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

In vivo effect of glucagon on blood-free fatty acid (FFA) concentration was investigated in rats adapted to 25 degree C and to 5 degree C. Intraperitoneal injection of glucagon in 100 or 25 mug/100 g body weight doses was followed by a triphasic response in blood FFA concentration: an immediate and marked rise at 5 min, a secondary depression at 60 min and a final rise at 120 to 240 min after the injectionss. For the 12.5 and 6.25 mug/100 g body weight injections, an initial increment was significantly lowered and no elevation at 240 min was observed. Concomitant elevations of blood glucose concentration were shown 5 min after glucagon injection of 100, 25, 12.5, and 6.25 mug/100 g body weight doses and their extents were not significantly different each other between these doses. However, rise in blood glucose level at 60 min was not seen at the 12.5 and 6.25 mug/100 g body weight doses. Blood lactate concentrations did not show any significant variations by the injections of glucagon. In fasting rats, glucagon at the 100 mug/100 g body weight dose caused similar increase in blood FFA as that in fed ones. In fed cold-adapted rats at 5 degree C glucagon at the dose of 100 mug/100 g body weight brought about similar effects in elevation of blood FFA level and its time-course as those in fed rats adapted to 25 degree C. However, under fasting condition cold-adapted animals exhibited greater increment in blood FFA level at 5 min than those adapted to 25 degree C, while an elevation of blood FFA at 240 min was not observed in the former animals. These results indicate for the first time an in vivo lipolytic action of glucagon in rats and further suggest an enhanced sensitivity to lipolytic action of glucagon in cold adaptation.
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PMID:In vivo lipolytic effect of glucagon in warm-adapted and cold-adapted rats. 117 71

The systolic time intervals and calculated parameters of PEP/LVET (pre-injection period/left ventricular ejection time-ratio) and 1/PEP2 before and after induction of anaesthesia with the barbiturate enibomal (Narcodorm) were studied noninvasively in eight surgical patients after pre-treatment with a bolus dose of glucagon. The mean difference between the PEP/LVET-ratio before and after induction was 0.06, and the mean difference between 1/PEP2 before and after induction was -8. The corresponding values in the control group consisting of 12 patients were 0.09 and -28, respectively, suggesting a somewhat greater depression of cardiac function in this group. However, no statistically significant difference at the 5% level was found between changes in the glucagon group and controls. The influence of barbiturates and glucagon on cardiac function is discussed.
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PMID:Influence of glucagon on systolic time intervals during induction of anaesthesia with barbiturate. 118 7

In experiments with rabbits, glucagon prolonged the half-period of absorption of sodium iodide 125J in the left ventricular myocardium. Regitine prevented acceleration of the heart rate and impairment of capillary flow after glucagon. In healthy rabbits hippurate 125J clearance was unaffected by glucagon. After injury of the heart muscle by injection of silver nitrate solution into the left ventricular wall and depression of blood pressure, glucagon partly normalized renal clearance of hippurate 125J.
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PMID:The influence of glucagon on the blood supply of the heart and kidneys in rabbits. 121 13

Quinolinic acid (Q.A.) which inhibits gluconeogenesis at the site of phosphoenolpyruvate (PEP) synthesis, reduced the content of PEP while elevating that of aspartate and malate in rat livers perfused with a medium containing 10 mM L-lactate. Glucagon at 10(-9) M did not affect Q.A. inhibition of lactate gluconeogenesis nor the depression of PEP level, but further elevated malate and aspartate accumulation. Exogenous butyrate had the same effect as glucagon on these parameters. Butylmalonate (BM), an inhibitor of mitochondrial malate transport, inhibited lactate and propionate gluconeogenesis to similar extents. The addition of 10(-9) M glucagon had no effect on BM inhibition of lactate gluconeogenesis, but almost completely reversed BM inhibition of propionate gluconeogenesis. These results suggest that glucagon may act on at least two sites, resulting in elevated hepatic gluconeogenesis. First, it may stimulate dicarboxylic acid synthesis (malate and oxaloacetate, specifically) through activation of pyruvate carboxylation. Secondly, it may stimulate synthesis of other dicarboxylic acids (fumarate, for example) by activating certain steps of the tricarboxylic acid cycle. The stimulatory effect of glucagon on gluconeogenesis in the perfused rat liver is well documented (1, 2). Exton et al., who earlier located the site of stimulation between pyruvate and PEP synthesis (3), proposed that glucagon stimulated PEP synthesis in the perfused rat liver (4), while reports from Williamson et al. (5) suggested the pyruvate-carboxylase reaction as the site of glucagon action. Stimulation at sites above PEP formation and of portions of the tricarboxylic acid cycle (4) by glucagon have also been suggested (6). In the present experiments, we have used substrates entering at different parts of the gluconeogenic pathway, and specific inhibitors to further resolve the action of glucagon.
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PMID:Effects of glucagon on gluconeogenesis from lactate and propionate in the perfused rat liver. 125 Aug 74

