Hyperdynamic circulatory response to iron deficiency, thalassaemia and sickle cell a anaemias

ABSTRACT

One of the most interesting areas of research in erythrocyte physiology is the interaction of haemoglobin with nitric oxide [NO]. These two molecules independently fulfill diverse and complex physiological roles, while together they delicately modulate microvascular perfusion in response to second-by-second changes in local metabolic demand, contributing to hypoxic vasodilatation. To highlight on pathophysiological mechanisms of hyperdynamic state in anemic patients as well as to investigate the relation between haemoglobin, NO, endothelin-1 [ET-1], cyclic guanosine monophosphate [c GMP] and endotoxins with hyperdynamic circulatory states in different anaemic patients. Forty five anaemic patients categorized in three groups each fifteen [Iron Deficiency Anaemic, Thalassaemic and Sickle Cell Anaemic patients] in addition to ten healthy controls. Pulse rate, systolic and diastolic blood pressure values were recorded for all subjects. Also, Haemoglobin types and level, serum iron and TIBC, NO, ET-1, c GMP and Endotoxin levels were measured for all. Significant increase in pulse rate and pressure, decrease in diastolic pressure in addition to elevation of NO, cGMP and Endotoxins whereas ET-1 significantly decline in all anemic patients. NO levels when correlated with Hb, ET-1 levels and diastolic blood pressure showed negative significant correlation, while. It was positively correlated with c GMP, Endotoxins, systolic blood pressure and pulse pressure in different anemic groups. Vasodilatation, the main cause of hyperdynamic accompanying anemia contributed to increase NO levels joint with reduction of ET-1 which mediated through c GMP pathway. Besides, en do endotoxemia may have some role in amplifying of NO production