A B S T R A C T The proposal that diastolic coronary flow is regulated by an intramyocardial "back-pressure" that substantially exceeds coronary venous and ventricular diastolic pressures has been examined in an open-chest canine preparation in which instantaneous left circumflex pressure and flow could be followed to cessation of inflow during prolonged diastoles. Despite correlation coefficients consistently >0.90, pressureflow data during individual diastoles were concave to the flow axis before and during pharmacologically induced maximum coronary vasodilation. Data were better fitted (P < 0.01) by second-order equations than by linear equations in >90% of cases. Second-order pressure-axis intercepts (Pf=o)l averaged 29±+7 (SD)

Ventilation (VE), pulmonary gas exchange (MO2 and MCO2), and arterial acid-base status (pH and PaCO2) were measured in immature green turtles. Chelonia mydas, equilibrated at 15, 25, and 35 degrees C. From 25 to 35 degrees C, pH decreased by 0.0134 U/degrees C and PaCO2 increased from 30.1 +/- 1.1 to 46.0 +/- 2.4 Torr (mean +/- SE, n = 8) in conformity with results from other ectotherms. From 15 to 25 degrees C, however, pH fell on the average by 0.06 U/degrees C but the change was not significant. PaCO2 rose over this range from 25.3 +/- 1.6 to 30.1 +/- 1.1 Torr. Calculated plasma [HCO3-], 27-28 meq/l, did not change over the entire temperature range. Both VE and MO2 increased with temperature, but the ratio, VE/MO2 (the air convection requirement), fell with temperature (1.01 +/- 0.10 l/mmol at 35 degrees C, 0.64 +/- 0.03 l/mmol at 25 degrees C, and 0.45 +/- 0.04 l/mmol at 15 degrees C). We conclude that the green turtle adheres to the typical ectotherm blood acid-base pattern over their usual temperature range (25-35 degrees C), but that pH control deviates from this pattern at temperatures below this range.

Bellamy's recent studies (1) suggest that coronary driving pressure is overestimated importantly when downstream pressure is taken as right atrial or left ventricular diastolic pressure. In these provocative observations the relationship between instantaneous left circumflex (LC) inflow and pressure showed a high correlation coefficient and was taken as linear over the range of pressure studied; extrapolation was frequently required in the determination of the pressure at which inflow ceased, i.e., the pressure-axis intercept or "zero flow" pressure (P~ = 0 ).The present studies were intended to define diastolic coronary pressure-flow relationships in settings in which LC diastolic inflow could be followed to zero during a single cardiac cycle, both with autoregulation intact and during sustained maximum vasodilation (carbocromen). Mean and phasic LC inflow and pressure were measured continuously with an electromagnetic flowmeter and downstream LC catheter in open-chest, heart-blocked dogs paced at 100 beats per minute. 66 prolonged postpacing diastoles in which LC inflow fell to zero were obtained in seven animals with stable systolic pressures of 100-125 mm Hg. Although instantaneous LC pressure and flow did show consistently high correlation coefficients during single diastoles (0.97 _ 0.01 [SD]), concavity to the flow axis developed at lower LC pressures and second-order equations gave statistically better fits than linear equations (p < 0.01) in 97 % of cases. Curvilinearity of the pressure-flow relationship was apparent in maximally vasodilated (n = 26) as well as autoregulating (n = 40) beds, indicating a role in the curvilinearity of factors not directly related to vascular smooth muscle. The pressure-axis intercept obtained from each second-990

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