Isoproterenol-induced myocardial hypertrophy in rats is heterogeneous, which may explain divergent functional characteristics reported in this model.
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Requires caution interpreting isoproterenol rat hypertrophy studies; leaves open standardization of induction protocols.
The aim of the present study was to analyse the possible lack of uniformity in isoproterenol (ISO)-induced myocardial hypertrophy. 2. Data obtained for isovolumic hearts isolated from 20 rats treated with ISO (0.3 mg/kg over 8 days) were divided into two groups (H1, n = 10; H2, n = 10) according to the volume (mean+/-SD) needed to change left ventricle diastolic pressure from 0 to 40 mmHg (H1, 184+/-30 microL; H2, 108+/-14 microL). Eight control rats (C; 165+/-37 microL) were used for comparison. 3. In addition to ventricular distensibility differences, the groups differed in terms of myocardial mass (mean+/-SEM: H1, 181+/-3 mg > H2, 166+/-3 mg > C, 136+/-3 mg; P < 0.001), of relaxation constant (H2, 43+/-4 msec > H1, 28+/-2 msec; P = 0.0012) and of maximum developed circumferential stress (C, 145+/-9 kdyn/cm2 = H1, 137+/-6 kdyn/cm2 > H2, 110+/-4 kdyn/cm2; P = 0.002). 4. Our results show that ISO-induced myocardial hypertrophy is not homogeneous. Data obtained for H2, taken as a whole and compared with H1 (smaller myocardial mass and impairment of relaxation, elastic stiffness and force generation), suggest that, in some animals, myocardial necrosis and reparative fibrosis may prevail over the stimulus for myocyte growth. The lack of uniformity of ISO-induced myocardial hypertrophy has not been previously reported and may have contributed to the divergence observed in the literature regarding the functional characteristics of the present model.
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Murad et al. (2000) studied this question.
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