Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. In the unanaesthetized cat, an injection of 0.75 mg of morphine into a lateral cerebral ventricle produced strong hyperglycaemia; on intravenous injection, 10 to 30 times larger doses were required. Other effects produced with both injections were shivering, pupillary dilatation, opening of the eyes, miaowing, periods of excitation, and analgesia. Between the periods of excitation the cat did not react to objects moving in front of its eyes and it had a vacant stare.2. Noradrenaline, adrenaline, and 5-hydroxytryptamine (5-HT) injected intraventricularly (250 mug, twice) depressed the hyperglycaemia due to intraventricular morphine, and noradrenaline also depressed the hyperglycaemia due to intravenous morphine. Adrenaline produced the strongest and 5-HT the weakest depression. 5-HT did not depress the other effects of morphine, but the catecholamines depressed most of them; only analgesia and the vacant stare appeared to be unaffected.3. Reserpine injected intraventricularly (0.5 mg, twice) greatly accentuated the hyperglycaemia as well as the other effects produced by intraventricular morphine, but pupillary dilatation and opening of the eyes no longer occurred; the protrusion of the nictitating membranes produced by the reserpine persisted.4. Pentobarbitone sodium injected intraperitoneally in an anaesthetizing dose practically abolished the morphine hyperglycaemia, but injected intraventricularly in a dose of a few milligrammes, it had a two fold effect: depression followed by enhancement of the morphine hyperglycaemia. The enhancement may be due to sensitization of the effect of the adrenaline released by morphine, since adrenaline hyperglycaemia was enhanced as well.5. Morphine did not seem to act on structures in the walls of either the lateral or third ventricle when producing its hyperglycaemic effect on intraventricular injection. The action may therefore be on more caudally situated parts of the neuro-axis, on the central grey, on structures in the floor of the fourth ventricle or of the lateral recesses, or even on structures near the ventral surface of the brain stem.
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PMID:The hyperglycaemic effect of morphine. 465 65

Daily oral administration of tiapamil (2 X 50-2 X 150 mg/kg, for 13 weeks) to spontaneously hypertensive rats (SHR) resulted in a dose-dependent inhibition of hypertension development, with complete prevention occurring at the highest dose. Tiapamil (2 X 100 mg/kg/day, p.o.) also prevented development of high blood pressure in deoxycorticosterone acetate-NaCl hypertensive rats (DOCA). A comparative hemodynamic analysis was carried out on age-matched (17-week-old) control SHR, tiapamil-treated (2 X 150 mg/kg/day, p.o.) SHR, and normotensive Wistar-Kyoto rats (WKY). Tiapamil-treated SHR and WKY had a significantly lower mean arterial pressure and total peripheral resistance as well as a higher cardiac output than untreated SHR. Vasoconstrictor responses to norepinephrine as well as to angiotensin I and II were significantly lower in tiapamil-treated than in untreated SHR. By contrast, isoproterenol elicited a fall in blood pressure in all three groups, the extent of which correlated directly with the magnitude of basal blood pressure levels. Tiapamil also caused a concentration-dependent depression of depolarization-induced vasoconstrictor responses in isolated mesenteric and renal arteries from SHR. The results of this study indicate that chronic administration of tiapamil will prevent the development of hypertension in SHR and DOCA rats as well as protect against accompanying hemodynamic alterations. This inhibitory effect on blood vessels that maintain peripheral resistance at elevated levels is a consequence of the vascular-selective calcium entry blocking properties of tiapamil.
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PMID:Chronic administration of tiapamil prevents hemodynamic alterations accompanying development of high blood pressure in hypertensive rats. 608 79

Continuously regenerating stratified squamous epithelia form an interesting model for examining mechanisms controlling the balance between rates of cell formation and cell maturation and death. In vitro assays of rates of glycolysis and amino acid incorporation of epidermal sheets free from dermal contamination were used to examine rates of metabolism in both normal and hyperplastic epidermis after treatment with various adrenergic agonists and cAMP. Epinephrine and isoproterenol over the concentration range of 1 x 10(-9) to 1 x 10(-5) M depressed the rates of glycolysis and amino acid incorporation in normal epidermis. Dibutyryl cyclic AMP produced a 73 to 78% depression in metabolic activity and its action was enhanced by the addition of theophylline. The alpha adrenergic agonist norepinephrine produced similar reductions. When epidermal samples were treated with hexadecane to induce a mild hyperplasia, depressant effects of isoproterenol and epinephrine were lost, but dibutyryl cyclic AMP and norepinephrine still reduced metabolic activity. The results suggest that adrenergic agents and their putative second messenger cAMP cause reductions in epidermal metabolic activity, an effect similar to their effects on cell proliferation, and that increased rates of proliferation are associated with loss of beta adrenergic responsiveness of the epidermis.
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PMID:The effects of alpha and beta adrenergic agonists and cyclic adenosine 3':5'-monophosphate on epidermal metabolism. 626 12

