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This letter is intended to extend the discussion of Bellamy's (1978) intriguing analysis of diastolic coronary artery pressure-flow relations in dogs during long diastoles. In reactive hyperemia (RH), he found practically linear diastolic pressure-flow relations. These linear pressure-flow relations led him to the conclusion that coronary resistance, R, remains constant during diastole, and consequently, extrapolation of this relation to zero flow was justified. The zero-flow pressure Pf-o found in this way varies during RH such that Pr-o is approximately 25 mm Hg immediately after release of a 15-second occlusion and progressively increases to a steady value of approximately 45 mm Hg. In mathematical terms, Bellamy presented his model of interpretation of the experimental results by Q = (Pa — Pr_o)/ R, where Q (= coronary flow) and P. (= aortic pressure) are varying during diastole, and Pf-o and R are constant during diastole but can vary from beat to beat. However, does the linear pressure-flow relation imply that coronary resistance is really constant? To examine this problem, I calculated pressure-flow relations, using a model based on assumptions contradictory to those of Bellamy. What would the pressure-flow relation look like if: (1) Pr_o remains constant during RH; (2) coronary resistance changes continuously during diastole of RH? The difference between the two models is elucidated with the aid of Figure 1. Points A and B are defined by the pressure and flow at beginning and end of the first RH diastole of Bellamy's Figure 6. Bellamy's model states that R is constant and, hence, a line might be drawn through A and B resulting in a Pf_o = 25 mm Hg. The present model assumes that Pr-o remains constant (40 mm Hg). Hence, the dotted lines through A and B represent imaginary pressure-flow relations holding at the instant of beginning and end of diastole, respectively. Would a time-varying coronary resistance lead to an apparently linear pressure-flow relation between A andB? For the present calculations, it was assumed that R during a diastole varied linearly with time between the average coronary diastolic resistance of that beat and that of the following one. The aortic pressure was assumed to decline exponentially from a value of 100 mm Hg at the beginning of diastole and with a time constant of 4.5 seconds. It was assumed that all diastoles are of 2.5 seconds duration. Coronary flow was then calculated as a function of time from the time-dependent P« and R but with constant Pr-o. Calculated diastolic flow-pressure relations are shown in Figure 2 by heavy lines. The calculated curves are only slightly nonlinear, and can be interpreted as being linear; by eye, they were extrapolated to zero flow. In Figure 2, these linear approximations are represented by broken lines. The deviation between the calculated curves and their linear approximations are well within experimental error, as far as can be judged from Bellamy's paper. Figure 2 shows essentially similar features to Figure 6 of Bellamy's paper. In both figures, the extrapolated apparent zero-flow pressure immediately after release of flow is as low as 20 mm Hg and increases during RH. In the present results, however, the apparent Pf_0 increases more rapidly than in Bellamy's study and also shows an overshoot during the course of RH. Nevertheless, the present analysis shows that (1) dynamic components of autoregulation may be significant but remain hidden within the scatter of the measurements, and (2) the determination of Pf_0 during RH is very sensitive to these dynamic components. Obviously, my intention was not to prove the validity of the present model. Bellamy points to the agreement in both the observed decreased diastolic coronary resistance and decreased zero-flow pressure at vasodilation obtained during RH, adenosine infusion, and decreased perfusion pressure (Mosher

Does coronary resistance change only during systole?