Gadolinium prevents stretch-mediated contractile dysfunction in isolated papillary muscles. Am J Physiol Heart Circ Physiol 2001 Mar;280(3):H1122-8
Date
02/17/2001Pubmed ID
11179055DOI
10.1152/ajpheart.2001.280.3.H1122Scopus ID
2-s2.0-0034977690 (requires institutional sign-in at Scopus site) 15 CitationsAbstract
We tested the hypothesis that overstretching the myocardium could induce and/or exacerbate contractile dysfunction via stretch-activated (SA) ion channels. Maximum developed tension (T(max)), normalized to a control value, was compared in guinea pig papillary muscles held at one of three resting lengths (physiological stretch, overstretch, and unloaded) for 85 min. Overstretched muscles exhibited decreased contractile force (T(max) = 0.77 +/- 0.03) compared with physiological and unloaded muscles (T(max) = 0.93 +/- 0.05 and 1.03 +/- 0.07, respectively). Gd(3+), an SA channel antagonist, eliminated the adverse effect of overstretching (T(max) = 0.98 +/- 0.06), but nifedipine, a dihydropyridine (DHP) antagonist of L-type calcium channels, did not (T(max) = 0.82 +/- 0.04). Exposure to modified hypoxia-reoxygenation (MHR) during physiological stretch resulted in decreased contractility (T(max) = 0.63 +/- 0.07), an effect that was exacerbated by overstretching (T(max) = 0.44 +/- 0.04). Gd(3+) mitigated the effects of overstretch during MHR (T(max) = 0.64 +/- 0.05), but DHP did not (T(max) = 0.48 +/- 0.04). These data suggest that overstretching of the myocardium contributes to contractile abnormalities via SA channels that are distinct from L-type calcium channels.
Author List
Nicolosi AC, Kwok CS, Contney SJ, Olinger GN, Bosnjak ZJMESH terms used to index this publication - Major topics in bold
AnimalsCalcium Channel Blockers
Calcium Channels, L-Type
Dihydropyridines
Gadolinium
Guinea Pigs
Heart Failure
Hypoxia
In Vitro Techniques
Ion Channel Gating
Muscle Contraction
Nifedipine
Oxygen
Papillary Muscles