Adrenocortical activity varies on a circannual basis with increased secretion in the winter and decreased secretion in the summer. One consequence of this variation is a circannual pattern in immune function. Adrenal corticosteroids, especially glucocorticoids, depress cellular immune function and seem to be more effective against T-suppressor cells. Thus, when adrenocortical activity is elevated, T-cell activity is depressed and B-cell activity is elevated. To the extent that T-cell "surveillance" is depressed in winter, there should be increased lymphoproliferative cancer risk during winter and in regions characterized by cold climates. This article presents data which suggest: (1) a winter, adrenal-corticoid induced, depression of T-cell function which is accompanied by elevated B-cell function; (2) elevated serum immunoglobulin levels in the winter; and (3) an inverse relationship between ambient temperature and serum immunoglobulin levels. The circannual pattern in immune function could help explain increased lymphoproliferative cancer risk, as a side effect of immunosuppression therapy during organ transplants, and as a function of latitude.
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PMID:Circannual changes in immune function. 634 40

The role of renal production of dopamine in mediating the natriuretic response to acute vascular volume expansion was investigated. The effect of infusion of 0.9% saline (30 ml/kg X h) over 2 h on urine excretion of sodium and catecholamines, as well as other hemodynamic and renal function parameters, was examined in seven dogs during control and carbidopa (1 mg/kg every 8 h for 24 h before saline infusion) treatment periods. Acute vascular volume expansion with saline resulted in a rise (P less than 0.01) in the renal excretion of dopamine and a depression (P less than 0.01) in renal excretion of norepinephrine which paralleled the natriuretic response to saline infusion. Epinephrine excretion was not altered by saline infusion. Carbidopa treatment was not associated with changes in left ventricular filling pressure, arterial blood pressure, glomerular filtration rate, renal blood flow, renal excretion of norepinephrine or epinephrine. However, carbidopa eliminated the increase in renal production of dopamine and markedly attenuated the natriuretic response to saline infusion. Since carbidopa blocks tissue conversion of dopa to dopamine, it appears that renal production of dopamine is an important mechanism mediating the natriuretic response to acute volume expansion.
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PMID:Relationship between urinary dopamine production and natriuresis after acute intravascular volume expansion with sodium chloride in dogs. 649 62

The investigation of catecholamine (CA) metabolism in animals subjected to various types of stress (different pain syndromes; cranial trauma; immobilization; cooling) and physical exercise shows considerable similarity among species in the sequence of changes, leading from the activation to the depletion of the sympathoadrenal system. The changes caused by physical exercise tend to be more pronounced in individuals with a genetic predisposition to greater stress responses. Stress adaption, induced by special training or by long-duration exposure to hypoxia, can substantially prevent the changes caused by physical exercise. Trained rats at rest show accelerated CA turnover, and after exercise, adaptive hypometabolic changes. Physical exercise causes both unspecific changes in CA metabolism, similar to those seen after other types of stress, and more specific ones, i.e., suppression of tissue CA synthesis and nonresponsiveness to exogenous L-tyrosine or L-DOPA. Adrenal CA synthesis could be restored in such animals by treatment with glucocorticoids and cyclic-AMP (c-AMP). The depression of CA synthesis after hard physical activity may be a mechanism for protecting the body from the injurious effect of the excessive CA release that would occur under stress.
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PMID:Effects of physical activity and other types of stress on catecholamine metabolism in various animal species. 654 Dec 42

