48 research outputs found
Long-term outcome of infective endocarditis: A study on patients surviving over one year after the initial episode treated in a Finnish teaching hospital during 25 years
To operate or not on elderly patients with aortic stenosis:the decision and its consequences
To operate or not on elderly patients with aortic stenosis:the decision and its consequences
To operate or not on elderly patients with aortic stenosis:the decision and its consequences
Percutaneous Transluminal Coronary Angioplasty in Patients with Failed Bypass Graft Surgery
Influence of heat and shear induced protein aggregation on the in vitro digestion rate of whey proteins
Beyond Brick and Mortar: The Experiences of U.S. Female Mobile Fashion Truck Entrepreneurs
Diaphragm adaptations in patients with COPD.
Contains fulltext :
70068.pdf ( ) (Open Access)Inspiratory muscle weakness in patients with COPD is of major clinical relevance. For instance, maximum inspiratory pressure generation is an independent determinant of survival in severe COPD. Traditionally, inspiratory muscle weakness has been ascribed to hyperinflation-induced diaphragm shortening. However, more recently, invasive evaluation of diaphragm contractile function, structure, and biochemistry demonstrated that cellular and molecular alterations occur, of which several can be considered pathologic of nature. Whereas the fiber type shift towards oxidative type I fibers in COPD diaphragm is regarded beneficial, rendering the overloaded diaphragm more resistant to fatigue, the reduction of diaphragm fiber force generation in vitro likely contributes to diaphragm weakness. The reduced diaphragm force generation at single fiber level is associated with loss of myosin content in these fibers. Moreover, the diaphragm in COPD is exposed to oxidative stress and sarcomeric injury. This review postulates that the oxidative stress and sarcomeric injury activate proteolytic machinery, leading to contractile protein wasting and, consequently, loss of force generating capacity of diaphragm fibers in patients with COPD. Interestingly, several of these presumed pathologic alterations are already present early in the course of the disease (GOLD I/II), although these patients appear not limited in their daily life activities. Treatment of diaphragm dysfunction in COPD is complex since its etiology is unclear, but recent findings indicate the ubiquitin-proteasome pathway as a prime target to attenuate diaphragm wasting in COPD