Hemodynamic effects of acute hyperglycemia in type 2 diabetic patients.

Abstract

Abbreviations: dBP, diastolic blood pressure; HR, heart rate; MBP, mean blood pressure; NO, nitric oxide; sBP, systolic blood pressure; SqT, squatting test; SqTs, squatting sympathetic ratio; SqTv, squatting vagal ratio.A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances. Hemodynamic Effects of Acute Hyperglycemia in Type 2 Diabetic PatientsOBJECTIVE -The aim of the present study was to evaluate the hemodynamic effects of acute hyperglycemia in type 2 diabetic patients and to see whether these effects are related to changes in nitric oxide (NO) availability.RESEARCH DESIGN AND METHODS -Twenty newly diagnosed complication-free diet-treated type 2 diabetic patients participated in the study. All patients underwent 3 hyperglycemic glucose clamps in random order: 1) the control study was performed with plasma glucose clamped at 18 mmol/l for 2 h; 2) the octreotide study with plasma insulin blocked at basal levels during the clamp; and 3) the L-arginine study with L-arginine (1 g/min) infused during the last 30 min of the clamp. A group of 8 patients also underwent a glutathione infusion (600 mg as an intravenous bolus followed by 5 mg/min infusion) during the clamp.RESULTS -During hyperglycemia, there were significant increments of systolic (sBP) (from 115.5 ± 9.1 to 120.3 ± 8.2 mmHg, P Ͻ 0.01) and diastolic (dBP) (from 70.3 ± 7.8 to 79.7 ± 5.3 mmHg, P Ͻ 0.01) blood pressure, as well as heart rate (from 75.2 ± 7.8 to 80.8 ± 5.4 beats/min, P Ͻ 0.01) and plasma catecholamines (P Ͻ 0.05). Squatting ratios, a measure of the baroreflex activity, significantly deteriorated after hyperglycemia (P Ͻ 0.01). The infusion of octreotide, used to avoid the possible confounding influence of insulin, did not change the hemodynamic effects of hyperglycemia. Glutathione, a free radical scavenger, completely prevented the vascular effects of hyperglycemia. L-Arginine produced a fall in sBP and dBP to baseline values and normalized squatting ratios.CONCLUSIONS -Acute hyperglycemia in newly diagnosed type 2 diabetic patients causes significant hemodynamic changes that are independent of endogenous insulin and are prevented by glutatione and reversed by L-arginine, suggesting an interference with endogenous NO availability. These observations could help explain the adverse cardiovascular effects of hyperglycemic spikes.

Squatting, a posture test for studying cardiovascular autonomic neuropathy in diabetes

“…In another study, the same researchers reported that these squatting ratios significantly deteriorated after acute hyper-glycaemia in T2DM patients (P<0.01) [24]. Such changes were prevented by glutathione and reversed by L-arginine, suggesting their possible interference with endogenous nitric-oxide (NO) availability.…”

Beyond postprandial hyperglycaemia: metabolic factors associated with cardiovascular disease

“…In support of this hypothesis these authors found, in another set of experiments, that in patients with newly diagnosed diabetes the adverse haemodynamic effects of acute hyperglycaemia (i. e. blood pressure rise and baroreflex responses) can be reversed by l-arginine infusion, a precursor of nitric oxide. Moreover, the adverse effects of acute hyperglycaemia could also be prevented by the anti-oxidant glutathione, enhancing nitric oxide availability [130]. Also insulin could have a direct effect on QTc.…”

Preventing end stage renal disease in diabetic patients — genetic aspect (part I)

“…66 A study in early Type 2 diabetes showed dramatic increases in blood pressure in response to two hours of hyperglycaemia, but the study was performed without an euglycaemic control period. 67 Two studies finding evidence of renal 50 and systemic 49 RAS activation after 12 hours of moderately elevated blood glucose also demonstrated a substantial increase in mean arterial blood pressure. Existence of a direct link between metabolic and systemic haemodynamic factors would certainly contribute to the understanding of mechanisms underlying the toxic effects of glucose.…”