This study's objective is to evaluate the ability of glucagon and amrinone to reverse propranolol induced cardiovascular depression in a canine model, compared to a control of normal saline. The study design included 18 animals which received intravenous propranolol (10 mg/kg) resulting in significant depression in heart rate, cardiac output, mean arterial pressure, maximal ventricular dP/dt and stroke volume. Each canine was randomly assigned to one of three treatment groups; controls (normal saline only), glucagon (20 micrograms/kg bolus) and amrinone (4 mg/kg bolus). Cardiovascular parameters were monitored at 1, 6, 11, 21 and 31 min after treatment was rendered. Multiple comparison procedures at each time period controlled the overall alpha-level at .05. Compared to control animals, both amrinone and glucagon were effective in reversing propranolol-induced depression of dP/dtmax at 6 and 11 min for glucagon and 11 min for amrinone and cardiac output at 1, 6 and 11 min for glucagon and 1 min for amrinone. Amrinone and glucagon significantly increased stroke volume over control values at 1 min and tended to do so at the remaining time periods. The two days caused a similar degree of arteriolar vasodilation which was significantly greater than that seen in control animals at 1 and 6 min. Beta blocker induced bradycardia did not respond significantly to amrinone while glucagon induced a tachycardia which is unique to canines. It is concluded that in this canine model, amrinone appears to be an effective therapeutic alternative to glucagon for reversing depressed dP/dtmax, cardiac output and stoke volume induced by propranolol toxicity. Unlike glucagon, amrinone appears to lack positive chronotropic activity which may limit its clinical utility in the treatment of beta blocker overdose.
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PMID:A comparison of amrinone and glucagon therapy for cardiovascular depression associated with propranolol toxicity in a canine model. 151 13

This study was designed to investigate the effect of short-term, submaximal training on changes in blood substrates, metabolites, and hormonal concentrations during prolonged exercise at the same power output. Cycle training was performed daily by eight male subjects (VO2max = 53.0 +/- 2.0 mL.kg-1.min-1, mean +/- SE) for 10-12 days with each exercise session lasting for 2 h at an average intensity of 59% of VO2max. This training protocol resulted in reductions (p less than 0.05) in blood lactate concentration (mM) at 15 min (2.96 +/- 0.46 vs. 1.73 +/- 0.23), 30 min (2.92 +/- 0.46 vs. 1.70 +/- 0.22), 60 min (2.96 +/- 0.53 vs. 1.72 +/- 0.29), and 90 min (2.58 +/- 1.3 vs. 1.62 +/- 0.23) of exercise. The reduction in blood lactate was also accompanied by lower (p less than 0.05) concentrations of both ammonia and uric acid. Similarly, following training lower concentrations (p less than 0.05) were observed for blood beta-hydroxybutyrate (60 and 90 min) and serum free fatty acids (90 min). Blood glucose (15 and 30 min) and blood glycerol (30 and 60 min) were higher (p less than 0.05) following training, whereas blood alanine and pyruvate were unaffected. For the hormones insulin, glucagon, epinephrine, and norepinephrine, only epinephrine and norepinephrine were altered with training. For both of the catecholamines, the exercise-induced increase was blunted (p less than 0.05) at both 60 and 90 min. As indicated by the changes in blood lactate, ammonia, and uric acid, a depression in glycolysis and IMP formation is suggested as an early adaptive response to prolonged submaximal exercise training.
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PMID:Early adaptations in blood substrates, metabolites, and hormones to prolonged exercise training in man. 178 5

Cold-restraint stress was found to produce a depression in hepatic glutathione content and to elevate circulating catecholamine levels in four mouse strains--ICR, NIH, B6C3F1, and ND/4. Serum norepinephrine concentrations were significantly elevated after cold-restraint (2--3 h) in all strains, and serum epinephrine levels were increased in the B6C3F1 and ND/4 strains. In time-course studies conducted using ND/4 mice, the decline in hepatic glutathione concentrations was found to slightly precede increases in serum epinephrine and norepinephrine concentrations. Also, pretreatment with phentolamine, an alpha-adrenoreceptor antagonist compound shown in previous studies to block epinephrine-induced hepatic glutathione suppression, had no effect on glutathione losses from cold-restraint. These observations are inconsistent with catecholamines as sole mediators of cold-restraint induced hepatic glutathione depression. Two other endogenous substances elevated during stress, corticosteroids and glucagon, were found to diminish glutathione concentrations in the liver in ND/4 mice when administered exogenously. The effects of catecholamines (epinephrine), corticosteroids (hydrocortisone) and glucagon were not additive, i.e. the depression in glutathione when these agents were administered in combination was generally no greater than that induced when the most effective agent was administered alone. It is postulated that during cold-restraint stress multiple endogenous agents are released which are independently capable of causing a depression in hepatic glutathione content.
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PMID:Examination of the role of catecholamines in hepatic glutathione suppression by cold-restraint in mice. 201 63

