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Fumio Yamamoto
Hajime Ichikawa
Toshihiko Shibata
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Ann Thorac Surg 1991;52:927-933
© 1991 The Society of Thoracic Surgeons

Articles

Harmful effects of inotropic agents on myocardial protection

Hiroyoshi Komai, MD, Fumio Yamamoto, MD*, Kazuhiko Tanaka, MD, Hajime Ichikawa, MD, Toshihiko Shibata, MD, Akitomo Koide, MD, Takeki Ohashi, MD, Hiroshi Yamamoto, MD, Nobuyuki Nakashima, MD, Yasunaru Kawashima, MD

Department of Cardiovascular Surgery, National Cardiovascular Center, Suita, Japan

* Address reprint requests to Dr F. Yamamoto, Department of Cardiovascular Surgery, National Cardiovascular Center, 5-7-1 Fujishiro-dai, Suita 565, Osaka, Japan.

Using an isolated working rat heart model, the pretreatment effects of positive inotropic agents on ischemiareperfusion injury were investigated. The experiment consisted of (1) working control perfusion; (2) working perfusion with isoproterenol (I), milrinone (M), a combination of these drugs (I + M) and dibutyl-cyclic adenosine monophosphate (DB) followed by ischemic arrest for 33 minutes at 37 °C or 150 minutes at 20 °C and Langendorff reperfusion; and (3) working perfusion. Under conditions of normothermic ischemia, percent recoveries of postischemic cardiac output (mean ± standard error of the mean) in the I, M, I + M, and DB groups were 37.8% ± 12.7%, 61.3% ± 3.1%, 0%, and 53.1% ± 5.2%, respectively. Under conditions of hypothermic ischemia, the percent recoveries in I + M and DB groups were 10.9% ± 7.9% and 29.8% ± 9.5%; they were all significantly lower than that in the control group. The addition of diltiazem or ryanodine at several concentrations and lowering of the Ca2+ concentration in the St. Thomas' cardioplegic solution did not prevent I + M-induced injury. Our data suggest that pretreatment by I + M aggravated ischemia-reperfusion injury, and adjustments in Ca2+ concentration were not sufficient to prevent that injury.






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