To test the effects of acute cold on muscle amino acid and protein 1) rats were exposed to 4 degrees C for 24 h, functionally hepatectomized (eviscerated) and accumulation in the blood used to indicate changes in amino acid release from the tissues; 2) other rats were left intact, and urinary excretion of 3-methylhistidine (proportional to muscle protein breakdown) determined during cold exposure. In the eviscerated group, cold enhanced loss of total amino acids from the tissues (as alpha-amino nitrogen), but the loss (213 +/- 14.8% of basal in 2 h) was not due to excess alanine (180 +/- 8.5%). By comparison, in fasted rats total amino acid was 182 +/- 12.3, alanine 309 +/- 17.2%. Also, the cold-induced loss resembled the effects of streptozotocin diabetes and depended on a depression by cold of serum insulin (to 35.7 +/- 2.3 muU/ml). Therefore it was prevented when insulin was restored by infusion (40 mU . 100 g-1 . h-1) or by adrenodemedullation before cold exposure. Epinephrine (10 micrograms/100 g sc) depressed insulin in the latter and permitted amino acid release to recur. In intact rats, 3-methylhistidine excretion was unaffected by cold. The results suggest that although cold fails to stimulate alanine synthesis or protein breakdown, it inhibits insulin release sympathetically, thereby diminishing the amount of amino acid incorporated into muscle protein.
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PMID:Effects of acute cold exposure on muscle amino acid and protein in rats. 704 71

Intravenous injection of xylazine (0.01-1 mg/kg) produced a dose-dependent mydriasis associated with a depression of tonic ciliary nerve activity in anesthetized cats. Xylazine-induced mydriasis was apparent in the sympathectomized iris but was absent in the parasympathectomized, physostigmine-treated iris. Epinephrine (30 micrograms/kg, i.v.) produced a slightly greater mydriasis in the sympathectomized iris than in the parasympathectomized, physostigmine-treated iris. The alpha 2-adrenergic blocking agent, yohimbine (0.5 mg/kg, i.v.) antagonized the pupillary dilation and reversed the depression of ciliary nerve activity induced by xylazine administration. In rats pretreated with reserpine (7.5 mg/kg, s.c., 20 h) and alpha-methyl-p-tyrosine (250 mg/kg, i.p., 5 h), intravenous injection of xylazine (0.01-1 mg/kg) resulted in mydriasis of similar magnitude as control animals. However, xylazine induced bradycardia in the control group but not in the pretreated animals. The results suggest that pupillary dilation produced by i.v. xylazine is primarily the result of a central inhibition of parasympathetic tone to the iris. It also appears that xylazine produces this effect via postsynaptic alpha 2-adrenergic mechanisms, while it produces bradycardia through a presynaptic alpha 2-adrenergic mechanism.
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PMID:Xylazine-induced mydriasis: possible involvement of a central postsynaptic regulation of parasympathetic tone. 734 35

The Authors have studied in a homogeneous group of rabbits the variations of intraocular pressure and of aqueous humour pH caused by instillation of timolol maleate at different concentrations. In the animals treated with drug concentration of 0,25% and 0,5% a constant reduction of IOP has been observed in comparison with controls, associated to acidification of aqueous humour: no evidence of this correlation it seems to be at low doses of timolol. Further studies are in course to indicate an eventual action of intermediate substances in the mechanism of IOP depression caused by timolol.
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PMID:[Preliminary study of acidification of the pH of the aqueous humor in rats treated with timolol maleate]. 745 18

Eight female patients (aged 51 to 65 years) with New York Heart Association class II angina pectoris, normal coronary angiograms, normal hyperventilation, and abnormal exercise stress tests (chest pain and ST depression), and 5 sex- and age-matched controls participated in this study. Epinephrine was given intravenously to both patients and controls at 5-minute intervals in doses of 0.1, 0.2, 0.3, 0.4, and 0.6 nmol/kg/min. After rest (15 minutes), the alpha-adrenoceptor antagonist phentolamine or placebo was administered intravenously to patients in a double-blind, crossover study on 2 separate occasions in doses of 250 micrograms/min for 5 minutes and 500 micrograms/min for the next 10 minutes; the epinephrine infusion was repeated. Blood pressure, heart rate, and electrocardiogram were monitored continuously and pain was estimated on the Borg CR-10 scale. On a third occasion, chest pain was induced in patients using the same epinephrine protocol during echocardiographic monitoring. In the control group, all patients received the maximal epinephrine dose. No chest discomfort or pain developed. In the patient group, the maximal tolerable epinephrine dose (0.39 +/- 0.19 nmol/kg/min) decreased diastolic pressure (-14 +/- 9 mm Hg, p < 0.01) and increased heart rate (+24 +/- 10 beats/min, p < 0.01), not statistically different from the control group. Pulse pressure increased in the patient group (27 +/- 17 mm Hg, p < 0.01) but not in the controls. Left ventricular ejection fraction at baseline was within reference limits (58% to 75%) and did not change during epinephrine infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of epinephrine infusion on chest pain in syndrome X in the absence of signs of myocardial ischemia. 757 75


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