The present study was performed to determine whether alterations in fuel reserves or energy substrate utilization might explain the performance decrements that occur in bacterial infections. Male Fisher-Dunning rats were studied at 24, 48, and 72 h after inoculation with Streptococcus pneumoniae. Rats were either sedentary or subjected to a 2-h swimming session at these three time points (N = 10 in each group). A more than 60% reduction (P less than 0.01) in performance capacity was observed on day 3 of infection compared with that in noninfected controls. This infection in the rat is characterized by fever (P less than 0.01), depression of plasma zinc (P less than 0.01) and free fatty acid (FFA) levels (P less than 0.01), inhibition of the two- to threefold increase in fasting ketonemia, and a decreased (NS) insulin:glucagon ratio, indicating a catabolic state. Glycogen stores were reduced in the heart (47%), liver (43%), and skeletal muscles (39%) but not in the carcass. Superimposed exercise resulted in a further reduction but not depletion of liver, muscle, and carcass glycogen stores, a less pronounced lactic acid accumulation, and a lower oxygen debt. However, plasma FFA and ketone body levels were still maintained or even elevated, suggesting that fat is supplied as fuel during swimming exercise in this infection. Thus, results indicate that unavailability of energy substrates or lactacidosis is not limiting for performance capacity during this severe infection.
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PMID:Metabolic responses to swimming exercise in Streptococcus pneumoniae infected rats. 205 98

Daily cyclosporine doses of 10 mg/kg body weight for 21 days in Wistar rats cause impairment in glucose homeostasis and changes in the amount of immunostainable hormones and in the ultrastructure of the cells of the pancreatic islets. CsA induces hyperglycemia and reduced glucose tolerance, and causes a decrease in immunoreactive insulin and an increase of somatostatin and pancreatic polypeptide (PP) immunoreactivities, leaving glucagon immunoreactivity unaffected. Ultrastructurally, different degrees of dilation of rough endoplasmic reticulum cisternae and enlargement of Golgi apparatus can be observed in B cells, together with a pronounced reduction in the number of secretory granules. Nevertheless, there were no apparent morphological changes of the other cytoplasmic organelles, suggesting that the drug, besides a depression of protein synthesis, as previously stated, also induces a substantial defect in granulogenesis, probably due to impairment in the intracellular transport of the hormone from the sites of synthesis to the secretory granules. The B cell alterations are not accompanied by any sign of B cell degeneration or death. Non-B cells did not show any of the ultrastructural changes found in B cells and were similar to those of the control rats. The above findings indicate that CsA at immunotherapeutic doses causes impairment in the secretory processes of B cells specifically. An hypothesis on the mode of action of CsA on B cells is drawn.
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PMID:Immunocytochemical and ultrastructural changes of islet cells in rats treated long-term with cyclosporine at immunotherapeutic doses. 218 26

Nine patients with psoriasis vulgaris were treated for 12 weeks with somatostatin analog, octreotide acetate (SMS 201-995) 50 or 100 micrograms by subcutaneous injection every 12 hours. The purposes of the study were to determine: (1) levels of insulin, glucose, glucagon, pancreatic polypeptide (PP), and SMS 201-995 after a subcutaneous injection of SMS 201-995 and ingestion of a standardized meal; (2) nocturnal (0200 h) thyroid stimulating hormone (TSH) levels before, during, and after treatment; and (3) the pharmacokinetics of SMS 201-995. Insulin peaks at 30 minutes were blunted from 65.8 +/- 11.0 mu U/mL without treatment to 26.7 +/- 8.6 mu U/mL and 7.7 +/- 2.0 mu U/mL after the 50- and 100-micrograms doses, respectively. Glucagon levels remained constant during the meal and were not affected by the 50-micrograms dose. Mean glucose levels were significantly elevated during insulin suppression. PP was also rapidly suppressed by SMS 201-995 and remained so for 4 hours after the injection. Nocturnal TSH was blunted after 12 weeks of treatment (P less than or equal to .05). T4 and T3 resin uptake showed no depression, and patients remained clinically euthyroid. The plasma peak of SMS 210-995 occurred 30 minutes postinjection and half-life was longer than 2 hours. After chronic administration of SMS 201-995, insulin was suppressed with resultant mild carbohydrate intolerance that persisted throughout the treatment course.
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PMID:Treatment of psoriasis with chronic subcutaneous administration of somatostatin analog 201-995 (sandostatin). II. Effect on pancreatic and thyroid hormone. 240 89


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