The responses of left ventricular end‐systolic pressure‐diameter relationship to acute pressure overload induced by aortic constriction

The aim was to investigate the responses of the left ventricular (LV) end-systolic pressure-diameter relationship (ESPDR) to acute pressure overload. ESPDRs were made by 2-min ascending and descending aortic constrictions before and after administration of propranolol and atropine sulphate (both 0.2 mg kg-1 i.v.) in eight open-chest dogs with the pericardium preserved. LV anterior-posterior diameter was measured with ultrasonic crystals. In the ascending aortic constriction, end-diastolic pressure (EDP) and end-diastolic diameter (EDD) were unchanged and ESPDR shifted to the left. In the descending aortic constriction, EDP and EDD increased from 6.8 +/- 0.7 to 8.8 +/- 0.9 mmHg (P < 0.01) and from 32.7 +/- 1.4 to 34.5 +/- 1.6 mm (P < 0.05) and ESPDR shifted to the right. After administration of propranolol and atropine sulphate, cases having smaller changes in EDD during 2 min constriction (0.3 +/- 0.3 mm in all cases of ascending, 0.3 +/- 0.2 mm in four cases of descending aorta) showed a leftward shift of ESPDR. The remaining four cases of descending aortic constriction with larger changes in EDD (1.8 +/- 0.8 mm, P < 0.05) showed a rightward shift of ESPDR. An inverse curvilinear correlation was found between percentage changes in EDD and in the slopes. These results suggest that the responses in ESPDR to acute pressure overload were determined by not only changes in the contractile state but also the interplay between adaptation to acute pressure overload (the Anrep effect) and pre-load.