Title:
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The effects of glycaemic perturbations on cognitive and vascular haemodynamic functions in adult humans
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Controlled hypoglycaemia can be induced experimentally using the hyperinsulinaemic glucose clamp technique and this method can be used to examine the effects of acute hypoglycaemia on cognitive performance. In general, tests that involve attention, concentration, psychomotor skill and the ability to ignore distracting information, tend to deteriorate when blood glucose declines below about 3.0 mmol/L. Memory, the cognitive process of storing, encoding and retrieving information, is one of the most crucial domains of cognition, yet memory function has seldom been examined during acute hypoglycaemia, and the few studies that have attempted to do this have provided inconsistent results. To protect the function and integrity of the central nervous system from hypoglycaemia and restore homeostasis as rapidly as possible, a hierarchy of responses are activated when blood glucose falls below 4.0 mmol/l. The rise in blood glucose is mediated by the secretion of counterregulatory hormones, of which adrenaline is one of the major components. Sympatho-adrenal stimulation provokes significant haemodynamic changes, including an increased heart rate and stroke volume, increased myocardial contractility and a rise in cardiac output. In addition, peripheral blood pressure is affected with an increase in systolic and decrease in diastolic pressure, while mean arterial pressure remains unchanged. Pressure values in the peripheral circulation are an inaccurate measure of central pressure because of amplification of the pressure pulse between central and peripheral arteries. Central systolic and diastolic pressures in the aorta are determinants of cardiac loading and perfusion and directly influence cardiac function. The aims of this research project were to examine the effects of acute hyperglycaemia on cognitive function and mood, the effects of acute hypoglycaemia on memory function, and to examine the central haemodynamic responses to acute hypoglycaemia.
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