2012
DOI: 10.1164/rccm.201209-1735ed
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Lipid Overload: Trigger or Consequence of Mitochondrial Oxidative Stress in Ventilator-induced Diaphragmatic Dysfunction?

Abstract: not measurable, but the clinicians felt the patient benefited from parental presence.There were a small but real percentage of responses that expressed concern regarding difficulties in carrying out the procedure (4%), ability to teach (9%), or clinical decision making (5%) while the parent was present. This highlights the importance of having processes in place to address the concerns. These difficulties were more marked with increasing complexity of the procedure and during resuscitation. This reinforces the… Show more

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Cited by 10 publications
(7 citation statements)
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“…However, these findings could not be reproduced in biceps muscle specimens . A causative link between lipid overload and mitochondrial dysfunction is not firmly established . Nevertheless, oxidative stress has been linked to activation of apoptic, proteasomal, and autophagocytic pathways, and expression of angiogenetic factors varies with the ventilation mode used …”
Section: Pathophysiology Of Respiratory Muscle Dysfunction and Vidd: mentioning
confidence: 98%
See 1 more Smart Citation
“…However, these findings could not be reproduced in biceps muscle specimens . A causative link between lipid overload and mitochondrial dysfunction is not firmly established . Nevertheless, oxidative stress has been linked to activation of apoptic, proteasomal, and autophagocytic pathways, and expression of angiogenetic factors varies with the ventilation mode used …”
Section: Pathophysiology Of Respiratory Muscle Dysfunction and Vidd: mentioning
confidence: 98%
“…83 A causative link between lipid overload and mitochondrial dysfunction is not firmly established. 84 Nevertheless, oxidative stress has been linked to activation of apoptic, proteasomal, and autophagocytic pathways, 85 and expression of angiogenetic factors varies with the ventilation mode used. 86 In conclusion, histopathological and biochemical changes of respiratory muscle dysfunction/VIDD in animal models could now be reproduced to some extent in human experiments.…”
Section: Pathophysiology Of Respiratory Muscle Dysfunction and Vidd: mentioning
confidence: 99%
“…Corroborando ainda com esses pressupostos, em um modelo experimental animal realizado com ratos adultos, um grupo de animais foi exposto à ventilação mecânica (VM) por 12 horas e compararam ao grupo controle (não expostos), concluiu-se que a ventilação mecânica promoveu desequilíbrio das principais defesas antioxidantes do diafragma, contribuindo para o dano na musculatura inspiratória 6,20 . Outro estudo com ratos expostos à VM por 18 horas evidenciou diminuição de miofibrila muscular em todos os tipos de fibras diafragmáticas, além de oxidação de proteínas e peroxidação lipídica 6,[21][22][23] .…”
Section: Discussionunclassified
“…irdly, mitochondrial oxidative stress induces a significant reduction of mitochondrial oxidative phosphorylation and increase of glycolysis, which may lead to an overall reduced energy supply to the muscle [43,55]. Lipid accumulation served as a stimuli to VIDD may result from both the accelerated glycolysis and the decreased breakdown of fatty acids due to compromised mitochondrial function, but the relationship between lipid accumulation and mitochondrial oxidative stress remains unclear [56,57]. Fourthly, mitochondrial oxidative stress modulates activity of enzymes for neurotransmitters in muscle.…”
Section: Mitochondrial Oxidative Stress In the Development Ofmentioning
confidence: 99%