Medical Journal of The Islamic Republic of Iran (MJIRI)
Iran University of Medical Sciences
Sat, Nov 23, 2024
[Archive]
Volume 17, Issue 4 (2-2004)
Med J Islam Repub Iran 2004 |
Back to browse issues page
Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
MOHAMMADI NAGHADEH M, MCGRATH J. VASODILATOR EFFECTS OF ACETYLCHOLINE IN AN EXPERIMEN TAL MODEL OF HEART FAILURE. Med J Islam Repub Iran 2004; 17 (4) :319-324
URL: http://mjiri.iums.ac.ir/article-1-669-en.html
URL: http://mjiri.iums.ac.ir/article-1-669-en.html
From the Department of Physiology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, I.R. Iran,
Abstract: (5280 Views)
The purpose of the work presented here was to investigate endotheliumdependent
relaxations in the rabbit coronary ligation model of heart failure. We
investigated endothelium-dependent relaxations at the level of larger vessels (thoracic
aorta and vena cava left renal artery and left renal vein lateral saphenous
artery and lateral saphenous vein and finally central ear artery and marginal ear
vein) in a model devised to mimic heart failure. The model presented here i s the
rabbit coronary ligation model in which myocardial infarction was produced in
male New Zealand white rabbits (2.6kg-3.0kg) by ligation of the marginal branch
of the left descending coronary artery. The development of chronic heart failure
was allowed to proceed over eight weeks. Animals were killed by overdose with
pentobarbitone sodium (i.v. injection). Arteries and veins were carefully removed
with as little connective tissue as possible and placed i n cold physiological salt
solution (PSS). The arterial and venous rings were mounted in 10mL isolated
organ baths, bathed in Krebs maintained at 37°C and gassed with 95% 02 plus 5%
CO2 , The rings were then placed under different resting tensions. Acetylcholine
(ACh) was chosen as endothelium-dependent vasodilator. After initial application
of tension, tissues were left to equilibrate for a 60 min period. Then all tissues
were precontracted with noradrenaline (1µM) nearly ten minutes before initial
application of vasodilator. This induced submaximal contraction in all vessels
with the exception of the ear vein. When the noradrenaline-induced contraction
reached a plateau, cumulative concentration-response curves (CCRC) to acetylcholine
were obtained by increasing the concentration in half-log increments. The
results led to two major conclusions with respect to the model. First, the relaxation
responses to acetylcholine were not impaired. Second, the results of our experiments in
this model of heart failure suggest that normal stimulation of endothelial NO is preserved
in peripheral conduit and capacitance vessels.
Type of Study: Original Research |
Subject:
Physiology
| Rights and permissions | |
 |
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License. |
