Key result
Inhibition of sodium/hydrogen exchange with MIA during acidosis and realkalinisation attenuated hypercontractility and abolished cell contracture, enhancing recovery of cell function.
Why the study?
Does inhibition of Na+/H+ exchange with MIA improve recovery of cell function in isolated guinea pig cardiac myocytes subjected to acidosis and realkalinisation?
Population
Isolated guinea pig cardiac myocytes subjected to lactic acid induced acidosis followed by realkalinisation
Comparison
Methylisobutylamiloride or phorbol 12-myristate… vs Untreated cells subjected to the same…
Design
Preclinical
Authors
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Does not support clinical adoption; hypothesis-generating for Na+/H+ exchange inhibition in myocardial recovery.
Does inhibition of Na+/H+ exchange with MIA improve recovery of cell function in isolated guinea pig cardiac myocytes subjected to acidosis and realkalinisation?
Inhibition of Na+/H+ exchange activity during acidosis and realkalinisation enhances the recovery of cellular function in isolated cardiac myocytes.
WARD et al. (1995) studied Lactic acid induced acidosis and realkalinisation. Methylisobutylamiloride (MIA) was evaluated on Intracellular calcium, intracellular pH, and unloaded cell shortening. Inhibition of sodium/hydrogen exchange with MIA during acidosis and realkalinisation attenuated hypercontractility and abolished cell contracture, enhancing recovery of cell function.
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