Abstract: A method to treat the chronic stage of heart injury after ischemia or reperfusion by administering Midkine to a subject in need of such treatment is described.

Abstract: The object is to find a nitric oxide synthase activator, a method for the administration of the activator, and the amount of the activator to be administered. Disclosed is a nitric oxide synthase activator comprising a midkine family protein or a midkine derivative as an active ingredient. Specifically disclosed is a nitric oxide synthase activator which is intended to be administered through the blood, a coronary artery or a vein and which comprises a midkine family protein or a midkine derivative as an active ingredient.

Abstract: The object is to find a nitric oxide synthase activator, a method for the administration of the activator, and the amount of the activator to be administered. Disclosed is a nitric oxide synthase activator comprising a midkine family protein or a midkine derivative as an active ingredient. Specifically disclosed is a nitric oxide synthase activator which is intended to be administered through the blood, a coronary artery or a vein and which comprises a midkine family protein or a midkine derivative as an active ingredient.

Abstract: A study was made on the therapeutic effect of midkine on an occlusive peripheral vascular disease, and it was found that midkine has an activity of promoting neovascularization and that a blood vessel can be proliferated and the blood flow in the upper and lower limbs can be improved (in other words, the condition of an ischemic disease in the upper and lower limbs can be ameliorated) by introducing midkine into a site affected by the occlusive peripheral vascular disease.

Abstract: The present inventors compared myocardial damages after ischemia/reperfusion in wild-type mice and Midkine (MK)-deficient mice to confirm the effects and functions of MK. MK administration was found to significantly prevent cardiomyocyte apoptosis in both cultured cardiomyocytes (in vitro) and mouse models (in vivo).

Abstract: [PROBLEMS] To prevent ventricular fibrillation. [MEANS FOR SOLVING PROBLEMS] A rectangular base material (10) is sewn to the epicardium surface of a left ventricle (38). Four cooling Peltier elements (12) are provided at the center of the base material (10), and temperature-detecting thermistors (18) are provided at part of their peripheries. A plurality of circular, flat potential sensors/energizing electrodes (14) for detecting the surface potential of the heart are arranged in a lattice form on the surface of the base material (10) at almost equal intervals. The potential sensors/energizing electrodes (14) are energizing electrodes for delivering a pulse voltage/current to the heart. When a rapid ventricular rate is detected, these Peltier elements (12) are energized to cool the heart.