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

A number of hemodynamic, pharmacologic and metabolic interventions were found to change the extent of acute ischemic injury of the myocardium and subsequent necrosis following experimental coronary artery occlusion. Reduction in myocardial damage occurred by decreasing myocardial oxygen demands (beta-adrenergic blocking agents, intra-aortic balloon counterpulsation, external counterpulsation, nitroglycerin, decreasing afterload in hypertensive patients, inhibition of lipolysis, and digitalis in the failing heart); by increasing myocardial oxygen supply either directly (coronary artery reperfusion or elevating arterial pO2), or through collateral vessels (elevation of coronary perfusion pressure by alpha-adrenergic agonists, intra-aortic balloon counterpulsation); or by increasing plasma osmolality (mannitol, hypertonic glucose); presumably by augmenting anaerobic metabolism (glucose-insulin-potassium, hypertonic glucose); by enhancing transport to the ischemic zone of substrates utilized in energy production (hyaluronidase); by protecting against autolytic and heterolytic damage (hydrocortisone, cobra venom factor, aprotinin). Augmentation of myocardial ischemic damage occurred as a consequence of increasing myocardial oxygen requirements (isoproterenol, glucagon, ouabain, bretylium tosylate, tachycardia); by decreasing myocardial oxygen supply either directly (hypoxia, anemia) or through reduction of collateral flow (hemorrhagic hypotension, minoxidil) or by decreasing substrate availability glycemia). Pilot studies have been carried out in patients with hyaluronidase, nitroglycerin, intra-aortic balloon counterpulsation, beta-blocking agents and Arfonad and have shown that these interventions may also reduce myocardial damage, suggesting that the concept of reduction in infarct size following coronary occlusion is applicable clinically.
 ...
PMID:Effects of metabolic and pharmacologic interventions on myocardial infarct size following coronary occlusion. 0 95

A number of hemodynamic, pharmacologic, and metabolic interventions were found to change the extent of acute ischemic injury of the myocardium and subsequent necrosis following experimental coronary artery occlusion. Reduction in myocardial damage occurred by decreasing myocardial oxygen demands (beta-adrenergic blocking agents, intra-aortic balloon counterpulsation, nitroglycerin, decreasing afterload in hypertensive patients, inhibition of lipolysis, and digitalis in the failing heart); by increasing myocardial oxygen supply either directly (coronary artery reperfusion or elevating arterial pO2), or through collateral vessels (evevation of coronary perfusion pressure by alpha adrenergic agonists, intra-aortic balloon counterpulsation); or by increasing plasma osmolality (manitol, hypertonic glucose); presumably by augmenting anaerobi metabolism (glucose-insulin-potassium, hypertonic glucoxe insulin potassium, hypertonic glucose); by enhancing transport to the ischemic zone of substrates utilized in energy production (hyaluronidase); by protecting against autolytic and heterolytic damage (hydrocortisone, cobra venom factor, aprotinin). Augmentation of myocardial ischemic damage occurred as a consequence of increasing myocardial oxygen requirements (isoproterenol, glucagon, ouabain, bretylium tosylate, tachycardia); by decreasing myocardial oxygen supply either directly (hypoxia, anemia), through reduction of collateral flow (hemorrhagic hypotension, minoxidil), or by decreasing substrate availability (hypoglycemia). Pilot studies have been carried out in patients with hyaluronidase, nitroglycerin intra-aortic balloon counterpulsation, beta-blocking agents and Arfonad and have shown that these interventions may also reduce myocardial damage, which suggests that the concept of reduction in infarct size following coronary occlusion is applicable clinically.
 ...
PMID:Effects of metabolic and pharmacologic interventions on myocardial infarct size following coronary occlusion. 76 15

Activation of noradrenergic afferents arising from the A1 cell group of the caudal VLM excites neurosecretory AVP cells of both the supraoptic and paraventricular nuclei, thus stimulating the release of this potent vasoconstrictor into the circulation. Although this effect is mimicked by application of alpha 1-adrenoreceptor agonists to AVP cells, the excitatory effects of A1 afferents may not be mediated by activation of post-synaptic alpha 1-receptors. Evidence has also been obtained that the actions of A1 afferents are not dependent upon the release of excitatory amino acids or NPY, although the latter is co-stored with NA in A1 cells and potentiates the actions of low concentrations of NA on AVP cells. Although a projection to AVP and OXY neurosecretory cells from the A2 NA cell group of the NTS has been established, this projection does not appear to contribute directly to the control of SON AVP cell activity. Rather, NTS stimulation excites SON AVP cells via a relay projection through the A1 cell group. This pathway is likely to correspond to that involved in the stimulatory effects of haemorrhage and caval constriction on AVP secretion, although it is uncertain whether the effects of these particular stimuli are contingent upon unloading of arterial baroreceptors and atrial stretch receptors, as commonly presumed, or upon the activation of other receptors such as ventricular mechanoreceptors or chemoreceptors. On balance, current evidence suggests that the A1 projection is unlikely to be critically involved in mediating the effects of arterial baroreceptor, arterial chemoreceptor, or atrial stretch receptor activation on AVP cells.
 ...
PMID:Control of neurosecretory vasopressin cells by noradrenergic projections of the caudal ventrolateral medulla. 269 23

