Cardiovascular changes during hypoglycaemia

Hilsted, J.

doi:10.1111/j.1475-097x.1993.tb00312.x

Cited by 10 publications

(6 citation statements)

References 39 publications

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“…Again with the sample size caveat, these findings suggest that the hemodynamic responses to hypoglycemia are largely the result of adrenomedullary, rather than sympathetic neural, activation. The relevant adrenomedullary secretory product is almost assuredly epinephrine (19).…”

Section: Discussionmentioning

confidence: 99%

“…Finally, increments in the plasma norepinephrine concentration were not observed during hypoglycemia in adrenalectomized humans (14,34). The hemodynamic responses to hypoglycemia, net vasodilation with increments in heart rate and cardiac output and widening of pulse pressure, have been attributed to increased adrenomedullary epinephrine secretion (in the context of the vasodilatory effect of the hyperinsulinemia used to produce the hypoglycemia) (19). Sympathetic neural activation may be a compensatory response that limits vasodilation and prevents hypotension (19).…”

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confidence: 99%

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Hypoglycemia and the sympathoadrenal system: neurogenic symptoms are largely the result of sympathetic neural, rather than adrenomedullary, activation

DeRosa

Cryer

2004

American Journal of Physiology-Endocrinology and Metabolism

109

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The relative contributions of the sympathetic nervous system and the adrenal medullae, the two components of the sympathoadrenal system, to the manifestations of hypoglycemia are largely unknown. We tested the hypothesis that the neurogenic symptoms of hypoglycemia are largely the result of sympathetic neural activation. To do so, we quantitated neurogenic symptoms, as well as norepinephrine (NE) kinetics and selected hemodynamic changes, during hyperinsulinemic euglycemic and stepped hypoglycemic clamps in 15 healthy control subjects (Controls) and four bilaterally adrenalectomized patients (ADX). Plasma epinephrine responses to hypoglycemia were virtually absent in ADX, as expected. Neurogenic symptom scores increased to higher values during the hypoglycemic compared with the euglycemic clamps in both Controls (P < 0.0001) (e.g., final scores of 7.8 +/- 1.2 vs. 3.0 +/- 0.7) and ADX (P < 0.0001) (e.g., final scores of 10.8 +/- 4.1 vs. 2.5 +/- 1.0). Plasma NE concentrations (P < 0.0001) and systemic NE spillover (P = 0.0007) increased during the hypoglycemic compared with the euglycemic clamps in Controls but not in ADX. Similarly, heart rate increased (P = 0.0104), diastolic blood pressure decreased (P = 0.0003), and forearm blood flow increased (P < 0.0001) during the hypoglycemic compared with the euglycemic clamps in Controls but not in ADX. These data indicate that the neurogenic symptoms of hypoglycemia are largely the result of sympathetic neural, rather than adrenomedullary, activation. They also suggest that the plasma NE and hemodynamic responses to hypoglycemia are largely the result of adrenomedullary, rather that sympathetic neural, activation.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Hypoglycemia and the sympathoadrenal system: neurogenic symptoms are largely the result of sympathetic neural, rather than adrenomedullary, activation

DeRosa

Cryer

2004

American Journal of Physiology-Endocrinology and Metabolism

109

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“…The finding that anesthesia and surgical stress did not affect islet perfusion indicated that local regulation of islet perfusion might be more predominant than neural regulation during hyperglycemia. Hypoglycemia induces systemic hemodynamic changes including increased cardiac output; increased blood flow to brain, skeletal muscle, and foregut; and decreased blood flow to kidneys and spleen (8). With regard to the splanchnic circulation, blood flow in the superior mesenteric artery increased by 53% in healthy subjects during hypoglycemia, as demonstrated using a Doppler technique (2).…”

Section: R1603mentioning

confidence: 98%

Pancreatic islet blood flow in conscious rats during hyperglycemia and hypoglycemia

