Volume 13, Issue 4 (2-2000)                   Med J Islam Repub Iran 2000 | Back to browse issues page

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MOHAMMADI NAGHADEH M, McGRATH J. VASODILATOR EFFECTS OF THE β -AGONIST ISOPRENALINE IN AN EXPERIMENTAL MODEL OF HEART FAILURE. Med J Islam Repub Iran. 2000; 13 (4) :283-286
URL: http://mjiri.iums.ac.ir/article-1-923-en.html
From the Department of Physiology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, I.R.lran
Abstract:   (2366 Views)
Heart failure is a clinical syndrome characterized by the inability of the heart to provide nutrient supply to tissues. In 75% of cases, the underlying pathology causing heart failure in patients with cardiac death is coronary heart disease. A rabbit model of heart failure with coronary ligation was produced to mimic coronary heart disease in humans. After producing the model, two arteries and two veins were investigated in the two groups (control and with coronary ligation). Arteries and veins were cut as rings and bathed in Krebs solution maintained at 37 DC, and gassed with 95% oxygen and 5% CO 2 , Then all tissues were placed under different resting tensions and allowed to equilibrate for 1 hour. Then all the tissues were contracted with U -46619 (0.1 µM) nearly ten minutes before initial application of isoprenaline. When the U -46619 (0.1 µM)-induced contraction reached a plateau, concentration-response curves to isoprenaline were obtained. Isoprenaline was chosen as a vasodilator, it's effect resulting from stimulating beta receptors in blood vessels. Isoprenaline induced relaxation in all tissues, but the renal artery was the most sensitive and showed maximum relaxation.20-26 Compared to acetylcholine, relaxation responses were small and maximum responses observed in the vena cava, aorta and renal vein were only 10 percent. In all tissues, relaxation responses to the vasodilator agent isoprenaline showed no significant difference between control and coronary ligated rabbits 8 weeks after operation.
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