American journal of physiology. Heart and circulatory physiology
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Am. J. Physiol. Heart Circ. Physiol. · Feb 2006
Mechanism of osmotic flow in a periodic fiber array.
The classic analysis by Anderson and Malone (Biophys J 14: 957-982, 1974) of the osmotic flow across membranes with long circular cylindrical pores is extended to a fiber matrix layer wherein the confining boundaries are the fibers themselves. The equivalent of the well-known result for the reflection coefficient sigma0 = (1 - phi)2, where phi is the partition coefficient, is derived for a periodic fiber array of hexagonally ordered core proteins. The boundary value problem for the potential energy function describing the solute distribution surrounding each fiber is solved by defining an equivalent fluid annulus in which the pressures and osmotic forces are determined. ⋯ Results for the reflection coefficient are presented in terms of two dimensionless numbers, alpha = a/R and beta = b/R, where a and b are the solute and fiber radii, respectively, and R is the outer radius of the fluid annulus. In general, the results differ substantially from the classic expression for a circular pore because of the large difference in the shape of the boundary along which the osmotic force is generated. However, as in circular pore theory, one finds that the reflection coefficients for osmosis and filtration are the same.
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Am. J. Physiol. Heart Circ. Physiol. · Feb 2006
Increased cross-bridge cycling rate in stunned myocardium.
Decreased Ca2+ responsiveness of the myofilaments underlies myocardial stunning. Given that cross-bridge cycling is a major determinant of myofilament behavior, we quantified cross-bridge cycling rate in stunned myocardium. After stabilization, rat hearts were subjected to 20 min of no-flow global ischemia and 30 min of reperfusion at 37 degrees C. ⋯ These results show that cross-bridge cycling is increased in stunned myocardium. Such increases are likely the result of increased transition rate from force-generating states to non-force-generating states. Thus stunned myocardium still maintains ATP consumption in spite of lower force development, rationalizing the long-standing paradox of decreased force but unchanged oxygen consumption in the postischemic heart.