Tetsuo Ohya

Effects of isoflurane and fentanyl on ischemic myocardium in dogs: Assessment by end-systolic measurements

The effect of anesthetics on ischemic myocardium to which blood was supplied by a stenotic coronary artery was investigated in dogs. The ischemia was assessed by regional wall motion (ultrasonic dimension technique) using fractional shortening (FS) [(EDL - ESL)/EDL x 100] and end-systolic pressure-segment length relationships (ESPLR). The latter is considered to be a more load-independent measure of regional myocardial function. Isoflurane and fentanyl were chosen as anesthetics of current interest. On reducing the left circumflex coronary artery (LCX) flow to approximately 50% of its resting value, a decrease in FS and a rightward shift in ESPLR were observed in myocardium perfused by the LCX. Simultaneously, increases in FS were observed in the nonischemic area perfused by the left anterior descending coronary artery (LAD), which was most likely due to the intraventricular unloading effect. No significant changes of ESPLR were observed in the area supplied by LAD. Isoflurane induced a dose-dependent decrease in FS and a rightward shift in ESPLR in the ischemic myocardial segment, whereas fentanyl caused an increase in FS and tended to shift ESPLR leftward in the same area. The results suggest that isoflurane may have deleterious effects on preexisting myocardial ischemia, whereas fentanyl may not when loading conditions are taken into consideration. Fractional shortening and ESPLR seem to provide similar information about regional myocardial function.

Discrepancy Between Slow Relaxation and Increased Myocardial Stiffness

The time constant of left ventricular pressure fall (TB, P = P0 + A. e-t /TB) is a good indicator of myocardial relaxation, but the physiological nature of the asymptote (P0) is not yet clear. The effects of hypoxia and the combined effects of hypoxia and DPI 201-106 (DPI, 10-6 M and 3 × 10-6 M), a new cardiotonic agent which increases the sensitivity of contractile elements to Ca2+, on diastolic myocardial function in isolated isovolumic rabbit hearts were investigated. There were close correlations between the change in left ventricular end-diastolic pressure (⊿A LVEDP) and ⊿P0 (r = 0.98, P < 0.01) and between ⊿TB and ⊿LVEDP (r = 0.73, P < 0.01) following hypoxia. The combination of hypoxia and DPI induced further increments in LVEDP (25 ± 8 mmHg, P < 0.05 vs hypoxia) and P0 (15 ± 7 mmHg, P < 0.05), and still there was a close linear correlation between ⊿LVEDP and ⊿P0 (y = 1.08x + 1.5, r = 0.90, P < 0.05). However, TB(52 ± 12 ms) was not altered and no relationship was observed between ⊿TB and ⊿LVEDP.