The sphincter of Oddi is the smooth muscle connection between the bile duct and the duodenum. Its physiological function is associated with a regular motility characterized by phasic contractions superimposed on the sphincter of Oddi baseline pressure. Recently introduced ERCP-manometry permits further studies of sphincter of Oddi pharmacology. A number of drugs have so far been studied. Sedatives of the diazepam type had no effect on the sphincter, while butylscopolaminium bromide, a typical neurotropic agent, brings about cessation of the sphincter motility for 3-8 minutes. Hymecromon lowered the sphincter baseline pressure from 9.8 to 7.8 mmHg. A 1.2 mg sublingual dose of nitroglycerin, a typical musculotropic agent, caused significant relaxation of the sphincter, and decreased baseline pressure from 8.9 mmHg to 2.9 mmHg; Sphincter motility was not affected. Morphine-like analgetics, in particular pentazocine, elevated sphincter baseline pressure, but buprenorphine and tramadol did not. Pharmacological doses of gastrointestinal hormones also affect the sphincter; CCK octapeptide, glucagon and secretin are able to decrease sphincter of Oddi baseline pressure, and CCK octapeptide abolishes sphincter motility. Sphincter of Oddi pharmacology is of clinical interest. The administration of sphincter-relaxing agents, in particular nitroglycerin and butylscopolaminium bromide, enables the endoscopist to extract small common bile duct stones without previous papillotomy. Analgetics that induce sphincter contraction and thus hinder the flow of bile and pancreatic juice, may be helpful for the treatment of pain in patients with pancreatico-biliary disease. Investigations into the effect of CCK on the healthy and diseased sphincter permit us to identify patients with sphincter dysfunction using a special CCK-provocation test.
 ...
PMID:Pharmacology of the sphincter of Oddi. 304 55

We sought to determine whether streamlining of portal venous blood occurs in normal anaesthetized rats under basal conditions and with variations in hepatic blood flow. We catheterized the ileocolic vein and injected 15 micron microspheres labeled with 85Sr and 141Ce into this vein and into the spleen, respectively. The hepatic lobar distribution of microspheres was studied in a group under basal conditions and after hepatic blood flow was increased (infusions of nitroglycerin or glucagon) or decreased (infusion of vasopressin or ligation of the superior mesenteric artery); this blood flow was measured with a constant infusion of indocyanine green. Measured results (expressed as proportion of total liver counts per minute) were compared with a reference group in which the portal vein of rats had been partially ligated 10 days prior to study and in which similarly injected microspheres that lodged in the liver were assumed to be completely mixed with portal blood. No differences were seen within groups and between the reference and experimental groups. We conclude that under these experimental conditions, portal venous blood flow appears to be distributed homogeneously between hepatic lobes.
 ...
PMID:Distribution of portal blood flow in the liver of the rat: a microsphere study. 643 27

Spasm of the sphincter of Oddi still occurs during cholecystectomy. Some reports indicate that the spasm, induced by morphine, can be reversed by injection of naloxone, nalbuphine, and glucagon. Others maintain that nitroglycerin or nifedipine can relax the sphincter of Oddi muscle. We recently encountered spasm of the sphincter of Oddi during a laparoscopic cholecystectomy and treated it successfully with intravenous nitroglycerin.
 ...
PMID:The use of intravenous nitroglycerin in a case of spasm of the sphincter of Oddi during laparoscopic cholecystectomy. 1160 16

A case of acute poisoning with amlodipine with deep hypotension, transient oliguria and clinical signs of acute heart failure was described. A woman of 23 years swallowed intentionally 60 tablets of amlodipine (600 mg). After eleven hours of ingestion she was admitted to Warsaw Poison Control Centre. She was in severe clinical condition; tachycardia and deep hypotension were the prominent signs of poisoning. There was not CNS depression. Intensive treatment with i.v. catecholamines (dopamine, norepinephrine), crystalloids (with continuous control of central venous pressure), and i.v. calcium salts (with control of plasma calcium concentration) was started immediately. The patient did not improve but got worse. Acute heart failure developed, especially of left ventricle, so i.v. crystalloids were stopped and dubutamin, morphine, nitroglycerin and glucagon were introduced. Because of oliguria and insufficient effect of high doses of furosemide four-hours hemodiafiltration was set in. The patient's condition slowly improve after third and forth day of hospitalization. The systolic blood pressure rose, heart work was really better and on sixth day--the stabilization of diastolic blood pressure was definitely achieved. The patient was discharge in good condition with heart ejection fraction of 65% measured echocardiographically.
 ...
PMID:[Deep hypotension with transient oliguria and severe heart failure in course of acute intentional poisoning with amlodipine]. 1186 80

