Serum glucagon and insulin levels and their relationship to blood glucose values in patients with acute myocardial infarction and acute coronary insufficiency

Willerson, James T.; Hutcheson, Donna R.; Leshin, Stephen J.; Faloona, Gerald R.; Unger, Roger H

doi:10.1016/0002-9343(74)90848-1

Cited by 66 publications

(20 citation statements)

References 9 publications

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“…or in dialyzed uremics (11+2 AU/ml, P < 0.05). 30 (P < 0.02), 60 (P < 0.05), 90 (P < 0.005), 120 (P < 0.005), and 180 min (P < 0.02).…”

Section: Resultsmentioning

confidence: 95%

“…Recent studies in our labora' fractional extraction ratio of glucagon acro in the intact dog and rat of 40%.3 After the renal failure by 75% nephrectomy, a consist take of glucagon is no longer observed.3 renal artery clamping (27) and ureteral lig dogs result in a rapid rise in plasma gluca trast, a decrease in circulating glucagon after successful renal transplantation in These data thus indicate that renal funct taken into account in interpreting plasr levels in a variety of pathological states. gonemia associated with traumatic shock myocardial infarction (30), diabetic ketoae and hyperosmolar coma (32) (Fig. 5).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Influence of uremia and hemodialysis on the turnover and metabolic effects of glucagon.

Sherwin¹,

Bastl²,

Finkelstein³

et al. 1976

J. Clin. Invest.

196

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A B S T R A C T To evaluate the mechanism and role of hyperglucagonemia in the carbohydrate intolerance of uremia, 19 patients with chronic renal failure (12 of whom had undergone chronic hemodialysis for at least 11 mo) and 35 healthy control subjects were studied. Plasma glucagon, glucose, and insulin were measured in the basal state, after glucose ingestion (100 g), after intravenous alanine (0.15 g/kg), and during a 3-h continuous infusion of glucagon (3 ng/kg per min) which in normal subjects, raised plasma glucagon levels into the upper physiological range.Basal concentrations of plasma glucagon, the increment in glucagon after infusion of alanine, and postglucose glucagon levels were three-to fourfold greater in uremic patients than in controls. The plasma glucagon increments after the infusion of exogenous glucagon were also two-to threefold greater in the uremics. The metabolic clearance rate (MCR) of glucagon in uremics was reduced by 58% as compared to controls. In contrast, the basal systemic delivery rate (BSDR) of glucagon in uremics was not significantly different from controls.Comparison of dialyzed and undialyzed uremics showed no differences with respect to plasma concentrations, MCR, or BSDR of glucagon. However, during the infusion of glucagon, the increments in plasma glucose in undialyzed uremics were three-to fourfold greater than in dialyzed uremics or controls. When the glucagon infusion rate was increased in controls to 6 ng/kg per min to produce increments in plasma glucagon comparable to uremics, the glycemic response remained approximately twofold greater in the undialyzed uremics. The plasma glucose response to glu- cagon in the uremics showed a direct linear correlation with oral glucose tolerance which was also improved with dialysis. The glucagon infusion resulted in a 24% reduction in plasma alanine in uremics but had no effect on alanine levels in controls. It is concluded that (a) hyperglucagonemia in uremia is primarily a result of decreased catabolism rather than hypersecretion of this hormone; (b) sensitivity to the hyperglycemic effect of physiological increments in glucagon is increased in undialyzed uremic patients; and (c) dialysis normalizes the glycemic response to glucagon, possibly accounting thereby for improved glucose tolerance despite persistent hyperglucagonemia. These findings thus provide evidence of decreased hormonal catabolism contributing to a hyperglucagonemic state, and of altered tissue sensitivity contributing to the pathophysiological action of this hormone.

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“…or in dialyzed uremics (11+2 AU/ml, P < 0.05). 30 (P < 0.02), 60 (P < 0.05), 90 (P < 0.005), 120 (P < 0.005), and 180 min (P < 0.02).…”

Section: Resultsmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

Influence of uremia and hemodialysis on the turnover and metabolic effects of glucagon.

Sherwin¹,

Bastl²,

Finkelstein³

et al. 1976

J. Clin. Invest.

196

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“…In addition, many states characterized by catecholamine excess are associated with hyperglucagonemia (9, [15][16][17][18][19][20]; nevertheless, a cause-effect relationship between sympathetic nervous system discharge or epinephrine release from the adrenal, and stimulation of glucagon secretion, especially in man, has not been identified. During hypoglycemia there is stimulation of glucagon secretion (9), increased sympathetic neural outflow, and increased adrenal medullary secretion with resultant increases in plasma and urinary epinephrine and norepinephrine levels (21,22).…”

Section: Discussionmentioning

confidence: 99%

Glucagon response to hypoglycemia in sympathectomized man.

