Objective: IGF-I possesses specific myocardial receptors and is able to promote cardiac remodelling and even inotropic effects in both humans and other animals. In fact, reduced cardiac mass and performance are present in GH deficiency and these alterations are counteracted by recombinant human (rh) GH replacement, restoring IGF-I levels. Recently, the acute administration of 60 mg/kg rhIGF-I has also been reported to be able to improve cardiac performance evaluated by echocardiography or

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... nce cardiography in normal subjects. The aim of our study was to verify the effects of a subcutaneous low dose of rhIGF-I (20 mg/kg) on cardiac performance in humans. Methods: In six healthy male adults (mean Ϯ S.E.M.: 35.7 Ϯ 4.3 years of age), the effects of rhIGF-I on left ventricular function evaluated by radionuclide angiocardiography and on circulating IGF-I, GH, insulin, glucose and catecholamines levels were studied. Results: Administration of rhIGF-I increased circulating IGF-I (peak at +150 min vs baseline: 330.2 Ϯ 9.6 vs 199.7 Ϯ 8.7 mg/l, P < 0.03) to levels which persisted similarly up to +180 min. Neither GH nor catecholamine levels were modified by rhIGF-I administration, while insulin and glucose levels showed a slight but significant decrease. Basal left ventricular ejection fraction (61.8 Ϯ 2.0%) significantly increased at +180 min after rhIGF-I (65.3 Ϯ 2.7%, P < 0.03). No change was recorded in mean blood pressure while a non-significant trend towards a reduction of heart rate was present by +120 min. Conclusions: These findings indicate that even subcutaneous administration of a low dose of rhIGF-I has acute inotropic effects as evaluated by radionuclide angiocardiography in healthy adults.