Relation between left ventricular systolic resistance and contractile rate processes.
To test the hypothesis that left ventricular (LV) systolic resistance is determined by the intrinsic rate processes of the contractile system, we studied 40 spontaneously hypertensive male rats (SHR). Thyroid hormone manipulation was used to alter isomyosin composition and consequently the rate processes of the contractile system. Seven groups of rats were studied: control (SHRC, n = 9); propylthiouracil (PTU) treated for 10 days (SHRP-10, n = 5), 20 days (SHRP-20, n = 5), and 30 days (SHRP-30, n = 6); and thyroxine treated for 5 days (SHRT-05, n = 5), 10 days (SHRT-10, n = 5), and 15 days (SHRT-15, n = 5). In situ (n = 40) and isolated (n = 14; 5 SHRP-30, 5 SHRC, and 4 SHRT-15) heart experiments were performed. In comparison to SHRC, we observed the following: 1) LV pump performance was not different in any of the thyroxine-treated groups, whereas with PTU, pump performance was significantly depressed in rats with greater than 80% slow myosin. 2) Normalized LV peak elastance (Emaxn) was significantly increased in the SHRP-30, whereas it was not altered after thyroxine. These observations were further confirmed in the isolated heart on the basis of peak isovolumetric stress-strain relations. 3) Thyroxine increased and PTU decreased theoretical maximum flow (Qmax; a measure of LV resistance); thus an inverse relation between Qmax and percent slow myosin was observed (r2 = 0.86). 4) The time to peak isovolumetric pressure was increased in SHRP-30 and decreased in SHRT-15. The relaxation process was significantly slower for SHRP-30 group and was unchanged for SHRT-15 group. These observations support our hypothesis that LV systolic resistance quantifies an intrinsic rate-dependent property of the myocardium and that isomyosin composition is one of its determinants. In addition, with changes in isomyosin composition toward predominantly slow myosin, the responses in Emaxn and Qmax are discordant, which may be responsible for the preservation of pump performance. This underscores the importance of quantifying both LV systolic resistance and elastance in the assessment of the functional status of the LV as a mechanical pump.
Shroff
S G
SG
Cardiovascular Institute, Michael Reese Hospital and Medical Center, University of Chicago Pritzker School of Medicine, Illinois 60616.
Naegelen
D
D
Clark
W A
WA
D000818:Animals; D001794:Blood Pressure; D001810:Blood Volume; D003971:Diastole; D004548:Elasticity; D006321:Heart / Q000033:anatomy & histology / Q000502:physiology*; D006352:Heart Ventricles; D006439:Hemodynamics; D066298:In Vitro Techniques; D007527:Isoenzymes / Q000378:metabolism; D008297:Male; D009200:Myocardial Contraction; D009206:Myocardium / Q000201:enzymology; D009218:Myosins / Q000378:metabolism; D009929:Organ Size; D051381:Rats; D011918:Rats, Inbred SHR; D013314:Stress, Mechanical; D013599:Systole
D007527:Isoenzymes; D009218:Myosins