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)

NH4Cl was infused into the left renal artery of anesthetized dogs at 50-125 mum/kg/min for up to 110 min. Renal blood flow declined early then increased to supra-control levels during infusion. Kidneys perfused at 125 mum/kg/min for 90 min showed patchy to confluent mixtures of cortical necrosis and tubular necrosis. Experimental kidneys invariably showed lower urine osmolality than contralateral controls 48 h after perfusion. Kidneys with necrosis showed depressed creatinine clearance as well. Renal artery infusion of NH4 acetate or intravenous infusion of NaHCO3 during arterial infusion of NH4Cl prevented significant acidosis and caused minimal histological changes, but depression of urine osmolality was not prevented. It is concluded that renal ammonium concentrations up to 40 mum/liter for 90 min does not cause tubular necrosis but does impair urine concentration. Severe tissue damage followed renal exposure to high ammonium concentrations in the presence of metabolic or renal acidosis.
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PMID:Some effects of ammonium salts on renal histology and function in the dog. 0 Jun 32

Urinary arylsulphatases (E.C.3.1.6.1) A and B were increased in male rats fasted for 24 hours. Excretion of non dialysable protein nitrogen decreased whereas creatinine excretion increased. On refeeding diet arylsulphatase A activity was restored to normal whereas arylsulphatase B was not normalised. A single oral supplementation of vitamin A acetate (20 000 IU) to rats fasted for 24 hours resulted in a significant reduction of both arylsulphatase A and B eventhough no further reduction of protein nitrogen excretion was evident. In vitamin A deficient male rats significant reduction in urinary excretion of both arylsulphatases A and B occured. In a smaller number of female rats depression of only arylsulphatase A was observed. This effect of vitamin A deficiency leading to reduced urinary arylsulphatase activity was evident even at the "weight plateau" stage when no reduction in food intake or growth had occurred. These results suggest a possible direct or indirect role for vitamin A on urinary excretion pattern of arylsulphatases presumably released from lysosomes of tissues.
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PMID:Studies on urinary arylsulphatase activity in vitamin A deficient rats. 0 3

In rats, a secretin (Jorpes) intravenous infusion superimposed on an intracolonic sodium acetate perfusion elicits, with respect to control values, a significant depression of Na+ absorption (0.16 mEq./h-0.00 mEq./h.) and mucus secretion (230-40 mg.). When the hormone is superimposed upon an intracolonic infusion of acetic acid, mucus secretion is also significantly inhibited (790-340 mg.). The influence of secretin on organic anion movement was pH related. At pH values of 7.0, absorption was unchanged (0.34--0.33 mEq./h.), at pH values of 2.9, absorption was significantly reduced (0.67-0.41 mEq./h). The secretin impairment of colonic mucus secretion could influence the transport of watersoluble (Na+) and lipid soluble (acetic acid) substances, probably through changes at the "unstirred layer" level.
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PMID:Does secretin influence rat colonic absorption and secretion? 3 Oct 88

Plasma glycoprotein synthesis in normal and vitamin A-deficient rats was investigated by injecting the rats with labeled carbohydrate precursors and then fractionating their plasmas on DEAE-Sephadex. Plasma from deficient rats showed a consistent depression of 30% in the uptake of label into a peak eluting with 0.23 M NaCl. The major component of this peak was identified as the rat alpha1-macroglobulin, based on its molecular weight (800,000), its mobility on cellulose acetate electrophoresis and its ability to bind trypsin. Although the alpha1-macroglobulin synthesis appeared to be depressed by 30%, its fractional turnover rate was not affected by vitamin A deficiency (t 1/2 = 18 hours). The trypsin-binding ability of this glycoprotein was used as a comparative measure of its concentration, and the results confirmed that serum levels of this glycoprotein were lower in deficient rats. In severe deficiency, alpha1-macroglobulin levels dropped to between 10% and 20% of normal levels.
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PMID:A plasma glycoprotein depressed in vitamin A deficiency in the rat: alpha 1-macroglobulin. 6 42

