Intravenous Injection Of Glucagon Research Articles

Cardiovascular responses to glucagon: Physiologic measurement by external recordings

The cardiovascular responses of normal subjects to intravenous injections of glucagon and glucagon diluent were assessed by noninvasive polygraphic techniques. A blinding procedure, which eliminated observer bias, was used during the reading of tracings. Analysis of group results showed that glucagon provoked uniformly significant (p < 0.001) changes, including increase in heart rate, blood pressure, pressure-rate product, and ejection time index, and decrease in pre-ejection period, mechanical and electromechanical systole, left ventricular ejection time, and the ratio, PEP LVET . The principal results correlated well with those of previous studies of the hemo-dynamic effects of glucagon. The pre-ejection period and its components responded in a bimodal pattern, the significance of which is unclear.

The early rise of plasma growth hormone (HGH) and immunoreactive insulin (IRI) in children following intravenous glucagon.

The effect of a rapid intravenous injection of glucagon (15 μg/kg body weight) in 28 children of short stature was studied. Significant elevations of growth hormone (HGH), insulin (IRI), and glucose were found to occur within two minutes. The peak response of HGH was found to compare favorably with other stimuli and to occur early. A direct action of glucagon on the pituitary is suggested.

Alterations in fetal and maternal carbohydrate metabolism in the primate fetus: Studies of glucose and insulin in response to intravenous injections of purified glucagon and cyclic adenosine monophosphate

An insulin-free glucagon preparation was obtained and studied in the primate by obtaining control and study plasma insulin and blood glucose measurements in the mother and fetus of the Macaca mulatta at 150 to 156 days of gestation. The experiment involved placement of polyvinyl catheters within the inferior vena cava of both the mother and fetus with the use of pentobarbital anesthesia. The intravenous injection of glucagon produced an insignificant immediate increase in the insulin output by the fetal pancreas. In addition, fetal injections of cyclic adenosine monophosphate failed to produce a fetal insulin rise whereas the fetal glucose and the maternal glucose and insulin levels increased. These data support the concept that the previously described fetal and neonatal responses to injected glucagon have been mainly due to the insulin contamination in the glucagon product.

The effect of glucagon on enterokinase secretion from Brunner's gland pouches in dogs.

ConclusionThe effects of glucagon on Brunner's gland secretion were studied in three mongrel dogs with pouches of the proximal duodenum. A continuous intravenous injection of glucagon given in a dose that produced maximal volume output caused sustained increases in volume, total protein, and enteropeptidase secretion from the pouches.

The effects of glucagon on sodium, potassium, and urine excretion in patients in congestive heart failure

The effects of 3 intravenous injections of glucagon on sodium, potassium, and urine excretion were determined in 8 patients with chronic congestive heart failure. Initial injections of 5 mg. of glucagon resulted in statistically significant average increments in sodium excretion from 84.8 to 210.4 μEq per minute in potassium excretion from 0.7 to 1.6 μEq per minute and in urine flow from 1.4 to 2.2 ml. per minute. Second and third injections of glucagon (3 to 10 mg.) sustained the natriuresis in only 4 patients. Six patients experienced nausea and 5 patients vomited, thus preventing the use of larger doses of glucagon. One patient, in a preliminary study in which glucagon was infused intravenously, developed a short episode of multifocal, ventricular tachycardia shortly after vomiting occurred. Because of the relatively limited diuresis and nausea and vomiting, we conclude that single injections of glucagon, in doses used in this study, did not offer advantages over existing methods of treatment in our patients.

Modification by glucagon of the splanchnic vascular responses to activation of the sympathicoadrenal system

The vasodilatory effect of glucagon on the splanchnic vascular bed was studied in anesthetized dogs during experimentally induced and simulated activation of the sympathicoadrenal system. Blood flow in the superior mesenteric artery was recorded using the electromagnetic technique. When the splanchnic blood flow had been reduced to about 50 per cent by bleeding, intravenous injection of glucagon restored the blood flow to approximately control level. When an activation of the sympathetic outflow to the splanchnic vascular bed was simulated by electrical splanchnic nerve stimulation, the vasoconstrictory response to the stimulation was abolished or modified by glucagon injection. Finally, the vasodilatory effect of glucagon in the mesenteric vascular bed could also be demonstrated when vasoconstriction due to catecholamine infusion was present. Glucagon did not, however, influence the vasoconstrictory response to catecholamines in other peripheral vascular beds. The mechanism for the vasodilatory action of glucagon is briefly discussed.

CARDIOVASCULAR EFFECTS OF GLUCAGON IN MAN

Abstract Cardiovascular effects of an intravenous injection of glucagon, 3 mg., were studied in 8 subjects during cardiac catheterization. In each study a prompt effect was noted, with an increase in heart rate, cardiac output, right ventricular dp/dt and right ventricular and systemic systolic pressures. Right ventricular end-diastolic pressure and systemic vascular resistance decreased. It is concluded that glucagon exerts positive inotropic and chronotropic effects upon the heart in man. Further studies are required to determine its proper clinical role and mechanism of action.

