Using an active cross-bridge model proposed by the authors, it has been established theoretically that cross-bridge activation rate (K
a) of the left ventricular myocardium, which might correspond to the rate of binding of Ca
2+ with troponin C, is approximately expressed as a simple formula: K
a=3/electromechanical systole (sec
-1), although no definitive biological proof has yet been provided for the equation. One hundred eighteen patients without significant cardiac disease and 6 patients who had atrioventricular block with a permanent pacemaker were evaluated to determine the K
a value of the normal human left ventricular myocardium (test 1), and to examine the effect of changes in heart rate (test 2) as well as afterloading (test 3) or dobutamine infusion (test 4) on K
a. The pacing rate was increased from 50 to 110 beats/min at 20-beat increments in test 2. Arterial pressure was elevated by angiotensin 11 infusion in test 3, and 7 subjects received a continuous dobutamine infusion in test 4. The K
a value was found to be related to heart rate, to be increased by dobutamine infusion, and to be decreased by myocardial lengthening due to afterloading. Dependence of K
a on heart rate appeared to result from changes in myocardial length. The K
a value corrected for heart rate (K
ac) had an average variation of only 4.6%, and was unrelated to age or myocardial length in individual subjects. Thus, the K
ac value of normal human left ventricular myocardium appears to be nearly constant between individuals but to be increased by catecholamine infusion or myocardial shortening.
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