Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of glucagon administered as a bolus (1 mg) followed by a continuous infusion (2 mg/h) for 8 h and a placebo was compared in 37 adults with urographically demonstrated ureteral calculi less than 6 mm. The bolus injection was given 20 min after start of intravenous urography, and the infusion was initiated immediately afterwards. No effect on pain relief or passage of calculi was found. Nausea and/or vomiting were recorded significantly more frequently in patients who had glucagon than in patients who had the placebo. It is concluded that glucagon is of no value in acute ureteral colic.
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PMID:Glucagon in acute ureteral colic. A randomized trial. 394 97

Beta antagonists competitively block beta 1-adrenoceptors that mediate both the rate and force of myocardial contraction. Their precise mechanism of anti-anginal action is uncertain. A reduction in oxygen demand may relative pain and improve effort tolerance. Alternatively inhibition of the adrenergic drive to contraction may offset the increased ventricular wall tension due to incomplete relaxation. Partial agonist activity in a beta-antagonist does not influence efficacy nor protect against airflow obstruction. Membrane stabilising activity is clinically trivial. Cardioselectivity makes airflow obstruction less likely at low but not at high blood concentrations of drug. Alpha-receptor antagonism may also prevent broncho-constriction; it has not been assessed in coronary vasospasm. The dosage and choice of drugs are based on pharmaco-kinetic and dynamic data in animals and man. The major side-effects of beta-blockade are heart failure and airflow obstruction. Cardiotoxicity from overdosage may be treated with isoprenaline, dopamine or glucagon while beta 2-agonists will reverse bronchoconstriction. Since beta-antagonists raise-peripheral vascular impedance, reduction of preload with nitrates enhances their antianginal efficacy. Combining a beta-antagonist with nifedipine seems especially useful. Beta-blockade is worth trying in angina with normal coronary arteries. In acute coronary insufficiency beta-blockade reduces both the work-load on the heart and the somatic features of anxiety, so preparing patients for investigations, like coronary arteriography, aimed at definitive treatment.
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PMID:Clinical pharmacology of beta-adrenoceptor antagonism in angina pectoris: an overview. 611 11

Single injections of epinephrine significantly lowered the hepatocellular levels of reduced glutathione (GSH) while producing small but significant elevations in serum glutamic-pyruvic transaminase (SGPT) activity. Hormones, i.e. glucagon and the corticosteroids, were also found to depress significantly hepatic glutathione. Based upon the agonist-antagonist studies performed, the hepatic GSH lowering effects of epinephrine appear to be mediated solely by alpha 2 receptors. Adrenergic antagonists with alpha 2 receptor blocking properties, phenotolamine and yohimbine, prevented the epinephrine-induced lowering of GSH while agonists with alpha 2 activity, clonidine and guanabenz, mimicked epinephrine's response. Antagonists with either alpha 1 or beta activity, i.e. prazosin, phenoxybenzamine and propranolol, did not prevent the epinephrine-induced lowering of hepatic GSH. Contrary to these findings antagonists with either alpha or beta receptor blocking activity significantly reduced the epinephrine-induced elevations in SGPT activity. Thus, there was no apparent relationship between the elevation of SGPT activity and the reduction in hepatic glutathione levels. It is concluded that the therapeutic administration of these compounds, or physiologic responses to stress or pain, may exacerbate the hepatotoxicity of compounds detoxified by GSH or alter important glutathione-mediated hepatocellullar processes.
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PMID:The perturbation of hepatic glutathione by alpha 2-adrenergic agonists. 613 90

Polypeptides are endogenous agents, involved in the regulation of many physiologic functions and the pathogenesis of several diseases. Polypeptide antagonists form a group of new chemical entities which may provide valid therapeutic agents. Some polypeptides (angiotensin, kinins) are released through the action of proteolytic enzymes (renin, kallikreins) and act as hormones or autacoids; others (substance P, neurotensin) are synthetized by nervous cells to serve as neurotransmitters or neuromodulators. The main homeostatic role of the renin-angiotensin system is to uphold high systemic arterial blood pressure. Overproduction of renin and insufficient checking of renin secretion are among the most common causes of arterial hypertension. Several forms of arterial hypertension (neurovascular, idiopathic) benefit from a reduction in renin-angiotensin system activity. This is achieved either through decreasing renin secretion, by inhibiting conversion of angiotensin I into angiotensin II, or through blocking the peripheral actions (at the receptor sites) of angiotensin II. Renin secretion is very significantly reduced by beta-blocking agents (propranolol); conversion of angiotensin I into angiotensin II is inhibited by teprotide, captopril and their derivatives; peripheral actions of angiotensin II are blocked by saralasin. Bradykinin and related agents produce vasodilation, increase vascular permeability and stimulate pain fibers. Kinins thus reproduce the cardinal features of inflammation and are held to be mediators of the inflammatory reaction. The substance P neuropeptide is found in the brain and bowel; it may act as a transmitter of the sensation of pain at the spinal cord and central nervous system sites. Among other effects outside of the brain, substance P is a potent vasodilator and inhibits renin secretion. Neurotensin is a neuropeptide which produces hypothermia, muscular relaxation and analgesia. Outside of the brain, this peptide is involved in the regulation of gastric secretion, intestinal motility and insulin and glucagon secretion. The vasoactive intestinal peptide, found in certain cholinergic nerve endings, is a large peptide which inhibits gastric secretion, intestinal motility and vascular tone.
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PMID:[Polypeptides and antagonists]. 620 6

