Granulocytosis and increased adhesion molecules after resistive loading of the diaphragm

Abstract

Upregulation of endothelial cell adhesion molecules, followed by an influx of granulocytes and macrophages, can contribute to exertion-induced skeletal muscle injury. The purpose of this study was to quantify circulating leukocyte subsets, diaphragm injury and infiltrating leukocyte subsets, and surface expression of vascular cell adhesion molecule (VCAM)-1 and intracellular adhesion molecule (ICAM)-1 in the diaphragm after inspiratory resistive loading (IRL).Eight New Zealand white rabbits underwent 1.5 h of IRL and seven control rabbits underwent a sham procedure. Blood samples, taken at baseline and 2, 6, 12, 24, 48 and 72 h after the onset of IRL or sham, showed that band cell counts had increased at 6 h post-IRL. Point counting of haematoxylin and eosin-stained cross-sections, sampled at 72 h post-IRL, showed greater injury in diaphragms from IRL rabbits compared with controls. Immunohistochemical processing showed increased expression of ICAM-1 and VCAM-1, and higher granulocyte and macrophage counts in IRL diaphragms than control diaphragms. Macrophages were the predominant inflammatory cells.Increased intracellular adhesion molecule-1 and vascular cell adhesion molecule-1 expression, and infiltration of granulocytes and macrophages may contribute to inspiratory resistive loadinginduced diaphragm injury.

Inspiratory muscle strength training improves weaning outcome in failure to wean patients: a randomized trial

“…Although we did not examine diaphragm samples for training-induced damage, we think that it is unlikely that the IMST program induced muscle damage for the following reasons: 1) the duration of muscle loading during each IMST training session was approximately one minute per day. In contrast, animal and human studies have documented diaphragm damage with prolonged, high resistance loads, lasting 1.5 [44,45] to 96 hours [46]. 2) Our IMST patients were able to inspire against increasing inspiratory loads on a daily basis.…”

Evolution of Diaphragm Thickness during Mechanical Ventilation. Impact of Inspiratory Effort

“…Given that increases in thickness over time were associated with both higher thickening fraction and higher SOFA scores in our study, it is possible that an injurious increase in thickness may result from excess inspiratory loads during ventilation or from systemic inflammation. High inspiratory loads can cause myofibrillar and sarcolemmal injury (44)(45)(46)(47)(48)(49)(50).…”

Respiratory drive in the acute respiratory distress syndrome: pathophysiology, monitoring, and therapeutic interventions

“…Few animal experimental studies show that high inspiratory effort due to excess inspiratory load might induce diaphragm inflammation [68,69] and promote diaphragm injury [70].…”