After transplantation, hepatocytes entering liver sinusoids are engrafted, whereas cells entrapped in portal spaces are cleared. We studied whether hepatic sinusoidal dilatation will increase the entry of transplanted cells in the liver lobule, improve cell engraftment, and decrease microcirculatory perturbations. F344 rat hepatocytes were transplanted intrasplenically into syngeneic dipeptidyl peptidase IV (DPPIV)-deficient rats. Animals were treated with adrenergic receptor blockers (phentolamine, labetalol), a calcium channel blocker (nifedipine), and splanchnic vasodilators (nitroglycerine, calcitonin gene-related peptide [CGRP], glucagon). Transplanted cells were localized by histochemistry. The hepatic microcirculation was studied with in vivo videomicroscopy. Changes in cell translocations were analyzed by injection of (99m)Tc-labeled hepatocytes. Pretreatment with phentolamine and nitroglycerine increased transplanted cell entry in liver sinusoids, whereas labetalol, nifedipine, CGRP, and glucagon were ineffective. Increased deposition of transplanted cells in sinusoids resulted in greater cell engraftment. In vivo microscopy showed disruption of sinusoidal blood flow immediately after cell transplantation with circulatory restoration requiring more than 12 to 24 hours after cell transplantation. However, in nitroglycerine-treated animals, sinusoidal blood flow was perturbed less. Nitroglycerine did not meaningfully increase intrapulmonary cell translocations. In conclusion, these findings indicate that hepatic sinusoidal capacitance is regulated by alpha-adrenergic- and nitroglycerine-responsive elements. Sinusoidal vasodilatation benefited intrahepatic distribution of transplanted cells and restored hepatic microcirculation after cell transplantation. This shall facilitate optimization of clinical cell transplantation and offers novel ways to investigate vascular mechanisms regulating hepatic sinusoidal reactivity.
 ...
PMID:Hepatic sinusoidal vasodilators improve transplanted cell engraftment and ameliorate microcirculatory perturbations in the liver. 1202 17

There is universal agreement that dentists require emergency drugs to be readily available. Opinions differ as to the specific drugs that should comprise an emergency kit. This article has provided one opinion. Oxygen, epinephrine, nitroglycerin, injectable diphenhydramine or chlorpheniramine, albuterol, and aspirin should be readily available in a dental office. Other drugs such as glucagon, atropine, ephedrine, hydrocortisone, morphine or nitrous oxide, naloxone, midazolam or lorazepam, and flumazenil should also be considered. There are differences in the level of training of dentists in the management of medical emergencies [25]. Therefore the final decision should be made by the individual dentist who is in the best position to determine the appropriateness of these agents for the particular practice. Despite the best efforts at prevention, emergencies may still arise. Plans to manage these events are needed and there is the possibility that the drugs discussed above may be required. Their presence may save a life.
 ...
PMID:Emergency drugs. 1244 34

The aim of our study was to compare the secretion of amylin, as well as glucose, insulin and C-peptide at baseline and in response to glucagon stimulation in 26 lean women with gestational diabetes mellitus (GDM) and in 19 age- and BMI-matched pregnant women with normal glucose tolerance (NGT). Intravenous 1-mg glucagon stimulation test was performed 6 weeks after delivery. Fasting and stimulated glucose levels were significantly higher in GDM patients than in subjects with NGT ( p<0.01 at 0 and 6 min; glucose area under the curve (AUC), 604.8+/-41.8 mg/6 min vs. 572.4+/-52.4 mg/6 min, p<0.05). Insulin AUC was also markedly higher in GDM subjects than in healthy controls (373.9+/-144.2 micro IU/6 min vs. 283.7+/-139.1 micro IU/6 min, p<0.05). There was no difference in fasting C-peptide levels between the groups studied, but stimulated concentrations, as well as C-peptide AUC were significantly higher in patients with GDM ( p<0.01 at 1 min and p<0.005 at 6 min; AUC, 27.4+/-11.3 pmol/6 min vs. 18.4+/-6.9 pmol/6 min, p<0.01). Amylin levels were higher in GDM group in comparison to healthy subjects ( p<0.005 at 1 and 6 min; amylin AUC, 113.3+/-51.2 pg/6 min vs. 72.5+/-15.7 pg/6 min; p=0.14), but in contrast to the other hormones, did not rise in response to glucagon injection. In conclusion, our results provide evidence that in patients with GDM in the post-partum period, the levels of amylin, as well as the secretion of insulin and C-peptide remain elevated, when compared to women with NTG. Further investigations are needed to clarify the significance of this elevation as a predictive factor for the development of late maternal type 2 diabetes.
 ...
PMID:Post-partum evaluation of amylin in lean patients with gestational diabetes mellitus. 1505 46


1 2 Next >>