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ABSTRACTThis present study was carried out to investigate the effect of Magnesium adaptation on Platelets to Lymphocytes ratio in acute myocardial infarction and oxidative stress. A total of 16 adult New Zealand rabbits of both sexes with average weight between 1.7-2.8kg were commercially obtained randomly and grouped into two (2) groups. The animals were allowed to acclimatize for two (2) weeks before the commencement of the experiment. The rabbits were randomly divided into two experimental groups of 8 rabbits each. Group one was fed with normal rabbit pellets and water ad libitum. Group 2 was fed with normal rabbit pellets and high magnesium (4.8mM)/day for 16 weeks (Magnesium adapted rabbits). At the end of the 16th weeks, each group was divided into 2 sub-groups (N=4) control and test (myocardial infarction (MI) + oxidative stress (OS) induction) through subcutaneous administration of adrenaline hydrochloride at a single dose of 1mg/kg/ on two consecutive days with an interval of 24 hours between applications and at the end of the 2nd day, oxidative stress was induced using carbon tetrachloride(CCL4) in a single dose of 1ml/kg/bd wt. Twenty-four hours after the induction of oxidative stress, each animal was anesthetized using chloroform vapour and 5ml of blood sample collected via cardiac puncture for analyses. The blood collected was allowed to clot and then centrifuged at 3000rpm for 3min. The serum was then collected with the aid of a Pasteur pipette in plain sample bottles and kept in the freezer till analysis. It was showed from my result that magnesium adaptation decreased the level of platelets-to-lymphocytes ratio in magnesium adapted rabbits induced with myocardial infarction and oxidative stress. This study showed that magnesium adaptation on platelets-to-lymphocytes ratio in acute myocardial infarction and oxidative stress significantly (p<0.05) prevented elevated levels of Troponin I, Creatinine Kinase and Malondialdehyde. This shows that magnesium adaptation serves as a protective measure against myocardial infarction and oxidative stress on platelets and lymphocytes.
