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

@entity235 @entity1406 @entity64 @entity432
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 @entity235 . 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 @entity235 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 @entity1406 . 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 @entity235 , a right heart bypass was performed to study the influence of @entity64 volume on the ESPVR by applying a pressure intervention under three conditions: with constant end-diastolic volume (decreasing @entity64 volume), Ees = 2.27 +/- 0.79 kPa/ml; with constant @entity64 volume, Ees = 1.59 +/- 0.51 kPa/ml; and with increasing @entity64 volume (and increasing end-diastolic volume), Ees = 1.36 +/- 0.49 kPa/ml. Analysis of variance revealed a statistically significant relation between Ees and @entity64 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 @entity432 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.