The antiarrhythmic activity of flecainide acetate (R-818), 2 mg/kg, was investigated in anesthetized, open-chest pigs. Ventricular arrhythmias were provoked by reducing the flow in the left anterior descending coronary artery (LAD) to 25% of control during 30 min. During this period ventricular fibrillation occurred in 33% (11 out of 33) of control animals against 12.5% (1 out of 8) of animals treated with flecainide. Ventricular tachycardias were seen in 42% (14 out of 33) of the untreated animals as compared to none of the animals previously treated with flecainide. Total number of ventricular arrhythmias was significantly lower in the treated than in the untreated animals (p less than 0.05). However, when the LAD was occluded completely at its distal part, ventricular fibrillation occurred in all animals (5 untreated and 6 pretreated with flecainide). Time to onset of ventricular fibrillation was the same for both groups of animals, despite a lower incidence of preceding ventricular arrhythmias in the pretreated group. Flecainide depressed myocardial contractility (LVdP/dt max), caused hypotension, and increased QRS width. Both myocardial depression and widening of QRS are related to arterial plasma levels of flecainide. Therefore, a slower infusion rate than the 1 mg/kg per minute used in this study is advisable when myocardial function is impaired.
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PMID:Antiarrhythmic and hemodynamic actions of flecainide acetate (R-818) in the ischemic porcine heart. 9 25

Previous in vitro studies of the metabolism of the peripheral nerve have been based on incorporation of radioactive precursor into components isolated from whole nerve. In this study we have determined incorporation secifically into myelin components of peripheral nerve by isolating myelin after incubating whole nerves with lipid or protein precursors and by determining the specific activity of the components of that membrane. The effect of diabetes on such incorporation was also studied. In the rat, in vitro incorporation of DL-[1-14C]leucine into protein components of myelin was decreased by 30-88% in diabetic animals as compared to controls. The major polypeptide constituent of rat sciatic nerve myelin (mol st 28,000; 58.5% of total mass of proteins) was not labeled in either the diabetic or the control group. In diabetes incorporation rate into a polypeptide of mol wt 23,000, which constitutes 21% of total mass, was approximately one half that of controls. In polypeptides of mol wt 38,000-49,000, which are heavily labeled in normal animals, but constitute only about 5% of total mass of proteins, depression of incorporation was e-en more marked in the diabetics. While these marked differences in incorporation between diabetic and control animals were observed, the amount of protein and its distribution among the constituent polypeptides was the same in both groups. In young rats made diabetic with streptozotocin and young rabbits made diabetic with alloxan, there was a lower rate of incorporation of the lipid precursors, [1-14C]sodium acetate or [3H]water, into myelin components. In older animals of both species incorporation in the controls was considerably lower than in the yount animals, and the effect of diabetes was no longer apparent. In nondiabetic animals, the in vitro addition of insulin (10-7 M) stimulated incorporation of DL-[1-14C]leucine into myelin proteins 1.6-3.1 times that of controls. This stimulation by insulin in vitro was not seen in diabetic animals. In animals in which diabetes had spontaneously recovered, however, incorporation rate in the in vitro experiments approached that of controls and were significantly above that in animals whose diabetes persisted. Since myelin is the palsma membrane of the Schwann cell, these studies provide evidence that the Schwann cell is affected by insulin and that some aspects of the metabolism of myelin are altered in insulin-deficient states.
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PMID:Metabolism of peripheral nerve myelin in experimental diabetes. 12 35

