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 |
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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. |
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ISSN: | 0363-6135 0002-9513 1522-1539 |
DOI: | 10.1152/ajpheart.1981.241.5.h740 |