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Stunning does not change the relation between calcium and force in skinned rat trabeculae
D L Dietrich1, G R van Leeuwen, G J Stienen
1Laboratory for Physiology, Free University, Amsterdam, The Netherlands.
Insights
Myocardial stunning after ischemia-reperfusion does not alter myofibril sensitivity to calcium. This study found no difference in force-calcium relations in stunned versus control heart muscle, suggesting other mechanisms are involved.
Area of Science:
- Cardiology
- Physiology
- Biochemistry
Background:
- Myocardial stunning is a post-ischemic dysfunction.
- The role of altered myofibril calcium sensitivity in stunning is debated.
Purpose of the Study:
- To investigate if myocardial stunning results from decreased myofibril sensitivity to calcium.
- To compare the isometric force-calcium relationship in stunned and control heart trabeculae.
Main Methods:
- Hearts underwent 40 minutes of ischemia followed by 30 minutes of reperfusion.
- Skinned trabeculae were isolated to determine the force-calcium relationship using the Hill equation.
- Control trabeculae were from aerobically perfused hearts.
Main Results:
- Left ventricular developed pressure significantly decreased in stunned hearts post-ischemia.
- Nucleotide content was reduced in stunned hearts, but creatine kinase levels remained similar.
- Maximal isometric force, force-calcium midpoint, and curve steepness were not significantly different between stunned and control trabeculae.
Conclusions:
- The contractile apparatus of stunned myocardium shows normal isometric force and calcium sensitivity.
- Structural changes in contractile proteins leading to reduced calcium sensitivity are unlikely to cause myocardial stunning.
Abstract:
To test the hypothesis that stunning is due to a decreased sensitivity of the myofibrils for calcium, we compared the isometric force-Ca2+ relation in skinned trabeculae from stunned and control hearts. Hearts were made ischemic for 40 min followed by 30 min reperfusion. In one group (Group 1) changes in left ventricular systolic and diastolic pressure were monitored. From another group (Group 2), trabeculae were isolated to determine the relation between force and Ca2+ concentration. Trabeculae isolated from hearts (Group 3) perfused aerobically for 90 min served as controls. Left ventricular developed pressure and end diastolic pressure were 5.9 +/- 0.7 kPa and 5.8 +/- 0.7 kPa, respectively in stunned hearts as compared to 9.9 +/- 1.2 kPa and 1.2 +/- 0.1 kPa prior to ischemia. The nucleotide content decreased from 24.9 +/- 3.4 mumol.g-1(dw) in control hearts to 9.3 +/- 0.8 mumol.g-1(dw) after ischemia and reperfusion while the creatine kinase levels were about the same. Force-Ca2+ relations obtained from trabeculae from control and stunned hearts were fitted to the Hill equation. Maximal isometric force, the midpoint and the steepness of the curves estimated for the two groups were not significantly different. We conclude that the maximum isometric force and the sensitivity of the contractile apparatus of skinned myocardium of stunned hearts do not differ from that of control hearts. This suggests that structural changes of the contractile proteins leading to a decreased sensitivity of the myofibrils to calcium are not involved in the mechanism responsible for stunning.