1 Introduction

The disproportion of myocardial demand of oxygen supply directs to necrosis of heart muscle known as MI. The higher levels of hypercholesterolemia and hyperlipoproteinemia of low density lipoprotein cholesterol (LDL-C), lower levels of high density lipoprotein cholesterol (HDL-C) are the leading risk factors for MI (Khader et al., 2003). The stress in the heart muscle is induced by ISO which is catecholamine that leads to necrosis of myocardium (Sushamakumari et al., 1989). The blockage in the arteries along with cardiovascular diseases (CVD) is caused by ISO elevates lipoproteins and lipids specifically LDL-C seen in blood circulation (Goldstein and Brown, 1984). MI is caused due to the release of oxygen free radicals by ISO (Singal et al., 1982). These oxygen free radicals and oxidative stress jointly leads to atherosclerotic lesions generation by formation of oxidized LDL from LDL, which is the base cause of MI (Libby, 2003). The failure of heart, neurohumoral axes gets active, along with the sympathetic nervous system. Myocardial remodelling, prognosis (Elser et al., 1997) and cardiac dysfunction levels have an effect on sympathetic activity. The sympathetic and inflammatory activities may partially antagonized by beta blockers, affecting hypertrophy and cardiomyocyte apoptosis which leads to attenuated development of ventricular remodelling and raise in ejection fraction (Fringerio and Roubina, 2005). Some experimental studies have established on how the beta-blockers shows an effect in falling mortality rate among patients with failure of heart in different functional classes (Domanski et al., 2003), and with recommend guidelines that left ventricular (LV) systolic dysfunction of the patient shall be treated with beta-blockers (ACC/AHA, 2005). To control the high blood β1-adrenergic blocking agent is used which is BOP a cardiac selective (Albouaini et al., 2007). To minimise the multiple doses of antihypertensive drugs instead it can be used once in a day for a long half life. Generally BOP is well suitable, due to the β1-adrenergic selectivity receptor and acts as a substitute to non-selective and β-blocker drugs use to treat of hypertension induced zebeta. Report clearly mentioned this use alone or in combination/alone with another drugs to manage hypertension (Albouaini et al., 2007). The patients suffer with COPD (chronic obstructive pulmonary disease) is useful for selective receptors in patients. Clinical and hemodynamic status was improved by BOP therapy, and the heart failure of different etiologies, cardiac function in COPD patients, it includes Chagas’ disease, though, improvement of exercise capacity and is not done. Other studies mentioned BOP was safe and tolerated well in different etiologies, in cardiac patients. Another study from the placebo-controlled and tolerated the medication rate is 76.5% (CIBIS, 1994) which is not different from the other report. Medication in Chagas’ disease tolerates the dose up to 10 mg, the symptoms are improved and functions of ventricular comparison to other etiologies patients. BOP and Chagas’ disease is the first report to use and attention of possibility of myocardiopathy and interaction of BOP mechanism. Oxidative modifications in specific sites are identified Ca-ATPase expressed and calmodulin (CaM) in membrane sarcoplasmic reticulum, it arise oxidative stress response (Gao et al., 1998b; Viner et al., 1999). CaM is oxidized to their equivalent methionine sulfoxides, and biological aging methionine and loss of functions where as specific nitration of tyrosines in the Ca-ATPases and related sites. The oxidation of methionines and regulatory role in signaling of calcium coupling and calcium are two types of modifications post translation and CaM function and cellular redox conditions (Sun et al., 1999; Squier and Bigelow, 2000; Yermolaieva et al., 2000). The present study to investigate the ISO induced heart failure rats and BOP dose response in plasma lipid profile, cardio marker enzymes and involvement of CaM mechanism.

