Hydrostatic forces limit swelling of rat ventricular myocardium

M. B. Pine, W. W. Brooks, J. J. Nosta and W. H. Abelmann To study ventricular cellular volume regulation when cell membranes and ion pumps cannot prevent swelling, rat ventricular sections were incubated in modified Krebs-Henseleit solutions in which 1) potassium was substituted for sodium, ion for...

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Veröffentlicht in:American journal of physiology. Heart and circulatory physiology 1981-11, Vol.241 (5), p.H740-H747
Hauptverfasser: Pine, M. B, Brooks, W. W, Nosta, J. J, Abelmann, W. H
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Sprache:eng
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Zusammenfassung:M. B. Pine, W. W. Brooks, J. J. Nosta and W. H. Abelmann To study ventricular cellular volume regulation when cell membranes and ion pumps cannot prevent swelling, rat ventricular sections were incubated in modified Krebs-Henseleit solutions in which 1) potassium was substituted for sodium, ion for ion; or 2) sodium chloride was reduced to decrease osmolarity to 228, 171, or 114 mosM. Ventricular water, [3H]inulin and [3H]mannitol spaces, potassium, sodium, chloride, and protein contents, and resting transmembrane potentials were measured. Increases in ventricular cellular volume were less than 30% in potassium-substituted and extremely dilute media (114 mosM), in contrast to increases of over 100% in identically treated renal cortical slices. In potassium-substituted solution, the fluid gained by ventricular cells during incubation was hypertonic with respect to the bathing medium. In dilute solution (171 and 114 mosM), ventricular, cellular, and extracellular osmolarities equilibrated only after substantial losses of cellular ions had occurred. These findings support the existence of mechanical limitations to ventricular cellular swelling, which may be caused by a unique network of interstitial collagen present in ventricular myocardium.
ISSN:0363-6135
0002-9513
1522-1539
DOI:10.1152/ajpheart.1981.241.5.h740