Iwase

Tashiro

Uchizono

et al. 2001

American Journal of Physiology-Regulatory, Integrative and Comp

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Anesthesia affects general hemodynamics and regulation of organ perfusion. We used colored microspheres to measure pancreatic islet blood flow in conscious rats at two time points, during either hyperglycemia or hypoglycemia. This method, using black and green microspheres, was validated by comparison with previous microsphere experiments and by lack of effect of a nonmetabolizable glucose analog, 3-O-methylglucose, on islet perfusion. Basal and glucose-stimulated islet blood flow levels were similar in pentobarbital sodium-anesthetized and conscious rats. However, the basal distribution of pancreatic blood flow was altered by anesthesia (fractional islet blood flow 5.8 +/- 0.4% in conscious rats, 7.9 +/- 0.8% in pentobarbital-anesthetized rats, P < 0.05). Insulin-induced hypoglycemia significantly increased whole pancreatic blood flow in conscious rats, whereas islet blood flow remained unchanged and fractional islet blood flow was decreased (5.8 +/- 0.5% in the basal state, 4.2 +/- 0.4% during hypoglycemia, P < 0.001). Methylatropine pretreatment significantly increased islet blood flow during hypoglycemia by 181%. This result suggests that prevention of hypoglycemia-induced increase in islet perfusion may be mediated, at least in part, by a cholinergic, vagal muscarinic mechanism.

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“…Hypoglycaemia can be associated with (1) activation of adrenergic response [23], (2) impaired flexibility in substrate shift in the diabetic myocardium [24], (3) QTc prolongation and cardiac rate/rhythm disturbances [25], and (4) excessive glucose fluctuations with marked activation of oxidative stress [26]. A further potential indicator of patient vulnerability is represented by diabetic autonomic neuropathy.…”

Section: Hypoglycaemia: a Trigger For CV Events?mentioning

confidence: 99%

Megatrials in type 2 diabetes. From excitement to frustration?

Prato

2009

Diabetologia

119

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Whether glycaemic control may result in a reduction of cardiovascular (CV) risk has been a matter of continuous discussion and investigation. Epidemiological analyses have extensively suggested a relationship between glycaemic control and CV events; however, the results of intervention trials have been less conclusive. The UKPDS reported a 16% reduction in the risk of myocardial infarction, but this reduction was not statistically significant. The results of the Kumamoto and PROactive studies could not allow any firm conclusions to be drawn either, because of limited size and the defined primary endpoint, respectively. The results of the Action to Control Cardiovascular Risk in Diabetes (ACCORD) and Action in Diabetes and Vascular Disease: Preterax and Diamicron Modified Release Controlled Evaluation (ADVANCE) trials and the Veteran Administration Diabetes Trial (VADT) were published in rapid succession over the second half of 2008 and at the beginning of 2009. A total number of almost 25,000 type 2 diabetic patients were recruited in these three trials, which assessed the effect of intensive glycaemic control vs conventional treatment on well-defined CV endpoints. In spite of the achievement and maintenance of strict glycaemic control (HbA 1c <7.0%), no beneficial effect of intensive therapy was apparent in any of the studies. At the same time these results were presented, the results of an analysis of the 10 year follow-up of the UKPDS also became available and provided a more optimistic view of the potential benefit of achieving good glycaemic control. The relative risk reductions for myocardial infarction and all-cause mortality were significantly lower in the patients who initially received the intensive treatment compared with those in the conventional treatment arm. Moreover, the initial benefit in terms of microvascular complications observed at the end of the intervention trial remained unaltered at follow-up. Once again the debate on the importance of glycaemic control in preventing macrovascular complications remains unsettled. These results, however, require some reconciliation, and the objective of this commentary is to analyse a series of elements, including the changes in the treatment approach to CV risk factors in type 2 diabetes, the effect of glucoselowering agents, and the characteristics of the patients included in the different trials, that should be taken into account when interpreting the results of intervention trials in type 2 diabetes.

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Cardiovascular changes during hypoglycaemia

Cited by 10 publications

References 39 publications

Hypoglycemia and the sympathoadrenal system: neurogenic symptoms are largely the result of sympathetic neural, rather than adrenomedullary, activation

Hypoglycemia and the sympathoadrenal system: neurogenic symptoms are largely the result of sympathetic neural, rather than adrenomedullary, activation

Pancreatic islet blood flow in conscious rats during hyperglycemia and hypoglycemia

Megatrials in type 2 diabetes. From excitement to frustration?

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