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Experimental Physiology 90.4 pp 635-644
DOI: 10.1113/expphysiol.2005.030460
© The Physiological Society 2005
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Detrimental effects after dobutamine infusion on rat left ventricular function: mechanical work and energetics

Chikako Nakajima-Takenaka1, Susumu Sakata1, Satoshi Kato12, Yoshimi Ohga1, Ken-ya Murata3, Shigeki Taniguchi2 and Miyako Takaki1

Departments of 1 Physiology II2 Thoracic-Cardiovascular Surgery, Nara Medical University School of Medicine, Kashihara, Nara 634-8521, Japan 3 Department of Neurology and Neurosurgery, Kanazawa Medical University, Kahoku-gun, Ishikawa 920-0293, Japan

We have previously reported that continuous infusion of dobutamine into the coronary artery induces positive inotropic effects but induces no detrimental effects in cross-circulated, excised normal rat hearts and even in Ca2+ overload-induced contractile failing rat hearts. However, we hypothesized that some detrimental effects on left ventricular (LV) function are induced after continuous dobutamine infusion and the following clearance of blood dobutamine, as is the case after ß-adrenergic receptor stimulation. To test this hypothesis, we investigated LV mechanical work and energetics in the same type of preparations that underwent continuous dobutamine infusion and clearance of blood dobutamine. We found that both mean end-systolic pressure and systolic pressure–volume area (PVA; a measure of total mechanical energy per beat) at midrange LV volume were significantly (P < 0.01) decreased. The mean myocardial oxygen consumption per beat {eph_154_mu1} intercept, which is composed of {eph_154_mu2} for the total Ca2+ handling in excitation–contraction coupling and basal metabolism, of the {eph_154_mu3} and PVA linear relation was also significantly (P < 0.05) decreased (n = 8). The mean slope of the linear relation was unchanged in such hearts. Post-dobutamine basal metabolism was unchanged (n = 5 of the 8 hearts). The moderate proteolysis of a cytoskeleton protein, {alpha}-fodrin was identified (n = 7 of the 8 hearts with the decreased {eph_154_mu4} intercept), after clearance of blood dobutamine. In agreement with our hypothesis, the detrimental effect of the post-ß-adrenergic receptor stimulation was induced by a moderate concentration of dobutamine; we found systolic dysfunction due to the impairment of Ca2+ handling in excitation–contraction coupling in the rat LV and proteolysis of a cytoskeleton protein, {alpha}-fodrin.

(Received 9 March 2005; accepted after revision 18 April 2005; first published online 22 April 2005)
Corresponding author M. Takaki: Department of Physiology II, Nara Medical University School of Medicine, 840 Shijo-cho, Kashihara, Nara 634-8521, Japan.  Email: mtakaki{at}naramed-u.ac.jp






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