Przejdź do zawartości
Merck

Adrenocorticotrope hormone fragment (4-10) attenuates the ischemia/reperfusion-induced cardiac injury in isolated rat hearts.

Antioxidants & redox signaling (2007-08-25)
Bela Juhasz, Peter Der, Peter Szodoray, Rudolf Gesztelyi, Istvan Lekli, Istvan Bak, Miklos Antal, Nilanjana Maulik, Arpad Tosaki, Miklos Vecsernyes
ABSTRAKT

The aim of our study was to investigate the contribution of the adrenocorticotropic hormone fragment, ACTH (4-10), on the recovery of postischemic cardiac function. Effects of ACTH (4-10) on caspase-3 activity, cardiomyocyte and endothelial apoptosis, and HO-1 protein expression were studied. Rats were treated with various doses of ACTH (4-10), and then 12 h later, anesthetized, hearts were isolated, perfused, and subjected to 30-min ischemia followed by 120-min reperfusion. Cardiac function including heart rate, coronary flow, aortic flow, and left ventricular developed pressure were recorded. After 120-min reperfusion, 200 mug/kg of ACTH (4-10) significantly improved the recovery of aortic flow, coronary flow, and left ventricular developed pressure from their untreated control values of 15.3 +/- 0.9 ml/min, 6.5 +/- 0.9 ml/min, and 10 +/- 0.6 kPa to 20.7 +/- 1.3 ml/min, 24.8 +/- 1.8 ml/min and 13.7 +/- 0.7 kPa, respectively. Heart rate did not show significant changes during reperfusion. ACTH (4-10) treatment resulted in a reduction in infarct size, caspase 3 activity, apoptosis, and an increase in HO-1 expression. When ACTH (4-10) was given at the moment of reperfusion, the drug failed to improve the postischemic recovery of the myocardium. Thus, ACTH (4-10) can be a useful tool for the prevention of the development of ischemia/reperfusion-induced injury.