Vagus Nerve Stimulation Attenuates Multiple Organ Dysfunction in Resuscitated Porcine Progressive Sepsis
Jazyk angličtina Země Spojené státy americké Médium print
Typ dokumentu časopisecké články
- MeSH
- elektrostimulační terapie MeSH
- hemodynamika MeSH
- hyperlaktatemie krev prevence a kontrola MeSH
- modely nemocí na zvířatech MeSH
- monocyty * MeSH
- multiorgánové selhání patofyziologie terapie MeSH
- myokard patologie MeSH
- náhodné rozdělení MeSH
- nervus vagus * MeSH
- počet leukocytů MeSH
- prasata MeSH
- progrese nemoci MeSH
- prospektivní studie MeSH
- sepse patofyziologie terapie MeSH
- srdce patofyziologie MeSH
- srdeční mitochondrie fyziologie MeSH
- vazokonstriktory terapeutické užití MeSH
- vyhodnocení orgánové dysfunkce MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- vazokonstriktory MeSH
OBJECTIVES: To investigate the potential benefits of vagus nerve stimulation in a clinically-relevant large animal model of progressive sepsis. DESIGN: Prospective, controlled, randomized trial. SETTING: University animal research laboratory. SUBJECTS: Twenty-five domestic pigs were divided into three groups: 1) sepsis group (eight pigs), 2) sepsis + vagus nerve stimulation group (nine pigs), and 3) control sham group (eight pigs). INTERVENTIONS: Sepsis was induced by cultivated autologous feces inoculation in anesthetized, mechanically ventilated, and surgically instrumented pigs and followed for 24 hours. Electrical stimulation of the cervical vagus nerve was initiated 6 hours after the induction of peritonitis and maintained throughout the experiment. MEASUREMENTS AND MAIN RESULTS: Measurements of hemodynamics, electrocardiography, biochemistry, blood gases, cytokines, and blood cells were collected at baseline (just before peritonitis induction) and at the end of the in vivo experiment (24 hr after peritonitis induction). Subsequent in vitro analyses addressed cardiac contractility and calcium handling in isolated tissues and myocytes and analyzed mitochondrial function by ultrasensitive oxygraphy. Vagus nerve stimulation partially or completely prevented the development of hyperlactatemia, hyperdynamic circulation, cellular myocardial depression, shift in sympathovagal balance toward sympathetic dominance, and cardiac mitochondrial dysfunction, and reduced the number of activated monocytes. Sequential Organ Failure Assessment scores and vasopressor requirements significantly decreased after vagus nerve stimulation. CONCLUSIONS: In a clinically-relevant large animal model of progressive sepsis, vagus nerve stimulation was associated with a number of beneficial effects that resulted in significantly attenuated multiple organ dysfunction and reduced vasopressor and fluid resuscitation requirements. This suggests that vagus nerve stimulation might provide a significant therapeutic potential that warrants further thorough investigation.
Biomedical Center Faculty of Medicine in Pilsen Charles University Pilsen Czech Republic
Department of Physiology Faculty of Medicine in Pilsen Charles University Pilsen Czech Republic
Citace poskytuje Crossref.org
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