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Hemodynamic effects of acute hyperglycemia in type 2 diabetic patients
R Marfella1, F Nappo, L De Angelis
1Department of Geriatrics and Metabolic Diseases, Second University of Naples, Italy. dagiugli@tin.it
Objective:
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 < 0.01) and diastolic (dBP) (from 70.3 +/- 7.8 to 79.7 +/- 5.3 mmHg, P < 0.01) blood pressure, as well as heart rate (from 75.2 +/- 7.8 to 80.8 +/- 5.4 beats/min, P < 0.01) and plasma catecholamines (P < 0.05). Squatting ratios, a measure of the baroreflex activity, significantly deteriorated after hyperglycemia (P < 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.
Insights
Acute hyperglycemia in type 2 diabetes causes harmful hemodynamic changes, impacting blood pressure and baroreflex activity. These effects are linked to reduced nitric oxide (NO) availability and can be mitigated by L-arginine.
Area of Science:
- Cardiovascular Physiology
- Endocrinology
- Metabolic Disorders
Background:
- Type 2 diabetes is characterized by hyperglycemia, which can lead to cardiovascular complications.
- The immediate hemodynamic impact of acute hyperglycemia and its underlying mechanisms in type 2 diabetes remain incompletely understood.
Purpose of the Study:
- To investigate the acute hemodynamic effects of hyperglycemia in patients with type 2 diabetes.
- To determine if these hemodynamic changes are associated with alterations in nitric oxide (NO) availability.
Main Methods:
- Twenty newly diagnosed, diet-treated type 2 diabetic patients underwent hyperglycemic glucose clamps.
- Interventions included a control clamp, octreotide to block insulin, L-arginine infusion, and glutathione infusion (in a subset of patients).
- Hemodynamic parameters (blood pressure, heart rate, baroreflex activity) and plasma catecholamines were measured.
Main Results:
- Hyperglycemia significantly increased systolic and diastolic blood pressure, heart rate, and plasma catecholamines.
- Baroreflex activity, measured by squatting ratios, significantly deteriorated.
- Glutathione prevented hyperglycemia-induced vascular effects, while L-arginine reversed them, suggesting a role for NO.
Conclusions:
- Acute hyperglycemia induces significant hemodynamic alterations in type 2 diabetes, independent of insulin.
- These changes are mediated by impaired nitric oxide (NO) availability.
- Findings suggest a mechanism for adverse cardiovascular events during hyperglycemic spikes in type 2 diabetes.