The effect of flow steps in coronary arterial flow (Qa) on myocardial oxygen consumption (MVo2) was investigated at different heart rates (HR) to further elucidate the dependency of myocardial oxygen consumption on perfusion. In six anesthetized goats the left main coronary artery and the great cardiac vein were cannulated. The hearts were paced alternately at 60 and 130 beats per min. Flow steps were applied at both HR during control and maximal vasodilation by adenosine. MVo2, in steady state before and after the flow step, was calculated by multiplication of Qa and arterio-venous oxygen content difference (Fick's law). Heart rate affected the MVo2 dependency on flow during control as well as during maximal vasodilation. With vascular tone present, the MVo2 dependency on flow (ΔMVo2/ΔQa), in μl O2/ml, was 16.0 ± 3.6 at HR 60 and 21.7 ± 3.9 at HR 130. During maximal vasodilation, these values were 9.5 ± 2.9 and 17.0 ± 5.3 at HR 60 and 130, respectively. The higher MVo2 dependency on flow at high HR may be explained via a dependency of MVo2 on microvascular pressure. The pressure change in the microvessels induced by a flow step is probably larger at high HR than at low HR because of increased venous resistance at high HR, due to increased compression by the heart contraction.@en

A functional distribution of coronary volume can be estimated from the response of arterio-venous O2 content difference (AVO2) to a flow step. However, the results depend on the assumed O2 exchange model. The previously used model consisted of a single mixed compartment with O2 exchange in series with an unmixed compartment without O2 exchange (reference model). The purpose of this study is to provide an estimate of the errors made in the volume estimations by not taking into account factors as flow heterogeneity, different mixing sites or Krogh-like O2 exchange. The approach is indirect: the response of the AVO2 to a flow step has been calculated with alternative O2 exchange models in which the factors mentioned are incorporated. These transients are fitted with the reference model. The resulting estimated volumes are different from the volumes assumed in the alternative models. Large differences are obtained with some of the alternative models, e.g. the model with Krogh characteristics. However, these models seem unrealistic because capillary pO2 is higher than venous pO2. Only small differences in volume are obtained with the more realistic models. Therefore, these results indicate that the coronary volumes are approximated well by the estimations obtained with the reference model. These volume estimations were 9.9 and 3.8 ml 100 g-1 for the O2 exchange vessels and the distal venous volume, respectively.@en

By fitting of simulations with an oxygen exchange model to measured responses of the arteriovenous oxygen content difference after a flow step, coronary volumes can be estimated. In this study the dependence of the volume estimates on the choice of the oxygen exchange model for the coronary circulation was investigated. A model consisting of a single well-mixed compartment results in smaller volume estimates than a series array of mixed compartments in which Po2 declines gradually (Krogh-like model). Use of the former model for data analysis resulted in realistic volume estimates. Thus, these results indicate that the oxygen exchange vessels are better represented by a single mixed compartment than by a cylinder having Krogh characteristics. This conclusion agrees with capillary Po2 being equal to or smaller than venous Po2 which cannot be explained by a Krogh model. From these arguments we conclude that though both models are rough representations of the coronary circulation, the coronary O2 exchange vessels of the beating heart can be represented better by a single mixed compartment than by a series array of mixed compartments which has Krogh characteristics.@en

In six open-thorax-anaesthetized dogs with paced hearts and a retrogradely cannulated epicardial lymph vessel, the sensitivity of myocardial lymph pres- sure to left ventricular pressure during systole and during diastole was determined. The lymph vessels were can- nulated using PE-90 tubing, and lymph pressure was measured by connecting the cannula to a microtip press- ure transducer. To obtain the systolic sensitivity, left ven- tricular pressure was changed by clamping the de- scending aorta, which caused left ventricular pressure to increase. The diastolic sensitivity was obtained from natural variation to left ventricular pressure caused by atrial contractions during induced long diastoles. The mean ratio of the pulse in lymph pressure to the pulse in left ventricular pressure was determined: systole: 0.069 + 0.013, n = 213, diastole: 0.76 -+ 0.16, n = 249 and, if possible, linear regression analysis between lymph and left ventricular pressure was performed. The systolic regression coefficients could be determined in six dogs and the diastolic coefficients in three dogs. Dur- ing long diastoles lymph pressure variations are on aver- age 76 per cent of those in the left ventricle. However, during systole, the sensitivity of lymph pressure to left ventricular pressure is more than ten times lower. It is not unlikely that the structural embedment of lymph ves- sels within the myocardium is such that volume vari- ations by cardiac contraction are limited. @en

1. We tested predictions of a mathematical formulation of a hypothesis of dynamic control of coronary blood flow by tissue oxygen tension. 2. The rate of change of adjustment of the coronary circulation to a step change in arterial perfusion was analysed in the cannulated main stem preparation of the anaesthetized goat. The variable studied was the ratio between driving pressure and coronary flow, each averaged per heart beat. The response of this ratio was measured following a sudden change in perfusion pressure with constant‐pressure perfusion and a sudden change in flow with constant‐flow perfusion. 3. The rate of change of the pressure‐flow ratio was quantified by t50, the time required to establish half of the completed response. For a pressure decrease t50 was 4.9 +/‐ 0.2 s (n = 35) (mean +/‐ S.E.M., n = number of individual measurements), 11.3 +/‐ 1.2 s (n = 25) for a flow decrease, 14.5 +/‐ 1.6 (n = 34) for a pressure increase and 25.1 +/‐ 2.3 (n = 19) for a flow increase. 4. No effect of the level of flow or pressure on t50 was found for a decrease in perfusion. Furthermore, with a flow increase, the t50 value did not depend on the level of flow, which is in agreement with the outcome of earlier experiments where the response to a change in heart rate was measured. With a pressure increase, the mean t50 value of the pressure‐flow ratio was lower at high perfusion pressure but the difference with low perfusion pressure was not significant (P = 0.11). 5. The t50 value in the cases of an increase in pressure and flow are similar to those found for a change of heart rate in an earlier study. 6. Unlike step changes of metabolic rate, some of the measured responses to mechanical step changes were not predicted by the oxygen hypothesis. It is suggested that the increased rate of coronary adjustment induced by the reduction of coronary perfusion is due to arteriolar smooth muscle mechanics which apparently differ in strength depending on the direction of change of the arteriolar dimensions. 7. This suggestion is strengthened by the results of experiments in which smooth muscle responses were abolished with adenosine.@en