**Acknowledgements**

*Apolipoproteins, Triglycerides and Cholesterol*

of the healthy volunteers. Also, there is greater decrease in ZP values of patients with Hypertension suffering from MI indicate the exacerbation in RBC deformity in patients. This may be due to hypertension induced complications. Higher ZP in treated patients indicates the increased stability of erythrocytes due to reduced

*Comparison between mean ZP values of normal volunteers, patients with hypertension and myocardial* 

*infarction patient and myocardial infarction patients on treatment.*

The exact mechanism of development of CVD is complex and is not yet fully understood. But from the literature survey it was clear that ROS plays an important role in the progression and development of CVD. Also, it was known that there is a strong relation between ROS and the pathophysiology of CVD. From the present research work it can be concluded that due ROS in Patients with Hypertension the erythrocytes are affected, their membrane gets oxidized resulting in various types of morphological deformity (Anisocytosis). Also, membrane potential (ZP) which is a characteristic property of RBC responsible for free flowing of RBC in the blood stream without aggregation, get affected. These conditions get exacerbated in erythrocytes of patients suffering from myocardial infarction. Development of membrane deformity directly reduces the membrane potential of RBC. Due to oxidation of RBC membrane by ROS, the membrane becomes fragile and therefore the fragility of erythrocytes increases in Patients with Hypertension and MI compared

Results obtained in our lab suggest that variations in erythrocyte morphology, zeta potential, lipid peroxidation and erythrocyte Fragility can act as a key indicator to determine the risk factor of myocardial infarction in hypertensive patients. In the present study, we have developed a greater understanding of effect of ROS on morphology of RBCs, effect on its membrane potential (ZP) due to deformity in the membrane and its erythrocyte fragility. This could be a new way to realize a better treatment in hypertensive patients and a prevention of cardiovascular complications (i.e.: myocardial infarction, TIA, etc.). However, more works in the near future are necessary to improve the detection and treatment of the ROS

**100**

oxidative stress.

**Figure 4.**

**4. Conclusion**

to healthy volunteers.

mediated dysfunction.

We are grateful to Dr. Varma Pathology Laboratory, Platina heart hospital, Nagpur and healthy voluntary donors of the Department of Pharmaceutical Sciences, Nagpur University, Nagpur.
