EFFECTS OF ANGIOTENSIN-CONVERTING ENZYME-INHIBITION ON CROSSBRIDGE PROPERTIES OF DIAPHRAGM IN CARDIOMYOPATHIC HAMSTERS OF THE DILATED BIO-53-58 STRAIN

Crossbridge properties of cardiomyopathic Syrian hamster (CSH) diaphra gm from the dilated Bio 53-58 strain were analyzed after 5-mo of treat ment with the angiotension converting enzyme (ACE) inhibitor perindopr il (1 mg/kg/d by oral gavage). Three groups were studied: control F1B hamsters (C; n = 14); CSH given placebo (PL; n = 11); and perindopril- treated CSH (PE; n = 11). Peak isometric tension was lower in PL than in C, in both twitch (21.4 +/- 1.5 versus 46.9 +/- 1.5 mN/mm(2); p < 0 .001) and tetanus (41.0 +/- 2.7 versus 90.5 +/- 3.3 mN/mm(2); p < 0.00 1). In PE, peak isometric tension was intermediate between C and PL, a nd was significantly lower than in C and higher than in PL. The single force of one crossbridge (II), the number (m) of crossbridges, the tu rnover rate of myosin adenosine triphosphatase (ATPase) (k(cat)), and peak mechanical efficiency (Effmax) were calculated from A.F. Huxley's equations; m was lower in PL than in C in both twitch (3.4 +/- 0.2 ve rsus 4.9 +/- 0.2 10(9)/mm(2); p < 0.001) and tetanus (4.0 +/- 0.3 vers us 8.9 +/- 0.7 10(9)/mm(2); p < 0.001); m was higher in PE than in Pk, in both twitch 4.3 +/- 0.5 versus 3.4 +/- 0.2 10(9)/mm(2); NS) and te tanus (6.2 +/- 0.4 versus 4.0 +/- 0.3 10(9)/mm(2); p < 0.01), with no change in Pi. In the three groups, Effmax correlated linearly with k(c at) (r = 0.93; p = 0.001) and showed a negative linear correlation wit h Pi (r = 0.996; p = 0.001). In conclusion, our results show that in e xperimental cardiomyopathy, ACE inhibitor mainly helps to prevent a de crease in the number of diaphragm muscle crossbridges, resulting in pr eserved peak isometric tension.