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Articles in PresS, published online ahead of print December 12, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00816.2002
Submitted on September 30, 2002
Accepted on December 9, 2002
1 Department of Biomedical Engineering, Marquette University, Milwaukee, WI, USA
2 Department of Biomedical Engineering, Marquette University, Milwaukee, WI, USA; Cardiovascular Research Center, VA Medical Center, Milwaukee, WI, USA
3 Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, WI, USA
4 Department of Biomedical Engineering, Marquette University, Milwaukee, WI, USA; Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, WI, USA; Department of Biomedical Engineering, Marquette University, Milwaukee, WI, USA
5 Department of Biomedical Engineering, Marquette University, Milwaukee, WI, USA; Pulmonary Medicine and Critical Care, Medical College of Wisconsin, Milwaukee, WI, USA; Cardiovascular Research Center, VA Medical Center, Milwaukee, WI, USA
* To whom correspondence should be addressed. E-mail: dfstowe{at}mcw.edu.
We modeled changes in contractile element kinetics derived from the cyclic relationship between myoplasmic [Ca2+], measured by indo-1 fluorescence, and left ventricular pressure (LVP). We estimated model rate constants of Ca2+ affinity for troponin C on actin (A) filament (TnCA) and A and myosin (M) cross-bridge (A.M) cycling in intact guinea pig hearts during baseline 37°C perfusion (P) and evaluated changes at 1) 20 min 17°C P, 2) 30 min reperfusion (RP) after 30 min 37°C global ischemia during 37°C RP, and 3) 30 min RP after 240 min 17°C global ischemia during 37°C RP. At 17°C P vs. 37°C P the model predicted: A.M binding was less sensitive, A.M dissociation was slower; Ca2+ was less likely to bind to TnCA with A.M present; and Ca2+ and TnCA binding was less sensitive in the absence of A.M. Model results were consistent with a cold-induced fall in heart rate from 260 (37°C) to 33 (17°C) beats/min, increased diastolic LVP and increased phasic Ca2+. On RP after 37°C ischemia vs. 37°C P the model predicted: A.M binding was less sensitive, A.M dissociation was slower; and Ca2+ was less likely to bind to TnCA in the absence of A.M. Model results were consistent with reduced myofilament responsiveness to [Ca2+] and diastolic contracture on 37°C RP. In contrast, after cold ischemia vs. 37°C P, A.M association and dissociation rates, and Ca2+ and TnCA association rates returned to pre-ischemic values, while the dissociation rate of Ca2+ from A.M was 9-fold faster. This cardiac muscle kinetic model predicted a better-restored relationship between Ca2+ and cross-bridge function on RP after an eight fold longer period of 17°C than 37°C ischemia.
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