According to medical studies, diabetic patients mostly die due to acute stroke than their disease. It is found out that diabetes mellitus is an independent predictor of the incidence of ischemic stroke that caused by many factors. However, between 20% and 40% of patients admitted with ischemic stroke are hyperglycemic. Although there is compelling evidence that hyperglycemia has an effect on stroke outcome. This condition is mostly prevalent during various pathophysiological conditions on the cardiovascular regulatory system and vasculature. In this connection, stroke volume was assessed from the non-invasive blood pressure signal by the arterial pulse contour method. Counter-regulation during hyperinsulinaemic hypoglycemia involves selective adrenomedullary sympathetic activation, and does not influence cardiac parasympathetic regulation or bar reflex control of heart rate. Usually, the autonomic deregulation is somewhat involved in metabolic and cardiovascular complications associated with hypoglycemia. The current exploratory study was conducted to be able to investigate both the sympathetic and parasympathetic regulatory responses to acute hyperinsulinaemia and hypoglycemia in healthy subjects by assessing changes in plasma catecholamine concentrations as markers of sympathetic hormonal regulation. Furthermore, heart rate variability (HRV) as a marker of cardiac parasympathetic regulation, blood pressure variability (BPV) as a marker of sympathetic vasomotor regulation, bar reflex sensitivity (BRS) as a marker of parasympathetic reflex control of heart rate, and haemodynamics during euglycaemic and hypoglycemic hyperinsulinaemic. Recent medical study shows that the degree of insulin resistance is being evaluated by the use of euglycaemic hyperinsulinaemic clamp technique.

(http://www.clinsci.org/cs/105/0315/cs1050315.htm)

Moreover, catecholamine stimulate glycogenolysis and gluneogenesis. However, it also controls the rate of glucose delivery by modulating vascular tone and blood flow. It therefore has the ability to mediate on the metabolic and the haemodynamic responses to hypoglycemia. And, because muscle sympathetic nerve activity to the heart or blood vessels is not measured, the tendency is the sympathetic activation of the cardiovascular organs cannot be evaluated. Though, plasma concentration of noradrenaline is a compromised indicator of general sympathetic activity, one might expect a more pronounced response of its concentration to hyperinsulinaemic hypoglycemia, in line with the response of adrenaline, unless the sympathetic response to hyperinsulinaemia and hypoglycemia is non-uniform. Since the nucleus of the solitary tracts is a central synapse of the bar receptor loop, and some of its efferent’s distributed with the vagus nerves synapse directly with parasympathetic fibers carried to the heart; it is possible that parasympathetic control of the heart is involved in hypoglycemic counter-regulation. Consequently, there are some evidences indicating the strength of the stimulus is relevant. It is found out that an 8 mmHg decrease in diastolic blood pressure and an 11 ml increase in stroke volume on average can evoke significant cardiovascular autonomic responses in normal circumstances. In addition, it emphasizes the relevance of the stimulus is that the subjects experienced marked hypoglycemic symptoms. In view thereof, the effects of catecholamine on haemodynamics depend on the relative excitation of a- and b-adrenoreceptors in the heart and blood vessels.

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