Perry Staltic
Member
- Joined
- Dec 14, 2020
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- 8,186
That was fairly widely known in early 2020. Pioneering work by Chestnut lol. Now he needs to go research how mechanical ventilation increases all of the biochemical markers he mentions (VGEF, adhesion molecules, selectins, etc). He might get it one day. Then it'll be - GUESS WHAT I FOUND! MY MOST IMPORTANT WORK YET!
I'll do him a favor and give him a head start so he can get a jump on everyone. He says this in that link:
14) Ang II synthesis both increased vascular permeability by promoting the expression and secretion of VEGF (vascular endothelial growth factor) (Chua et al, 1998; Kitayama et al, 2006; Suzuki et al, 2003), and induced the expression of endothelial adhesive molecules including molecules-1 (ICAM-1) and their ligands, the integrins (Alvarez et al, 2004; Piqueras et al, 2000; Pueyo et al, 2000). Ang II also promotes endothelial dysfunction through COX-2 activation, which generates vasoactive prostaglandins and ROS (Welch, 2008; Wu et al, 2005). Moreover, Ang II favours the recruitment of infiltrating inflammatory cells into tissues by stimulating the production of specific cytokine/chemokines.
Those are increased by mechanical ventilation
Ventilator-induced endothelial activation and inflammation in the lung and distal organs - Critical Care
Introduction Results from clinical studies have provided evidence for the importance of leukocyte-endothelial interactions in the pathogenesis of pulmonary diseases such as acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), as well as in systemic events like sepsis and...
ccforum.biomedcentral.com
Ventilator-induced lung injury increases expression of endothelial inflammatory mediators in the kidney
In critical illness, such as sepsis or the acute respiratory distress syndrome, acute kidney injury (AKI) is common and associated with increased morbidity and mortality. Mechanical ventilation in critical illnesses is also a risk factor for AKI, but ...
www.ncbi.nlm.nih.gov
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