Abstract

B-type natriuretic peptide (BNP) and adiponectin play important role in the cardiovascular homeostasis regulation. We investigated BNP and adiponectin serum levels followed by isoproterenol (ISO) administration to rats and explored the relationship between them. Cardiac troponin I (cTnI) blood level was used as biochemical evidence of myocardial damage development. Adult male Wistar rats (average body weight 273.33 ± 21.63 g) were distributed into groups: control group received saline (n=6) and ISO groups (n=12) treated with ISO (subcutaneous single dose 100 mg/kg of rat body weight). ISO group was divided into two groups according to the time of BNP, adiponectin and cTnI determination: ISO I (n=6; 2 hours after ISO administration); ISO II (n=6; 4 hours after ISO administration). Blood for determination of parameters was taken from rat abdominal aorta. BNP, adiponectin and cTnI were determined by ELISA method. Data were statistically analysed by using SPSS version 13 computer program. P value less 0.05 was considered statistically significant. Blood BNP and adiponectin were lower at 2 hours after ISO administration in comparison with control group (p=0.004 for BNP and p=0.174 for adiponectin). Four hours after ISO administration, we have noted significant elevation of both parameters compared to ISO I group (p=0.004 for BNP; p=0.02 for adiponectin). Test of correlation have showed significant relation between their blood levels during experimental period (rho=0.577; p=0.01). BNP and adiponectin are not simple indicators of myocardial damage development. They have possible associated and additive effects in cardiovascular homeostasis regulation.

Highlights

  • It has not been established laboratory markers linking clinical and preclinical testing of heart functional disturbance followed by myocardial damage

  • The mean values of body weight, adiponectin, Cardiac isoform of troponin I (cTnI) and median B-type natriuretic peptide (BNP) values obtained in experiment were given in Table

  • Control group of rats were treated with saline and hours after that we noted circulated values of adiponectin . ± . ng/ml, BNP . ( . - . ) pg/ml and ng/ml for cTnI

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Summary

Introduction

It has not been established laboratory markers linking clinical and preclinical testing of heart functional disturbance followed by myocardial damage. Cardiac fibroblasts produce BNP but its circulated amounts are released from cardiac myocytes as main source [ ]. BNP is released into circulation after ischemia and necrosis of myocardial cells, systolic and diastolic dysfunction and increased wall stress of the left ventricle in acute myocardial infarction [ ]. Lower adiponectin blood level is connected to greater disease severity and poor outcome in acute coronary syndrome and congestive heart failure. Based on these facts, circulating adiponectin concentractions may represent both a protective or it should be harmful instead of harmuful signal [ ]. Cardiac isoform of troponin I (cTnI) is specific biochemical marker of cardiomyocytes damage but its blood elevation could not explain mechanism of cardiac damage [ ].

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