Palmer¹,

Henry²,

Benson³

et al. 1976

J. Clin. Invest.

109

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A B S T R A C T Hypoglycemia stimulates immunoreactive glucagon (IRG) secretion and increases the activity of the sympathetic nervous system. To ascertain if the augmented alpha cell activity evoked by glucopenia is mediated by the adrenergic nervous system, the glucagon response to insulin-induced hypoglycemia of five subj ects with neurologically complete cervical transections resulting from trauma, thereby disrupting their hypothalamic sympathetic outflow, was compared to six healthy volunteers. In addition to clinical neurological evaluation, completeness of sympathectomy was verified by failure to raise plasma norepinephrine levels during hypoglycemia compared to the two-to threefold increase observed in controls. Total IRG response (IRG area above basal 0-90 min) and peak IRG levels achieved were the same in the quadriplegics and the controls. Although the glucagon rise tended to be slower, and the peak levels attained occurred later in the quadriplegic patients than in the controls, this response was appropriate for their sugar decline, which was slower and reached the nadir later than in the control subjects.These observations that the glucagon release during insulin-induced hypoglycemia is normal in subjects whose hypothalamic sympathetic outflow has been interrupted provide strong evidence that the sympathetic nervous system does not mediate the glucagon response to hypoglycemia. INTRODUCTIONIn addition to the control of insulin and glucagon secretion by circulating levels of substrates such as amino

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“…Hyperglycemia in the acute stage of AMI is also associated with an increased risk of in-hospital mortality independent of the presence or absence of diabetes. 32 Whether hyperglycemia occurs secondary to a larger infarction and therefore a larger area of no reflow, 33 or whether it contributes to the no-reflow phenomenon, is not known. Hyperglycemia by itself impairs endotheliumdependent vasodilatation, enhances leukocyte adhesion to endothelial cells by increasing circulating adhesion mole- cules, and attenuates the beneficial impact of ischemic preconditioning.…”

Section: No-reflow Phenomenonmentioning

confidence: 99%

Microvasculature in Acute Myocardial Ischemia: Part II

2004

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I n the setting of suspected acute myocardial infarction (AMI), a cardiologist needs to know three things: (1) whether there is actually an ongoing infarction, (2) whether reperfusion therapy has succeeded, and (3) how much myocardium was salvaged by reperfusion. Myocardial contrast echocardiography (MCE) can answer the first question by demonstrating the presence of a perfusion defect resulting from reduced microvascular flow because of the presence of a thrombus in an epicardial coronary artery. In a recent multicenter study of 203 patients without ST-segment elevation who presented to the emergency department with chest pain, 21 had AMI, and MCE only missed 1 such patient (sensitivity of 95%). 1 Panel A in Figure 1 demonstrates a MCE perfusion defect in a patient presenting to the emergency department with chest pain who was subsequently ruled in for an AMI. The success of reperfusion and degree of myocardial salvage are equally important to know in patients even with ST-elevation AMI. Coronary angiography is not reliable in this regard. 2 The success of attempted reperfusion can also be accurately assessed with MCE. Most currently used clinical and electrocardiographic parameters are accurate in Ϸ75% of the cases, whereas MCE has an almost 100% accuracy. Panel B in Figure 1 depicts MCE images that were obtained immediately after thrombolysis and showed that most of the myocardium was reperfused. A small region in the apex showed no reflow and failed to exhibit improvement in function weeks later, whereas the reperfused myocardium showed complete recovery in function. In several cases of STelevation AMI, perfusion is normal at the time of cardiac catheterization despite a wall motion abnormality, and when angiography is performed, the infarct-related artery is found to be open, either spontaneously or from treatment with aspirin and heparin. No-Reflow PhenomenonAlthough MCE immediately after reperfusion can provide an accurate assessment of the success of reperfusion, it might underestimate the degree of no reflow because of reactive hyperemia. 3,4 The degree of reactive hyperemia is influenced by the amount of capillary damage and the degree of residual stenosis in the infarct-related artery. The no-reflow zone also changes dynamically in the first several hours after reperfusion because of vasospasm, myocardial edema, etc. Therefore, the ideal time to measure no reflow to determine the extent of myocardial necrosis is after 48 hours following reperfusion. 5,6 At that time, dynamic changes in resting tissue perfusion have subsided, and the extent of no reflow correlates well with infarct size and denotes a region of irreversible tissue damage.The "no-reflow" phenomenon in the heart was originally described in a canine model of coronary artery ligation followed by reperfusion. 7 Despite an open infarct-related artery, regions within the myocardium showed low flow, which were located exclusively within irreversibly injured myocardium. Consequently, the size of the no-reflow zone approximated infarct size. Elec...

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Serum glucagon and insulin levels and their relationship to blood glucose values in patients with acute myocardial infarction and acute coronary insufficiency

Cited by 66 publications

References 9 publications

Influence of uremia and hemodialysis on the turnover and metabolic effects of glucagon.

Influence of uremia and hemodialysis on the turnover and metabolic effects of glucagon.

Glucagon response to hypoglycemia in sympathectomized man.

Microvasculature in Acute Myocardial Ischemia: Part II

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