175 women of reproductive age, with hirsutism of differing degrees and different pathogenetic causes (ovarian, adrenal, iatrogenic) or idiopathic, and acne were treated with two different combinations of Cyprotrone acetate and ethinyl estradiol (SH 8.1041 and SH B209AB). 90 patients were given SH 8.1041 and 10 were given SH B209AB. 75 received both preparations. The total number of treatment cycles was 1534. Clinical, hormonal and biochemical assessments were made before, during and after treatment. The degrees of hirsutism and acne, and of seborrhea and hair loss when present, were scored by means of a modified version of the Ferriman and Gallway criteria. SH 8.1041 brought about a significant improvement in the majority of the patients. SH B209AB was generally used as maintenance therapy for hirsutism and severe acne. It was the initial treatment of choice in patients with milder acne. Reduction of hirsutism was usually apparent after the fourth cycle of therapy and acne regressed after the first month. Both combinations were well-tolerated biochemically. In a few patients on SH 8.1042, slight and transient increases in BSP, SGOT, SGPT and bilirubin were observed, but cessation of treatment was not necessary. Some patients on SH 8.1041 complained of transient frigidity, mild depression, breast discomfort and nausea.
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PMID:Treatment of hirsutism and acne in women with two combinations of cyproterone acetate and ethinylestradiol. 14 May 76

These experiments were designed to examine the mechanisms involved in the renal excretion of the non-nutritive sweetener, saccharin. Renal transport of saccharin in female rats was quantitatively evaluated using renal cortical slices in vitro and renal clearances in vivo. Renal cortical slices actively accumulated saccharin. Accumulation was oxygen dependent, saturable and reduced in the presence of metabolic inhibitors (2,4-dinitrophenol and sodium azide) and other organic anions 1p-aminohippurate (PAH) and probenecid]. Furthermore, addition of acetate or lactate to the medium stimulated saccharin uptake whereas reducing potassium concentration in the medium significantly decreased saccharin accumulation. Addition of saccharin to medium containing PAH and N-methylnicotinamide produced a dose-related depression of PAH accumulation. Although N-methylnicotinamide accumulation also was reduced, the depression was not dose-related. The saccharin/inulin clearance ratio of 3.76 indicates that saccharin, like PAH, undergoes tubular secretion. These findings suggest that the primary route of renal elimination of saccharin is active tubular secretion. It is also suggested that saccharin and PAH may share a common transport system.
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PMID:Renal tubular transport of saccharin. 14 38

Experiments on cats determined that ammonium acetate injected intravenously (2-4 mM/kg) supressed the processes of primary afferent depolarization (PAD) which are thought to be responsible for the presynaptic inhibition of spinal reflexes. The supression was transient and proceeded in paralle to depression of postsynaptic inhibition of monosynaptic reflexes. Ammonium acetate slightly decreased the amplitude of the negative postsynaptic potentials recorded form the dorsal surface of lumbar cord in response to stimulation of hind limb afferent nerves and increased polysynaptic reflex discharges in appropriate ventral roots. These findings make it unlikely that the ammonium depression of PAD is a result of impairment of interneuronal activity. A suggestion is made that ammonium depression of PAD results from diminition of the EMF for synaptic currents producing PAD.
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PMID:[Effect of ammonium acetate on depolarization processes in the central terminals of primary afferents]. 19 May 47

A synthetic steroid compound derived from testosteron (isoxazol-ethisterone), Danazol, with gonadotropin-depressing activity, was used in the treatment of 4 cases of idiopathis sexual precocity (age 2 1/2 to 4 years) and in 10 cases of severe pubertal gynaecomastia. In sexual precocity the suppression of menstruation as well as of breast-enlargement was good, while the suppression of acceleration of longitudinal growth and bone maturation was inferior compared with cyproteron-acetate. In most boys with gynaecomastia a marked regression of breast enlargement occurred within a few weeks or months. With the dosage used (200-300 mg/day in the sexual precocity patients, 300-400 mg in the gynaecomastia patients) the changes in plasma hormone levels (LH, FSH, progesterone, estradiol, testosterone) were within a non significant range. Depression of testosterone seemed to be a rather regular finding. No untoward side-effects of the medication were noticed in the 14 patients studied. In summary, Danazol did not show any advantages compared with the compounds used in the treatment of isosexual precocity sofar. In contrast, the drug proved to have useful effects in pubertal gynecomastia, a condition which in severe degrees certainly deserves medical treatment.
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PMID:[A new antigonadotropin in the treatment of precocious puberty and pubertal gynaecomastia (author's transl)]. 19 73


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