Heart failure (HF) is a multifactorial and progressive disease that
has been linked to activation of the renin-angiotensin and sympathetic
systems.
Carvedilol competitively blocks beta 1, beta 2 and alpha 1
receptors with potent antioxidant property, carvedilol has emerged as an
effective treatment modality for heart failure. Nevertheless, the
mechanism for improved cardiac function seen with f3-blocker treatment
remains largely unknown.
Valsartan is a potent and specific angiotensin II type I receptor
antagonist that has been proven to be an effective antihypertensive drug.
Valsartan has been claimed to posses prophylactic effect in cases of
myocardial infarction and heart failure.
In this study, cardioprotective effect of carvedilol (vasodilator beta
adrenoreceptor blocker and valsartan (ARBs) were studied in model of heart
failure induced by isoprenaline and in a model of acute myocardial
infarction induced by isoprenaline.
The main objective of the present study was to evaluate the
cardioprotective effect of chronic carvedilol treatment, vasodilator non
specific beta adrenoreceptor blocker versus valsartan specific angiotensin
II type I receptor antagonist on arterial blood pressure, heart rate, infarct
size assessed by triphenyltetrazolium chloride stain in heart failure
induced experimentally by isopemaline in rats.
The results of the present study showed that chronic carvedilol
treatment (1mg/kg) and valsartan (3mg/kg) by gastric gavage for four
weeks significantly decreased the arterial blood pressure and produced
insignificant decrease in heart rate in heart failure induced experimentally
by isoprenaline. And there was insignificant difference between both
drugs on blood pressure lowering effects or change in heart rate. |
