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Mechanical ventilation impairs sarcomeric protein function in rat diaphragm single fibers
Author(s) -
Ahn Bumsoo S.,
Sollanek Kurt J.,
Smuder Ashley J.,
Wiggs Michael P.,
Powers Scott K.,
Ferreira Leonardo F.
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.939.3
Subject(s) - isometric exercise , diaphragm (acoustics) , chemistry , biophysics , medicine , calcium , respiratory system , mechanical ventilation , ventilation (architecture) , cardiology , endocrinology , biology , loudspeaker , engineering , mechanical engineering , physics , acoustics
Mechanical ventilation (MV) is a widely used clinical intervention for patients unable to maintain alveolar ventilation. Although a life‐saving measure for patients suffering from respiratory failure, MV promotes diaphragm atrophy and contractile dysfunction. The cellular basis of contractile dysfunction remains unclear. The mechanisms of contractile dysfunction are important to understand because MV‐induced diaphragm weakness can delay the weaning process. We studied triton‐permeabilized diaphragm single fibers from rats after 12 hrs of spontaneous breathing (SB) and MV (n = 4/group). Key parameters of isometric contractile properties were maximal specific tetanic force (sPo), rate constant of tension redevelopment (ktr), and calcium sensitivity (pCa50). In type I diaphragm fibers, sPo did not differ between groups. MV slowed ktr by ~6% and decreased the pCa50 such that calcium concentration eliciting 50% sPo increased by ~20%. In type II diaphragm fibers, MV diminished sPo by ~32% and slowed ktr by ~22%. However, pCa50 did not differ between groups. Together, our data suggest that MV impairs diaphragm sarcomeric protein function as evidenced by diminished specific force and calcium sensitivity, and slowing of cross bridge cycling kinetics in membrane‐permeabilized single fibers. Funding support: NIH R00‐ HL098453 (LFF) and HL087839 (SKP)