Osteonectin and osteopontin, two secreted matricellular proteins, have a variety of functions that are exerted through interaction with matrix components. These proteins appear in response to tissue injury. To test our hypothesis that osteopontin and osteonectin are expressed with spatially and temporally different patterns in myocardial infarct tissue, we investigated osteonectin and osteopontin expression in experimentally induced myocardial infarction in rats, in comparison with Type I collagen expression. Northern blotting demonstrated that osteonectin mRNA did not markedly increase on Day 2 after the infarction, but it increased on Days 7 and 14 by 1.7+/-0.12- and 1.8+/-0.01-fold compared to that in preligation hearts. In contrast, osteopontin mRNA was increased on Day 1 (41.9+/-11.3-fold increase) and on Day 2 (58.3+/-7.6-fold increase), and then it declined on Days 7 and 14 (24.8+/-9.0- and 13.5+/-4.7-fold increase, respectively). In situ hybridization revealed that osteonectin mRNA signals were observed in fibroblasts, myofibroblasts and macrophages around infarct necrotic tissue on Days 7 and 14. Osteopontin mRNA signals were observed in macrophages in the infarct marginal zone on Day 2. Immunopositive staining for both osteonectin and osteopontin showed the same pattern as that obtained by in situ hybridization. The time course of osteonectin mRNA was almost parallel with that of Type I collagen mRNA, while that of osteopontin was not. These results demonstrated spatially and temporally different expression patterns of osteonectin and osteopontin in myocardial infarction and suggest that osteonectin appears to be involved in the pathological course in the late phase after infarction concomitantly with Type I collagen, while osteopontin may play a role in the early phase.

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The present results demonstrated the time-dependent increase in the expression of dermatopontin mRNA in parallel with that of decorin mRNA in the infarct zone. Coexpression of dermatopontin mRNA with decorin and type I collagen mRNAs suggests that dermatopontin plays a role in ECM (fibrillar collagen matrix) reformation in the infarct along with decorin and type I collagen.

The heart rate (HR) is closely coupled with cardiac performance [1]. In response to changes in the oxygenated blood requirements of the body due to exercise, the HR changes with the alteration of cardiac output. The HR is also closely related to myocardial oxygen consumption [2]. Impaired response of heart rate to exercise has recently been demonstrated to be predictive of increased mortality and coronary heart disease incidence [3,4]. Quantitative analyses of the HR response are thus important with respect to cardiac accidents.In high-intensity bicycle ergometer-exercise (120 W), the HR at first increased rapidly followed by a continuous and gradual increase, and this response was fitted to a second-order exponential function [5][6][7][8][9]. In moderate-intensity exercise (50-75 W), the HR increased and reached a plateau level, and this response was fitted to a first-order exponential function [5][6][7][8][9]. In unloaded or low-intensity exercise, the HR increased transiently and then declined, and an adequate equation fitting this response has not yet been obtained [10]. In these previous analyses, it was difficult to determine, in certain cases, whether the first-or second-order exponential equation was appropriate for fitting. It is also reasonable to expect that the central nervous command system regulates smoothly (not suddenly with a switching point) the change of balance between parasympathetic and sympathetic tone. It would be more theoretically reasonable for one single equation to fit all these different HR changes, and such an equation would be very helpful for analyzing the HR changes induced by constant-load exercise Key words: kinetics, regression, least-squares method, electrocardiography. Abstract:We attempted to fit heart rate (HR) changes induced by constant exercise loads of different intensities to an exponential hyperbolic sine curve by the least-squares method, and we compared the results with the fitting of the changes to exponential curves. Seven healthy male volunteers performed three different intensities of constant-load exercise on a bicycle ergometer. The exponential hyperbolic sine function adequately fitted the HR responses induced by all three different intensities of loads: low (30 W: correlation coefficient, rϭ0.68Ϯ0.13, meanϮSD), moderate (75 W: rϭ0.93Ϯ0.07) and high (125 W: rϭ0.97Ϯ0.02). The first-order exponential curve fitted only the moderate load response. Although the second-order exponential equation fitted the HR response for both the moderate and high loads, the equation did not fit the low-load response (rϭ0.43Ϯ0.26). In lowload exercise, the sum of the power of the residuals for the exponential hyperbolic sine curve fitting was significantly smaller than that for the first-or second-order exponential curve fitting. In conclusion, the exponential hyperbolic sine function is useful for quantitative analyses of the HR response to exercise loads of various intensities.

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