P410The impact of ischaemia reperfusion on aging rat heart physiological and molecular parameters

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Introduction: Heart muscle is largely dependent on uninterrupted blood flow, which guarantees delivery of substrates and washout of harmful products of metabolism. During aging, a lot of degenerative changes occur at the levels of all organs and heart is not an exception. Ischemia is a frequent phenomenon associated with aging and this means the decrease or cessation of myocardial blood flow, which leads to changes in myocardial metabolism The concept of "self regulation" is based on the axiom that the heart is a regulatory system, integrating many internal and external functional units. The aim of study: Was to point out how physiological parameters of cardiac contractility such as: H.R.(heart rate),C.F.(coronary flow),and LVPD(left ventricle developed pressure) are affected, by 45 minutes ischemia followed by 60 minutes reperfusion as well as to assess left ventricle for apoptosis.

Material and methods: Our study has been done on 12 female Wistar rats aged 6 and respectively 32 months old. The animals have been anesthetized i.p. with Na Phenobarbital (60mg/kg body weight) and Heparin(300 U i.p.).

After the abolishment of reflexes, hearts were excised and placed in ice cold perfusion medium and quickly mounted in Langendorff retrograde perfusion system. A 45 minutes ischemia by stopping perfusion fluid has been followed by 60 minutes reperfusion. Has been investigated the impact of oxidative stress generated by ischemia-reperfusion upon physiological parameters of rat heat of different ages respectively: C.F., H.R. and LVPD. Molecular modifications induced by the oxidative stress have been followed by pointing out DNA fragments detected by DNA laddering kit Cat.Nr.TA 4630 purchased from R&D Systems England.

Results: Our data have pointed out a constant decrease in cardiac frequency during experiment in both animal groups. In old rats H.R. presented net elevated values versus controls. LVPD presented lower values in old rats during experiment while C.F. has recorded higher values versus controls. Myocyte apoptosis from left ventricle has been pointed out on gel electrophoresis by DNA internucleosomal fragmentation.

Conclusions: Oxidative stress of ischemia-reperfusion generated modifications of H.R. in old rats and of C.F. which can be explained by adaptation of old heart rat to the new experimental conditions which at the molecular level have been reflected by appearance of apoptosis phenomenon in ventricular myocytes.

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