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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Exocrine pancreatic function was investigated by means of the Lundh test model in dogs with chronic duodenal and gastric fistulas. The test was standardized and the effect of glucagon on exocrine pancreatic secretion was evaluated. The mean tryptic activity detected in 18 tests in 6 dogs was 32.25 +/- 5.25 muEqH+/minute/ml, which is considerably higher than that observed in man. The administration of glucagon was followed by a significant decrease (30.8%) in the volume of the duodenal contents and a more pronounced depression of the enzyme concentrations (trypsin 59%, chymotrypsin 53.3%). It is concluded that the Lundh test affords a valuable experimental model for the investigation of exocrine pancreatic function in dogs.
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PMID:Influence of glucagon on exocrine pancreatic function as determined by the Lundh test in dogs. 59 92

The electrocardiogram was monitored in 100 patients undergoing oesphago-gastro-duodenoscopy. Premedication differed: 25 patients each were given either (Group I) atropine 0.5 mg, hyoscine-N-butylbromide 20 mg, and diazepam 5 mg, or (Group II) hyoscine-N-butyl-bromide 20 mg and diazepam 5 mg, or (Group II) diazepam 5 mg and glucagon 0.2 mg, or (Group IV) only diazepam 5 mg intravenously. After injection of the parasympatholytic drugs (Groups I and II) there was a significantly higher heart rate duringthe entire length of the examination than in groups III and IV. Nine of the ten cases of ascending S-T depression were found in Groups I and II, while descending (ischaemic) S-T changes occurred equally frequently in patients of all four groups. Two of the three more serious arrhythmias were registered after atropine. Since parasympatholytic drugs fail to inhibit arrhythmias and ST-T changes, while accentuating the rise in heart rate, it is recommended that premedication for oesophago-gastro-duodenoscopy should not include such drugs.
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PMID:[Cardiac side-effects of oesophago-gastro-duodenoscopy in relation to premedication (author's transl)]. 68 92

It has previously been shown that nicotinic acid (NA)-induced depression of free fatty acids (FFA) stimulates the secretion of GH and glucagon. To evaluate this hormonal response further, we studied the influence of different doses of glucose administered by continuous iv infusion on the GH and glucagon increase during NA-induced FFA depression. In ten male non-obese volunteers, FFA depression by the infusion of NA (2.3 g over a period of 210 min) resulted in a late rise (from 150 min on) of GH (From 1.1 to 25.9 ng/ml) and an early increase (from 30 min on) of glucagon (from 71.7 to 138.2 pg/ml). When glucose was infused (approximately 60, 120 and 180 g, respectively, over a period of 270 min) during NA-induced FFA depression, the GH rise was reduced and delayed in relation to the amount of glucose infused, but could not be completely abolished (maximal GH concentration during the three NA-plus-glucose infusions: 16.5, 8.0 and 6.1 ng/ml, respectively). The glucagon rise was entirely reversed by the high glucose dose. Insulin did not rise during NA infusion alone. Its secretion in response to glucose infusion was not significantly influenced by FFA depression. Thus, during NA-induced FFA depression the secretion of two lipolytic hormones--GH and glucagon--is stimulated while the secretion of the lipogenetic hormone insulin remains low. Glucose has an inhibitory effect on the GH and glucagon response which, however, is different for each of the hormones.
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PMID:Growth hormone, glucagon, and insulin response to depression of plasma free fatty acids and the effect of glucose infusion. 83 44

Glucagon and L-epinephrine stimulate gluconeogenesis from 20 mM L-lactate, the effect being about 3 times greater in liver cells from fed rats than in those from fasted rats. The rate of pyruvate kinase flux was estimated to be less than 10% of the rate of gluconeogenesis from lactate in hepatocytes from fasted rats, and neither glucagon nor epinephrine lowered the absolute rate significantly. In hepatocytes from fed rats, however, the rate of pyruvate kinase was nearly one-half that of gluconeogenesis. Glucagon caused a marked depression of pyruvate kinase flux, with 1 muM glucagon lowering the rate to nearly the level found in cells from fasted rats Epinephrine at concentrations from 10(-8) to 10(-6) M actually increased pyruvate kinase flux during gluconeogenesis from lactate in cells from fed rats. These results are in accord with the view that the effects of glucagon and epinephrine on gluconeogenesis are not identical.
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PMID:Role of pyruvate kinase in the regulation of gluconeogenesis from L-lactate. 84 45

The study investigated the respective influences of nicotinic acid and somatostatin on plasma concentrations of blood glucose, free fatty acids, glucagon, growth hormone and cortisol in insulin-dependent diabetic subjects. After administration of nicotinic acid alone, marked depression of plasma FFA was accompanied by significant increases of plasma glucagon, growth hormone and cortisol. The glucagon and growth hormone responses to nicotinic acid were significantly reduced when plasma FFA were raised by intravenous administration of heparin and triglycerides. Somatostatin alone induced a significant decrease in blood glucose, plasma glucagon and growth hormone concentrations. Plasma FFA remained unchanged. Somatostatin did not modify the nicotinic acid-induced fall in plasma FFA, but completely blocked the corresponding increments in glucagon and growth hormone. The cortisol rise was not altered by somatostatin. Rebound of glucagon and growth hormone levels were seen upon discontinuation of the somatostatin administration. These results demonstrate that the plasma FFA concentration plays a role in the regulation of glucagon and growth hormone secretion in insulin-dependent diabetics. Furthermore, they indicate that somatostatin, previously shown to be capable of negating the stimulatory effect of various factors on glucagon and growth hormone secretion, also affects the response of these hormones to FFA depression.
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PMID:Effect of somatostatin on metabolic and hormonal changes induced by nicotinic acid in insulin-dependent diabetics. 97 35