Recent neuroanatomical and behavioral evidence has indicated that vasopressin (VP) increases pain thresholds. In the present study intracerebroventricular (ICV) administration of both arginine VP (AVP: 75-500 ng) and 1-deamino-8-D-arginine vasopressin (DDAVP: 150-500 ng) elevated tail flick latencies. Oxytocin (OXY, ICV), also elevated tail-flick latencies (150-1000 ng); however this increase was accompanied by "barrel-roll" seizure activity. VP analgesia was eliminated by pretreatment with 1-deamino-penicillamine-2(O-methyl)tyrosine-AVP (dPTyr(me)AVP: 500 ng, ICV), a VP antagonist, but not naloxone (1 or 10 micrograms, ICV), suggesting that VP modulates nonciceptive thresholds through its own binding sites. Conversely, pretreatment with naloxone (1 micrograms, ICV) but not dPTyr(me)AVP (1 microgram, ICV) attenuated the analgesic efficacy of systemic morphine (10 mg/kg), further dissociating VP and central opiate analgesic processes. Finally, systemic pretreatment with dexamethasone potentiated VP analgesia. These data support the notion that VP is a specific non-opioid pain inhibitor.
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PMID:Vasopressin analgesia: specificity of action and non-opioid effects. 649 25

This study is a review of all cases of intussusception from December 1971 to December 1981 at the Erlanger Medical Center in Chattanooga. Only 24 cases were found. A disproportionate number of patients were white (92%). The male to female ratio was 2 to 1. There was no regular seasonal variation. Several patients were below the third percentile in weight for their ages. The most common signs and symptoms were vomiting, pain, and bleeding per rectum. The occurrence of anatomic lead points was high, and the success rate for hydrostatic reductions was low. The use of glucagon before barium enema increased the success rate of hydrostatic reduction by 75%, from four successful reductions to seven of 20 attempts.
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PMID:Intussusception: a case review. 670 21

A randomised prospective double-blind study of the effect of 1 mg glucagon intravenously was done on 51 consecutive patients with acute uretic colic. No significant difference between glucagon and placebo could be demonstrated as to pain relief or passage of calculi.
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PMID:Glucagon and ureteric colic. 671 56

Seventy-one patients with a clinical diagnosis of painful biliary tract disease have been entered into a double-blind trial of glucagon. Twenty-eight were excluded as gallstones were not proved: of the remainder, 21 patients received glucagon and 22 placebo. Glucagon-treated patients were pain free 14.26 h (+/- 2.77 s.e.m.) after commencing treatment compared to 29.14 h (+/- 6.01 s.e.m.) for the placebo group (P less than 0.05). Tenderness in the right hypochondrium showed a significant improvement when assessed at 12 h (P less than 0.02) and 24 h (P less than 0.1) for those given glucagon. A significant difference in blood glucose levels was seen between the two groups (P less than 0.05). No serious side effects were observed. Glucagon relieves the pain and tenderness associated with painful biliary tract disease more effectively than conventional therapy.
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PMID:A trial of glucagon in the treatment of painful biliary tract disease. 675 55

In a prospective clinical-experimental study, 15 consecutive patients with chronic pancreatitis, operated on because of severe pain, were examined for the effects of a duodenum-preserving resection of the pancreas head on endocrine pancreas function. This was done by means of oral and intravenous glucose tolerance testing before the operation, on the 10th or 11th day postoperatively, and 3 months after the operation. In addition to glucose levels in the peripheral venous blood, levels of insulin, C-peptide, glucagon, and pancreatic polypeptide were determined. As indicated by the k value, glucose tolerance improved postoperatively in 10 patients (66.6%); three patients (19.9%) showed no change, and one patient (6.6%) was worse. Only one patient (6.6%) developed evident diabetes mellitus immediately postoperatively. Pre- and postoperative levels of insulin and C-peptide showed no significant differences. The fasting levels of glucagon were significantly lower postoperatively than before the operation (p < 0.01). The stimulation of pancreatic polypeptide after oral glucose was significantly lower postoperatively (p < 0.01). Duodenum-preserving pancreas head resection does not lead to an impairment of glucose tolerance in the majority of patients; a deterioration was observed only in few cases (13.3%).
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PMID:Glucose homeostasis and endocrine pancreatic function in patients with chronic pancreatitis before and after surgical therapy. 810 71

To study the role of abnormal visceral perception in the pathophysiology of the irritable bowel syndrome (IBS), we evaluated colonic tone and visceral perception during intracolonic distension using a flaccid balloon connected to a computerized barostat and placed in the descending colon of IBS patients and healthy controls. In the first part of the study, basal colonic tone and response to pharmacological (neostigmine and glucagon) and physiological (1000-kcal meal) stimuli were recorded in nine IBS patients. Colonic tone increased by 72 +/- 27% after injection of neostigmine and decreased by 88 +/- 62% after glucagon. After the meal, the maximal increase in colonic tone was 76 +/- 31% with the total response to the meal lasting 109.7 +/- 32.0 min. In the second part of the study, symptomatic responses (discomfort and pain thresholds) and pressure variations were evaluated during two different methods of distension (stepwise and intermittent) in a randomized order in the nine IBS patients and six healthy controls. Each distension method was repeated twice in IBS patients to study reproducibility. In IBS patients, the mean discomfort threshold volume was 172 +/- 76 ml when using stepwise and 167 +/- 43 ml when using intermittent distension. The mean pain threshold volume was 250 +/- 25 ml when using stepwise and 211 +/- 22 ml when using intermittent distension, this difference being statistically significant (P < 0.02). Discomfort and pain threshold volumes recorded during the first session of the same distension method were not different from those recorded during the second one.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of colonic sensory thresholds in IBS patients using a barostat. Definition of optimal conditions and comparison with healthy subjects. 813 79


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