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KMID : 0378119850120010103
Chungnam Medical Journal
1985 Volume.12 No. 1 p.103 ~ p.115
Influence of pH Changes on the Contractility of Cardiac Muscle


Abstract
The effects of extracellular pH changes on excitation-contraction coupling were studied in isolated. rabbit papillary muscles.
All expertments were performed in nonbicarbonate-buffered Tyrods slution, using phosphate buffer system for acidosis (PH 7.0, 6.4 or 6.0) and Tris tuffer system for alkalosis (pH 7.8),which was aerated with 100% O©ü and kept at 35¡É. Action potentials were measured by conventional microelectrode technique in the papillary muscles. The slow response action potentials(SRAP) were induced by superfusing the muscles to a Tyrode solution containing 27 mM KCI and 10^(-5)% histamine and stimulating them with stow and intense stimuli (from 0.5Hz, 5V to 0.1 Hz, 20V).
The results obtained were as follows;
1. Acidosis elicited a degree-dependent negative inotropic effect, whereas alkalosis induced a positive inotropic effect. The increase in isometric tension at pH 7.8 was 150%, cempared tothat at normal pH, but the decrease at pH 6.4 was about 50%.
2. The acidosis-induced depression of contractility was restored rapidly to normal level by the addition of Ca2+ to the Tyrode solution or administration of agonists, histamine (10^(-6)M) ornorepinephrine (10^(-4)M).
3. The parallel changes in resting msmbrane potential (depolarization) and overshoot, and the obvious shortening of action potential duration were observed after a change from control solution to the alkalotic Tyrode solution (pH 7.8). In acidosis (pH 7.0), however, the parallel declines in resting membrane potential (hyperpolarigation) and overshoot were observed, and the duration was almost no changed.
4. SRAP, which were eliminated by Ca^(2+) antagonists (verapamil or Mn^(2+)), were potentiated in amplitude and duration at high pH 7.8, but inhibited obviously at low pH 6.4.
The results of this experiment suggest that the alteration in cardiac contractility by extracellular pH change is due to the influence upon slow inward Ca^(2+) current.
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