Contractile reserve but not tension is reduced in monocrotaline-induced right ventricular hypertrophy

Abstract

The objective of this study was to evaluate the role of right ventricular hypertrophy on developed tension (Fdev) and contractile reserve of rat papillary muscle by using a model of monocrotaline (Mct)-induced pulmonary hypertension. Calcium handling and the influence of bicarbonate ([Formula: see text]) were also addressed with the use of two different buffers ([Formula: see text] and HEPES). Wistar rats were injected with either Mct (40 mg/kg sc) or vehicle control (Con). Isometrically contracting right ventricular papillary muscles were studied at 80% of the length of maximal developed force. Contractile reserve (1 – Fdev/Fmax) was calculated from Fdev and maximal tension (Fmax). Calcium recirculation was determined with postextrasystolic potentiation. Both groups of muscles were superfused with either [Formula: see text] (Con-B and Mct-B, both n = 6) or HEPES (Con-H and Mct-H, both n = 6) buffer. With hypertrophy, contractions were slower but Fdev was not changed. However, Fmax was decreased ( P < 0.05). With [Formula: see text], Fmax decreased from 23.8 ± 6.5 mN·mm–2 in Con-B, to 13.7 ± 3.3 mN·mm–2 in Mct-B. With HEPES, it decreased from 16.3 ± 3.5 mN·mm–2 ( n = 6, Con-H) to 8.3 ± 1.6 mN·mm–2 (Mct-H). Contractile reserve during hypertrophy was therefore also decreased ( P < 0.05). With [Formula: see text], it decreased from 0.73 ± 0.03 (Con-B) to 0.55 ± 0.04 (Mct-B). With HEPES, it decreased ( P < 0.001) from 0.64 ± 0.07 (Con-H) to 0.19 ± 0.06 (Mct-H). The recirculation fraction decreased ( P < 0.05) from 0.59 ± 0.04 in Con-B to 0.44 ± 0.04 in Mct-B. We conclude that contractile reserve and recirculation fraction are impaired during hypertrophy, with a stronger effect under HEPES than [Formula: see text] superfusion.