Am J Physiol Cell Physiol Journal of Neurophysiology
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Am J Physiol Cell Physiol 278: C739-C746, 2000;
0363-6143/00 $5.00
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Vol. 278, Issue 4, C739-C746, April 2000

Cellular basis for contractile dysfunction in the diaphragm from a rabbit infarct model of heart failure

Niall G. MacFarlane, G. Murray Darnley, and Godfrey L. Smith

Institute of Biomedical Sciences, University of Glasgow, Glasgow G12 8QQ, United Kingdom

Abnormal respiratory muscle function is thought to contribute to breathlessness and exercise intolerance in heart failure but little is known about possible alterations in the function of such muscle. We have measured tetanic force and intracellular Ca2+ concentration ([Ca2+]i) in isolated, arterially perfused hemidiaphragm preparations from a rabbit coronary artery ligation model of heart failure. Increasing stimulation frequency (10-100 Hz) caused a progressive increase of force and [Ca2+]i in control preparations, whereas force and [Ca2+]i only increased between 10 and 25 Hz stimulation (decreasing at higher frequencies) in preparations from ligated animals. Cyclopiazonic acid produced a dose-dependent shift in the relationship between stimulation frequency and [Ca2+]i in control preparations that was similar to the shift observed in the diaphragm of coronary-ligated animals. These data indicate that the in vitro contractile characteristics of the diaphragm are significantly altered in our model and that altered [Ca2+]i regulation contributes to the reduced diaphragm strength observed in heart failure.

calcium; respiratory muscle; sarco(endo)plasmic reticulum; contractility


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