2 Experimental methodology

3 Results and discussion

Observed results that exposed in ISO treated rat leads to heart injury with significant increased change in the cardiac marker enzymes CK, LDH, AST and ALT. In ISO + BOP treated group IV results were nearly normal levels and BOP treated alone group also same when compared to controls rats in (Fig. 1). Blood glucose, serum urea, uric acid, creatinine in group II ISO treated rats has a significant increase and it showed a significant increase in the levels of these parameters. Plasma protein contents increase in experimental subjects of ISO, ISO + BOP rats but not BOP group III when compared to control group I (Fig. 2). Anandan et al. reported (2007) involvement of lipids plays important role in cardivalcular disease (CVD). Hypercholesterolaemia and hyperlipidaemia are the very important factors in cardiac risk and MI progress. ISO treated and MI includes elevated lipid levels are circulatory. Our reports, ISO treated rat’s shows increase levels of TGs, Total cholesterol significantly in plasma levels with increase free fatty acids (Fig. 3). Cardiovascular disturbances and MI is the primary risk factors to increased level of TGs (Sushama Kumari et al., 1990). Increased levels significant in plasma phospholipids of ISO treated rats and ISO + BOP treated rats were clearly observed that the levels are decreased near to normal control range which might be appropriate to the decrease of hypolipidemic and hypocholesterolaemic activities in present reports are supported to previous results (Anandan et al., 2007). ISO create hypoxia or relative ischemia with the effect of coronary hyperactivity in myocardium and hypotension in heart (Bloom and Davis, 1991), the overload of cytosolic Ca2+ induces myocardial ischemia in ISO group (Singal et al., 1983). The level of glucose in blood increased while comparing with the controls. The difference increase may be appropriate to the improved lipolysis and glycogenolysis, with the start of phosphorylase kinase enzyme and β-adrenergic receptor. On testing enzymes in the heart tissue is at a low level and microscopic myocardial necrosis and gross is produced by ISO treated rats. Though there are many beneficial effects and drugs are well standardized model studies to cardiac functions in clinical and mimics of MI due to ischemia in rats induces ISO (Harada et al., 1993). In CVD lipids are major role played by not only development of atherosclerosis and hyperlipidaemia, and modification of cell composition and stability of structure of cell membranes (Rajadhurai and Prince, 2005). Increased lipid values in plasma that are administrated rats with ISO. The ISO treated rat’s shows increase in plasma triglycerides and cholesterol this might be due to increase in adenosine monophosphate in cardiac cycle followed by biosynthesis of lipids (Paritha and Devi, 1997). The key role of eukaryotic cells in deciphering the signalling of Ca2+ is due to the CaM that acts as primary indicator of intracellular calcium (Ca2+). Being the secondary messenger, the CaM interacts/reacts with large number of proteins which is not unusual (Fig. 4). Every lobe is exposed with hydrophobic patches this firm changes are due to the binding of CaM and it helps to bind hydrophobic anchor residues in large that is present in canonical Ca2+ loaded CaM (CaCaM) which is a target binding sequences. The channels NaV1.5 are huge, consisting subunit (a) pore-forming (∼220 kDa) and subunit (b) one of four auxiliary (b1–4, 30–35 kDa) in heterooligomeric assemblies which involve in function and channel trafficking. The cytosolic subunit (b) joins as the linker region in connecting DI and DII, adapt CaV1.2 voltage dependent activation and inactivation in ISO + BOP administrated rats (Yamniuk and Vogel, 2004; Bodi et al., 2005; Nerbonne and Kass, 2005; Abriel, 2010; Catterall, 2011).

Close

Fig. 1

Effect of isoproterenol and bisoprolol administration on cardiac marker enzymes. Values are expressed as Mean ± SEM, on each bar followed by the same symbol are not significantly different (P ≤ 0.05) from each other according to Duncan’s Multiple Range (DMR) test, n = 8, Control = Control rats.

Export to PPT

Close

Fig. 2

Effect of isoproterenol and bisoprolol administration on plasma components Values are expressed as Mean ± SEM, on each figure/bar followed by the same symbol are not significantly different (P ≤ 0.05) from each other according to Duncan’s Multiple Range (DMR) test, n = 8, Controls = Control rats.

Export to PPT

Close

Fig. 3

Effect of isoproterenol and bisoprolol administration on plasma lipid profile. Values are expressed as Mean ± SEM, on each bar followed by the same symbol are not significantly different (P ≤ 0.05) from each other according to Duncan’s Multiple Range (DMR) test, n = 8, Controls = Control rats.

Export to PPT

Close

Fig. 4

3D structure of Ca2+ bound calmodulin (PBD:1OSA).

Export to PPT

4 Conclusion

Rats were administered BOP parameters were close to control rats. Reports clearly stated that ISO treated rat tissue of heart damage was reduced when compared to treated ISO + BOP rats. The models were treated with ISO + BOP to defend against hyperlipidaemia and tissue of cardiac damage followed by MI. Hence, to investigate biochemical BOP mechanism against MI risk in rats. More in strength studies are needed to interact of BOP and ISO treated experimental animals.

5 Statistical investigation

The consequences are states that mean ± SEM. (DMR) impact was set at (P ≤ 0.05).