Sensitivity of left ventricular end-systolic pressure-volume relation to type of loading intervention in dogs

The influence of different types of loading intervention on the resulting end-systolic pressure-volume relation (ESPVR) of the left ventricle in situ was investigated in anesthetized open-chest dogs. Left ventricular volume was measured by conductance catheter and pressure was measured by tip-micromanometer. Two loading interventions were applied: a pressure intervention (INp) by gradually occluding the descending aorta and a volume intervention (INv) by rapidly infusing 180 ml blood into the vena cava. The pressure-volume loops during an intervention always showed a linear ESPVR, the slope of which, Ees, was calculated. Possible method-related artifacts were assessed and could be excluded. Results from 16 dogs show that Ees(INp) was always larger (1.37 +/- 0.45 kPa/ml) than Ees(INv) (0.73 +/- 0.32 kPa/ml) (p less than 0.001). This difference was enhanced by beta-blockade through metoprolol. The same phenomenon was found for the slope (SdPV) of the relation between dP/dtmax and end-diastolic volume: SdPV(INp) = 45.17 +/- 22.63 kPa/ml/sec and SdPV(INv) = 20.55 +/- 11.13 kPa/ml/sec. In seven dogs, a right heart bypass was performed to study the influence of stroke volume on the ESPVR by applying a pressure intervention under three conditions: with constant end-diastolic volume (decreasing stroke volume), Ees = 2.27 +/- 0.79 kPa/ml; with constant stroke volume, Ees = 1.59 +/- 0.51 kPa/ml; and with increasing stroke volume (and increasing end-diastolic volume), Ees = 1.36 +/- 0.49 kPa/ml. Analysis of variance revealed a statistically significant relation between Ees and stroke volume (p less than 0.01). From the right heart bypass experiments, we conclude that shortening-related deactivation plays a role in the observed behavior of the ESPVR. However, the results from the series with intact circulation indicate that aortic occlusion has an additional effect on the slope of the ESPVR, leading to increased myocardial inotropism, perhaps mediated through a peripheral stimulus in response to decreased perfusion.