The effects of carbohydrate (CHO) restriction on the hypoglycemic phase of the glucose tolerance test were studied in ten normal subjects. The mean nadir plasma glucose was 64 +/- 4 mg/dl (x +/- SEM) for the control test, and 48 +/- 4 mg/dl (P less than 0.01) after 3 days of an isocaloric low CHO diet. Following the low CHO diet, six of ten subjects had a nadir plasma glucose less than 50 mg/dl, and five of these six had mild symptoms of hypoglycemia compared to no biochemical or symptomatic hypoglycemia during the control test. Hormone secretory patterns under the two experimental conditions were measured. CHO restriction produced a significant decrease in early insulin release followed by excessive insulin relative to the control test at 3-4 h of the test. Glucose ingestion produced a depression of plasma, glucagon from fasting levels during the control test, which was impaired following CHO restriction. Plasma growth hormone and cortisol responses were not different under the two experimental conditions. These studies demonstrate that CHO restriction followed by concentrated CHO ingestion produces hypoglycemia in normals. They emphasize the need to consider dietary history in evaluation of hypoglycemia. CHO restriction may provide a useful model for further study of the mechanisms of hypoglycemia.
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PMID:Effects of carbohydrate restriction on the hypoglycemic phase of the glucose tolerance test. 99 13

The incidence of significant arrhythmias and ST segment changes during barium enema examination (BE) was evaluated by Holter monitoring of 58 unselected patients over the age of 60 years. Forty percent of the group developed new significant arrhythmias of which the most common were frequent and/or multifocal premature ventricular contractions. Seven percent demonstrated ST segment depression. Administration of glucagon did not diminish the incidence of arrhythmias. Predictive factors for ECG abnormalities were advancing age, abnormal pre-BE-ECG, and pre-BE orthostatic hypotension. Analysis of arhythmias and response to phywiologic tension. Analysis of arrhythmias and response to physiologic manoeuvres suggested that the abnormalities were related to increased sympathetic tone which may be intensified by hypovolaemia resulting from routine bowel preparation.
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PMID:Predictive factors and mechanism of arrhythmias and myocardial ischaemic changes in elderly patients during barium enema. 100 Jan 70

Animal experiments have suggested a FFA control mechanism for glucagon secretion. In man, the potent effect of FFA on HGH secretion and the similarity of the secretory control mechanisms for HGH and IRG also support a role of FFA in IRG secretion. Our studies in man in which plasma FFA were elevated by either an oral lipid emulsion (Lipomul) or an intravenous lipid suspension (Intralipid)suggest only a minor role of lipids in control of IRG secretion. Plasma FFA and triglyceride elevations did not suppress arginine- or hypoglycemia-induced plasma IRG elevations, but an inhibitory effect of Intralipid on basal plasma IRG concentrations was observed. Although nicotinic acid administration, which caused a depression in plasma FFA, did elevate plasma IRG, the IRG elevation was considered more likely a consequence of stress induced by the drug. The failure of lipids to inhibit IRG secretion at FFA concentrations inhibiting HGH secretion indicates a dissociation in the secretory control mechanisms of the two hormones.
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PMID:Effect of lipids on glucagon secretion in man. 111 Jun 25

The tissue response to exogenously administered glucagon was examined in 5 obese subjects (180 plus or minus 20 percent ideal body weight) and compared with the response in 5 normal weight controls (plus or minus 10 percent of ideal body weight). In all control subjects, glucagon (1 mug/kg) caused an increase in plasma free fatty acids and betahydroxybutyrate concentrations. In contrast, not only did the obese subjects fail to demonstrate a similar catabolic response, but 4 of the 5 obese subjects actually responded with a depression of plasma free fatty acid concentration and 3 of the 5, a decrease in betahydroxybutyrate. The potential mechanisms responsible for this defect are discussed, and it is suggested that the observation of an abnormal tissue response to a pharmacological stimulus warrants further investigation utilizing physiological lipolytic stimuli.
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PMID:Altered tissue response to glucagon in obesity. 112 83

Glucagon in a dose of 50 mug/kg body weight was studied for its cardiovascular effects in hypovolemic dogs in which coronary blood flow was reduced to an average 40% of its control value and cardiac depression was evident. Myocardial contractility, as judged mainly by dP/dt and acceleration of aortic blood flow, was brought to a normal level for a short time. Systemic and coronary vascular resistances were markedly reduced. These effects were similar in normovolemic dogs. The inotropic, chronotropic, and peripheral vascular effects of glucagon can be evoked also in hypovolemic dogs in which coronary blood flow is less than normal and myocardial metabolism is impaired.
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PMID:Cardiovascular response to glucagon in hypovolemic dogs. 113 18


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