Recovery mechanisms from acute hypoglycaemia in complete tetraplegia

Corrall, R. J. M.; Frier, Brian M.; McClemont, Elizabeth; Taylor, Sue; Christie, N E

doi:10.1038/sc.1979.60

Cited by 13 publications

(10 citation statements)

References 7 publications

(6 reference statements)

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“…By studying patients with autonomic deficits, the increment in heart rate has been found to be mediated via sympathetic activity. This response is absent in tetraplegic patients who have a pre-synaptic sympathectomy caused by traumatic transection of the cervical cord [60], and it appears to be mediated via β 1 adrenoceptors [61]. The blood pressure changes are thought to be caused by epinephrine via α and β 2 adrenoceptors, and can be reproduced by infusing epinephrine intravenously [61].…”

Section: Physiological Changes In the Heartmentioning

confidence: 96%

Vascular disease and diabetes: is hypoglycaemia an aggravating factor?

Wright

Frier

2008

Diabetes Metabolism Res

296

231

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Acute hypoglycaemia provokes profound physiological changes affecting the cardiovascular system and several haematological parameters, principally as a consequence of sympatho-adrenal activation and counter-regulatory hormonal secretion. Many of these responses have an important role in protecting the brain from neuroglycopenia, through altering regional blood flow and promoting metabolic changes that will restore blood glucose to normal. In healthy young adults the cardiovascular effects are transient and have no obvious detrimental consequences. However, some of the effected changes are potentially pathophysiological and in people with diabetes who have developed endothelial dysfunction, they may have an adverse impact on a vasculature that is already damaged. The acute haemodynamic and haematological changes may increase the risk of localized tissue ischaemia, and major vascular events can certainly be precipitated by acute hypoglycaemia. These include myocardial and cerebral ischaemia and occasionally infarction. Established diabetic retinopathy often deteriorates after strict glycaemic control is instituted, the latter being associated with a threefold increase in frequency of severe hypoglycaemia, and enhanced exposure to mild hypoglycaemia. The possible mechanisms underlying these hypoglycaemia-induced effects include haemorrheological changes, white cell activation, vasoconstriction, and the release of inflammatory mediators and cytokines. The concept that acute hypoglycaemia could aggravate vascular complications associated with diabetes is discussed in relation to evolving comprehension of the pathogenesis of atherosclerosis and blood vessel disease.

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Section: Physiological Changes In the Heartmentioning

confidence: 96%

Vascular disease and diabetes: is hypoglycaemia an aggravating factor?

Wright

Frier

2008

Diabetes Metabolism Res

296

231

View full text Add to dashboard Cite

show abstract

“…The time at which the hypoglycaemic reaction (R) ensued varied between individuals and the clock was reset at R to ensure that subsequent time points during the recovery phase were comparable between subjects. If resetting had not occurred at this point, data from variable points of recovery from hypoglycaemia would have been pooled leading to inaccuracies in data interpretation [5]. Serial measurements were repeated at intervals for the next 120 min.…”

Section: Methodsmentioning

confidence: 99%

Increased splanchnic blood flow after hypoglycaemia in diabetic and normal man: evidence against glucagon as a mediator

et al. 1999

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Superior mesenteric artery blood flow increases significantly after hypoglycaemia in healthy humans. Glucagon has vasoactive properties but its role in hypoglycaemic hyperaemia is unclear. To assess this role, we studied the superior mesenteric artery blood flow response to hypoglycaemia of patients with uncomplicated Type 1 (insulin-dependent) diabetes mellitus of at least 10 years duration; a group known to have defective glucagon response to hypoglycaemia. Hypoglycaemia was induced using an intravenous infusion of soluble human insulin (2.5 m-units.min-1.kg-1) discontinued at a plasma glucose of 2.5 mmol/l. Superior mesenteric artery blood flow was measured using transcutaneous duplex Doppler ultrasound. Plasma samples were assayed for glucose, insulin, glucagon, catecholamines, growth hormone and cortisol. Plasma glucose concentration fell to a nadir of 1.8 (0.3) mmol/l in patients and 1.4 (0.1) mmol/l in controls. Plasma glucagon concentration was unchanged in patients from a baseline level of 111.7 (13.1) ng/l but rose in controls from 105 (8.5) to a peak of 239 (3.1) ng/l (P<0.001). Superior mesenteric artery blood flow increased in both groups: from 385 (29) to 921 (100) ml/min (140% increase; P<0.05) in patients and from 517 (50) to 790 (67) (53% increase; P<0.001) in controls. This study shows that patients with Type 1 diabetes have a normal splanchnic vascular hyperaemic response to hypoglycaemia despite defective glucagon counter-regulation. These results support our previous work suggesting that glucagon is not a major mediator of this response; it seems likely that circulating adrenaline is the major regulatory mechanism.

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“…Therefore, to ensure comparison of responses over a standardized time scale, R was taken to represent time zero. Statistical comparisons were made between data collected after or before R. It has previously been demonstrated that, unless comparison is made with reference to R in studies into hypoglycaemia, pooling of data from variable points of recovery occurs, and such pooling leads to inaccuracies in interpretation [6].…”

Section: Methodsmentioning

confidence: 99%

Physiological control of splanchnic blood flow by adrenaline: studies during acute hypoglycaemia in man

PARKER¹,

BRAATVEDT²,

HALLIWELL³

et al. 1999

Clinical Science

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Superior mesenteric artery blood flow (SMABF) increases significantly during and after the hypoglycaemia reaction in healthy humans. To investigate the mechanisms controlling this phenomenon, SMABF and plasma catecholamines were measured in healthy human volunteers. In 10 controls, hypoglycaemia was induced by insulin infusion (2.5 m-units.min-1.kg-1). In six subjects, beta-blockade by propranolol infusion (0.7 microgram.min-1.kg-1) preceded insulin infusion and was continued throughout the study. Following the hypoglycaemia reaction, the glucose nadir was similar in both groups. In controls, increases in SMABF [42.4+/-6.1% (mean+/-S.E.M.); P<0. 001], cardiac output (34.3+/-2.3%; P<0.001) and pulse rate (from 63. 9+/-2.7 to 82.5+/-3.1 beats/min; P<0.001) occurred. Superior mesenteric artery resistance fell by 32.4+/-3.3% (P<0.001). Under beta-blockade, decreases in SMABF (34.8+/-2.9%; P<0.001) and pulse rate (from 59.5+/-0.2 to 51.8+/-2.2 beats/min; P<0.001) occurred. Superior mesenteric artery resistance increased (peak +30.8+/-12.3%; not significant). Subjects showed greater increases in adrenaline (P<0.006) and noradrenaline (P<0.022) concentrations than controls. Mesenteric hyperaemia associated with hypoglycaemia in man appears to be mediated by a beta-adrenergic mechanism that is activated by increased circulating levels of adrenaline.

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Recovery mechanisms from acute hypoglycaemia in complete tetraplegia

Cited by 13 publications

References 7 publications

Vascular disease and diabetes: is hypoglycaemia an aggravating factor?

Vascular disease and diabetes: is hypoglycaemia an aggravating factor?

Increased splanchnic blood flow after hypoglycaemia in diabetic and normal man: evidence against glucagon as a mediator

Physiological control of splanchnic blood flow by adrenaline: studies during acute hypoglycaemia in man

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