التفاصيل البيبلوغرافية
| العنوان: |
Gentisic acid sodium salt, a phenolic compound, is superior to norepinephrine in reversing cardiovascular collapse, hepatic mitochondrial dysfunction and lactic acidemia in Pseudomonas aeruginosa septic shock in dogs |
| المؤلفون: |
Mink, Steven, Roy Chowdhury, Subir, Gotes, Jose, Cheng, Zhao-Qin, Kasian, Krika, Fernyhough, Paul |
| بيانات النشر: |
BioMed Central Ltd. |
| سنة النشر: |
2016 |
| المجموعة: |
BioMed Central |
| مصطلحات موضوعية: |
Lactic acidosis, ATP, Electron transport chain, Vasopressors, Antioxidants, Vasodilation, Infection, Septic shock, Mitochondria, Norepinephrine, Gentisic acid |
| الوصف: |
Background The development of lactic acidemia (LA) in septic shock (SS) is associated with an ominous prognosis. We previously showed that the mechanism of LA in SS may relate to impaired hepatic uptake of lactate, but the mechanism was not clear. Uptake of lactate by the liver occurs by a membrane-associated, pH-dependent, antiport system known as the monocarboxylate transporter. In the hepatocyte, lactate can then be metabolized by oxidative phosphorylation or converted to glucose in the cytosol. In the present study, we examined (1) whether hepatic mitochondrial dysfunction accounted for decreased uptake of lactate in a canine model of Pseudomonas aeruginosa SS, (2) whether norepinephrine (NE) treatment by increasing mean arterial pressure (MAP) could improve mitochondrial dysfunction and LA in this model, and (3) whether gentisic acid sodium salt (GSS), a novel phenolic compound, was superior to NE in these effects. Methods In anesthetized/ventilated dogs, we infused the bacteria over ~10 h and measured hemodynamics in various treatment groups (see below). We then euthanized the animal and isolated the hepatic mitochondria. We measured hepatic mitochondrial oxygen consumption rates using the novel Seahorse XF24 analyzer under conditions that included: basal respiration, after the addition of adenosine- diphosphate to produce coupled respiration, and after the addition of a protonophore to produce maximal respiration. Results We found that in the septic control group, mean arterial pressure decreased over the course of the study, and that mitochondrial dysfunction developed in which there was a reduction in maximal respiration. Whereas both NE and GSS treatments reversed the reduction in mean arterial pressure and increased maximal respiration to similar extents in respective groups, only in the GSS group was there a reduction in LA. Conclusions Hepatic mitochondrial dysfunction occurs in SS, but does not appear to be required for the development of LA in SS, since NE improved mitochondrial ... |
| نوع الوثيقة: |
report |
| اللغة: |
English |
| العلاقة: |
http://www.icm-experimental.com/content/4/1/24Test |
| الإتاحة: |
http://www.icm-experimental.com/content/4/1/24Test |
| حقوق: |
Copyright 2016 The Author(s). |
| رقم الانضمام: |
edsbas.8F77C76A |
| قاعدة البيانات: |
BASE |
