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D A Eisner

Publications and source records attributed to D A Eisner.

154 records · Page 9Linked to original sources
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The effects of lactic acid production on contraction and intracellular pH during hypoxia in cardiac muscle.

During hypoxia cardiac contraction declines and there is an intracellular acidosis. We find that, if this acidosis is abolished by decreasing pCO2 there is little restoration of force. Therefore the acidosis is not the major cause of the decline of force. The acidosis may partly result from the generation of lactic acid. No acidosis, is however, seen in isolated cardiac cells. Furthermore a theoretical model shows that lactic acid production would be expected to produce a transient acidosis. We suggest that the observed maintained acidosis may be a consequence of extracellular lactic acid accumulation affecting intracellular pH.

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PubMedDate not supplied

The control of sarcoplasmic reticulum Ca content in cardiac muscle.

Most of the calcium that activates contraction in the heart comes from the sarcoplasmic reticulum (SR) and it is therefore essential to control the SR Ca content. SR Ca content reflects the balance between uptake (via the SR Ca-ATPase, SERCA) and release, largely via the ryanodine receptor (RyR). Unwanted changes of SR Ca are prevented because, for example, an increase of SR Ca content increases the amplitude of the systolic Ca transient and this, in turn, results in increased loss of Ca from and decreased Ca entry into the cell thereby restoring cell and SR Ca towards control levels. We discuss the parameters that affect the steady level of SR Ca and how these may change in heart failure. Finally, we discuss disordered Ca regulation with particular emphasis on the condition of alternans where successive heartbeats alternate in amplitude. This behaviour can be explained by excessive feedback gain in the processes controlling SR Ca.

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PubMedDate not supplied

Oscillations of intracellular Ca2+ in mammalian cardiac muscle.

Contraction of cardiac muscle depends on a transient rise of intracellular calcium concentration ([Ca2+]i) which is initiated by the action potential. It has, however, also been suggested that [Ca2+]i can fluctuate in the absence of changes in membrane potential. The evidence for this is indirect and comes from observations of (1) fluctuations of contractile force in intact cells, (2) spontaneous cellular movements, and (3) spontaneous contractions in cells which have been skinned to remove the surface membrane. The fluctuations in force are particularly prominent when the cell is Ca2+-loaded, and have been attributed to a Ca2+-induced Ca2+ release from the sarcoplasmic reticulum. In these conditions of Ca2+-loading the normal cardiac contraction is followed by an aftercontraction which has been attributed to the synchronization of the fluctuations. The rise of [Ca2+]i which is thought to underlie the aftercontraction also produces a transient inward current. This current, which probably results from a Ca2+-activated nonspecific cation conductance, has been implicated in the genesis of various cardiac arrhythmias. However, despite the potential importance of such fluctuations of [Ca2+]i their existence has, so far, only been inferred from tension measurements. Here we present direct measurements of such oscillations of [Ca2+]i.

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