO1 P. aeruginosa strain, which do not produce ExoU. Finally, after PA103 infection, mice with a targeted deletion of the PAFR gene exhibited higher brain capillary density and lower leukocyte adhesion to venule endothelium, as well as lower increase of systemic inflammatory cytokines, when compared to wild-type mice. Altogether, our results establish a role for PAFR in mediating ExoU-induced cerebral microvascular failure in a murine model of sepsis.

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“…The mechanisms are related to altered blood flow to and within the liver, as seen in experimental models. [5][6][7] The alteration in sinusoidal blood flow coincides with an intense increase in metabolic demand by both hepatocytes and KC. Therapeutic interventions, including positive end-expiratory pressure (PEEP), or concurrent right ventricular dysfunction and tricuspid valvular regurgitation also serve to increase sinusoidal pressure.…”

mentioning

confidence: 99%

The Liver in Critical Illness

Damm

2016

Critical Care Clinics

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Early adverse changes in liver microvascular circulation during experimental septic shock are not linked to an absolute nitric oxide deficit

Cited by 6 publications

References 24 publications

Mechanical Ventilation Preserves Diaphragm Mitochondrial Function in a Rat Sepsis Model

Mechanical Ventilation Preserves Diaphragm Mitochondrial Function in a Rat Sepsis Model

Contribution of the platelet activating factor signaling pathway to cerebral microcirculatory dysfunction during experimental sepsis by ExoU producingPseudomonas aeruginosa

The Liver in Critical Illness

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