Cardiovascular effects of glucagon in man

Cardiovascular effects of an intravenous injection of glucagon, 3 mg., were studied in 8 subjects during cardiac catheterization. In each study a prompt effect was noted, with an increase in heart rate, cardiac output, right ventricular dp/dt and right ventricular and systemic systolic pressures. Right ventricular end-diastolic pressure and systemic vascular resistance decreased.It is concluded that glucagon exerts positive inotropic and chronotropic effects upon the heart in man. Further studies are required to determine its proper clinical role and mechanism of action.

INSULIN RESERVE IN PATIENTS WITH CHRONIC PANCREATITIS

Sixteen patients with unequivocal evidence of chronic pancreatitis were subjected to intensive β-cell stimulation by combined intravenous injection of glucagon and tolbutamide after oral glucose. The serum-immunoreactive-insulin responses of the whole group were significantly impaired when compared with normal controls. The degree of impairment seemed to be proportional to the degree of glucose intolerance. It is postulated that the diabetic syndrome of chronic pancreatitis represents an example of acquired insulinopenia and is thus a valuable clinical model for assessing the effects of this in man.

BETA-CYTOTROPHIC EFFECTS OF GLUCOSE, GLUCAGON, AND TOLBUTAMIDE IN MAN

Rapid increases in plasma-levels of immunoreactive insulin were observed after intravenous injection of glucagon or tolbutamide. Injections of both agents simultaneously doubled the maximum response of either alone. Pretreatment with oral carbohydrate notably enhanced the response to either alone or both combined.

Oxytetracycline and hypoglycemia with convulsions in pancreatectomized dogs.

SummaryAddition of oxytetracycline to intravenous fluid used to maintain pancrea-tectomized dogs brings about a state of hypo-glycemia with staggering and convulsions that only infrequently responds to administration of glucose. The liver glycogen of these dogs is usually normal and occasionally elevated. During the state of hypoglycemia with staggering and convulsions the rise of the blood glucose following intravenous injection of adrenalin or glucose (glucose tolerance test) is transient; the rise of the blood glucose following intravenous injection of glucagon is large and sustained.

The glucagon response of fasting obese subjects

The storage of liver glycogen in 7 obese fasting subjects was assessed by observing the response of peripheral blood glucose to the intravenous injection of glucagon. Three subjects who were receiving liberal diets prior to the study showed a subnormal response within the first 4 days of total food deprivation. As the fast continued, the rise in peripheral blood sugar was gradually restored. During a second fast, these same subjects maintained a normal blood sugar response to glucagon. Another group of 4 subjects who had been on restricted diets prior to the study maintained their blood sugar response to glucagon during a similar fasting regimen. These observations indicate that in prolonged fasting or in periods of restricted dietary intakes, glycogen formation and gluconeogenesis are enhanced following a brief period of glycogen depletion.

The effect of glucagon, epinephrine and vasopressine on the plasma concentration and renal excretion of electrolytes in man.

Rapid intravenous injection of glucagon and epinephrine to normal man first caused a shortlasting increase of the serum potassium concentration. Subsequent to this increase a more longlasting decrease was found. If the hormones were given slowly no hyperkalemia was observed.Vasopressine infusion, giving a marked increase in blood glucose, resulted in a serum potassium increase which returned to normal after end of infusion.

The hepatic response to glucagon in the unanesthetized dog.

Intravenous administration of crystalline glucagon 02 mg.⁄kg. was used to study hepatic glycogenolysis and associated events in the unanesthetized dog. An increase in hepatic blood flow and hepatic glucose output regularly occurred following glucagon administration. Approximately 9.6 gm, of glucose were released from the liver during the first hour after a single intravenous injection of glucagon; this represents a net increase over control values of about 6 gm. Depletion of glycogen stores induced by fasting was associated with a decreased or absent response of hepatic blood flow and hepatic glucose output to glucagon. Hepatic uptake of alpha amino nitrogen increased after glucagoninduced glycogenolysis; this increase began promptly and reached a maximum about 45 minutes after glucagon administration. These changes were interperted as reflecting increased gluconeogenesis following depletion of liver glycogen stores. GLYCOGENOLYSIS may be induced in the liver in a controlled fashion by means of glucagon a...

The preventive effect of glucagon (HGF) against the diabetogenic action of alloxan and its antagonism by insulin.

SUMMARY The intravenous injection of glucagon (0·4 mg/kg) 12–30 min before the administration of a diabetogenic dose of alloxan (60 mg/kg) prevents the development of alloxan diabetes in dogs. The protection obtained with glucagon is abolished by a subcutaneous injection of insulin (2 i.u./kg) administered 2 hr previously. The possible mechanism of this protection and of its antagonism by insulin is discussed.

Absence of hyperglycemic effect of glucagon in the eviscerate rat.

SummaryEviscerated rats were given continuous intravenous injections of glucose. The intravenous injection of glucagon failed to affect the level of blood glucose in eviscerated rats but did cause hyperglycemia in normal rats.