Key points are not available for this paper at this time.
Isovolumetrically contracting left ventricle of the anesthetized dog was used to evaluate the end-diastolic pressure-volume relationship LVEDP (P)-LVEDV (V) relationship (curve) following changes in heart rate, ischemia and administration of beta-adrenergic blocking drug. At the same time, relaxation indices were also obtained. Initial left ventricular volume (14.8 ± 7.6 ml, mean ± SD, n = 11) was set at the end-diastolic pressure of 2.0 ± 0.7 mmHg. Comparison of each parameters after intervention was done when each initial left ventricular volume was increased by 10 ml. With increase in heart rate, LVEDP increased significantly from 5.1 ± 2.1 to 14.0 ± 2.2 mmHg (at 160 bpm, p<0.02, vs 100 bpm) and to 24.0 ± 1.0 mmHg (at 180 bpm, p < 0.001, vs 100 bpm). Regional ischemia also increased LVEDP significantly from 6.4 ± 1.4 to 12.8 ± 4.1 mmHg (after 30 min, p < 0.01, vs control) and to 14.1 ± 4.7 mmHg (after 45 min, p < 0.01, vs control). However, global ischemia produced by decreasing coronary perfusion pressure to 50 mmHg, or administration of propranolol (1.0/kg) brought about no significant changes in LVEDP. Among the relaxation indices, peak negative dP/dt decreased significantly following global ischemia, regional ischemia and administration of propranolol (from 1101 < 131 to 733 < 49 mmHg/sec, p < 0.01 ; from 888 425 to 268 94 mmHg/sec after 45 min, p < 0.01 and from 562 160 to 291 100 mmHg/sec, p<0.01, respectively). On the other hand, time constant (T) of the left ventricular pressure fall was prolonged significantly following regional ischemin from 44.7 5.2 to 72.0 8.6 msec (after 30 min, p < 0.001 ) and 95.4 26.0 msec (after 45 min, p < 0.01 ). Therefore, it is concluded that LV diastolic compliance decreases by tachycardia (160 and 180 bpm) and regional ischemia, while the changes of the relaxation indices were not necessarily parallel to those of the LV compliance.
Sakamoto et al. (Fri,) studied this question.