Shoji Kojima

Changes in left ventricular diastolic function after left ventriculography: A comparison with iopamidol and urografin

Changes in left ventricular (LV) diastolic indices after left ventriculography (LVG) with iopamidol or urografin were studied in 42 subjects. Increase in heart rate and decrease in LV systolic pressure were more significant with urografin than with iopamidol (p less than 0.05 to 0.001). LV end-diastolic pressure was elevated more with urografin than with iopamidol (p less than 0.005 to 0.05) 1 to 3 minutes after LVG. LV peak negative dP/dt decreased significantly with urografin immediately (10 to 15 seconds, -511 and 30 seconds, -376 mm Hg/sec; p less than 0.0005 to 0.02), but with iopamidol it did not decrease significantly after LVG. Time constant, T, was elongated with iopamidol (10 to 15 seconds, +13 and 30 seconds, +6 msec; p less than 0.0005), but this elongation was significantly less than urografin (10 to 15 seconds, +34; 30 seconds, +25; 1 minute, +15; and 2 minutes, +10 msec; p less than 0.05 to 0.0005). We conclude that iopamidol disturbed LV diastolic function to a lesser degree than did urografin.

Examination of the Direct Effects of Nicorandil, Verapamil, Propranolol, and Nitroglycerin on the Hypoxic Canine Myocardium

Effects of intracoronary administration of verapamil (VER), nitroglycerin (TNG), propranolol (PRO), and nicorandil (NIC) on regional hypoxia were examined in 39 open-chest dogs. Distal left anterior descending coronary artery was perfused for 5 min with deoxygenated Krebs-Henseleit solution (KHS) in group 1 (n = 9), VER-containing (1.3 mg/dl) KHS in group 2 (n = 9), TNG-containing (0.5 mg/dl) KHS in group 3 (n = 7), PRO-containing (0.4 or 0.8 mg/dl) KHS in group 4 (n = 7), and NIC-containing (0.5 or 2.5 mg/dl) KHS in group 5 (n = 7). Transmural biopsy at 5 min revealed a less severe metabolic deterioration in the hypoxic myocardium in groups 2, 4, and 5, as evidenced by higher ATP content (2.99 ± 0.73, 2.81 ± 0.35, and 3.14 ± 1.20 μmol/g in groups 2,4, and 5, respectively) and lower lactate accumulation (5.16 ± 0.59, 5.62 ± 1.44, and 5.05 ± 1.12 μmol/g in groups 2, 4, and 5, respectively) compared with those in group 1 (2.09 ± 0.45 μmol/g in ATP and 8.77 ± 2.34 μmol/g in lactate). Metabolic preservation by VER, PRO, and NIC were not mediated by changes in hemodynamics and regional myocardial contraction. On the other hand, any significant protective effects were not noted in group 3, despite a significant reduction in rate-pressure products. Under an aerobic condition these agents affected regional myocardial contraction in a different manner from each other.

Comparative effects of intracoronary administration of propranolol with systemic administration on hypoxic canine myocardium

Myocardial protective effects of intracoronary administration of relatively small doses of propranolol were examined and compared with systemic administration in 20 open-chest dogs. In group 1 (n = 6) rate-pressure-product (R X P) did not change during 5-minute left anterior descending artery (LAD) perfusion with deoxygenated Krebs-Henseleit solutions (KHS). However, R X P decreased by the same degree in group 2 (n = 7), which received perfusion with KHS containing 0.4 or 0.8 mg/dl of propranolol, and in group 3 (n = 7) given LAD perfusion with original KHS and systemic administration of 0.02 to 0.04 mg/kg of propranolol. Total administered doses of propranolol were the same for groups 2 and 3. Transmural biopsy after 5 minutes of perfusion revealed less severe metabolic deterioration of hypoxic myocardium in group 2 when compared with that in group 1, as evidenced by higher ATP (adenosine triphosphate) (2.81 +/- 0.35 versus 2.23 +/- 0.45 mumol/g, p less than 0.05) and lower lactate content (5.62 +/- 1.44 versus 9.01 +/- 2.62 mumol/g, p less than 0.05). On the other hand, significant metabolic preservation was not noted in group 3. Sequential changes in regional myocardial contraction did not differ among the three groups. In conclusion, intracoronary administration of propranolol showed myocardial protective effects that were not mediated by the changes in hemodynamics and myocardial contraction.