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)

Rats fed a Purina or low-iodine diet (LID) for varying periods were serially sampled before and after a single iv injection of T4, T3, iodide or saline. Suboptimal replacement doses of T4 and T3 were given to rats fed LID for 2 months or 1 year (basal TSH, approximately 1000 and 2000 muU/ml, respectively). Both 1 mug T4 and 0.25 mug T3/100 g BW dropped plasma TSH to 70% of the initial level at 15 min and to 10--20% at 4 h. By 12 h TSH had begun to rise in 2-month LID rats, followed by a secondary decline 3--5 days after injection. Statistical comparison of the slopes of the initial TSH decline indicated there was no significant difference between the effect of T4 and T3. There effect of graded doses of T3 (0.01--0.3 mug/100 g) was also examined. There was a highly significant correlation of the magnitude of TSH suppression with the dose of T3 administered. Saline had no effect but 0.65 mug iodide/100 g BW (equal to that in 1 mug T4) had a delayed effect, depressing TSH to a minimum of 25% of the initial value at 48 h in 2-month LID rats. There was no difference in the effect of these doses of T4, T3, or saline in purina-fed rats (basal TSH, 170 muU/ml). T4 or T3 in physiologically equivalent doses thus produces an identical prompt rate of decrease in plasma TSH, indicating that both hormones possess intrinsic hormonal activity. The delayed effect of iodide is presumably because it must first be incorporated into T4 and T3 and secreted by the thyroid gland. The similarity of depression of plasma TSH by thyroid hormones or saline injection in Purina-fed rats is believed due to a nonspecific stress effect in these animals with a low basal rate of TSH secretion. The non-specific inhibition of TSH secretion is minimal in the iodine-deficient rats with a much higher basal rate of TSH secretion, presumably because of relative vectorial influences.
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PMID:Acute effects of thyroxine, triiodothyronine, and iodide on thyrotropin secretion. 119 14

A radioimmunoassay for rabbit luteinizing hormone (rLH) in which rLH shows no significant cross-reaction with human LH (hLH) or human chorionic gonadotropin (HCG) was employed to test for the existence of a short-loop feedback for LH in the rabbit. Two weeks after castration, hCG and hLH were administered intravenously to rabbits, and the effects on circulating rLH were measured. Purified hLH (10 ng or 100 IU) produced significant depression of blood rLH within 30-60 min of intravenous injection. Saline administered to the same animals produced no changes in rLH. Injection of hCG (2,000 IU) under the same conditions also produced a significant fall in rLH. However, hCG administered to rabbits castrated 6 wk prior to study failed to suppress endogenous rLH. These data demonstrate, by direct radioimmunoassay quantification of blood hormones, the existence of a short-loop negative feedback for LH in the rabbit. They also suggest that the sensitivity of the short-loop changes with time after castration.
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PMID:Short-loop feedback control of luteinizing hormone in the rabbit. 126 22

Saline extracts of burn eschar (CEBE) and normal skin (CENS) caused inhibition to mitochondrial respiration and inner membrane function. Ethyl acetate extracts from CEBE (D1) and CENS (D'1) caused depression of the Respiratory Control Ratio, (RCR), an inhibition of respiration rate in state 3 and stimulation to state 4 respiration. Excellent linear correlations exist between the degree of inhibition to state 3, rate of stimulation to state 4 respiration and the logarithm of doses of D1 and D'1. The effective dose ranges (0.75-0.25 mg/ml for D1 and 4-1 mg/ml for D'1) differ by one order of magnitude. The activity of NADH dehydrogenase and succinate dehydrogenase of mitochondria after incubation with the highest toxic dose of D1 or D'1 remained normal. Dinitrophenol (DNP)-stimulated respiration was moderately inhibited by D1 and D'1. No change of oligomycin-sensitive ATPase activity was demonstrated. Exogenous malondialdehyde (MDA) did not show any inhibitory effect. Preliminary studies show that D1 contains a family of free fatty acids (FFA). Incubation of normal mitochondria with D1 increased the content of saturated FFA and a decrease of unsaturated FFA. The role of other peroxidative products is under investigation.
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PMID:Inhibition of mitochondrial respiratory function by an organic solvent extractable component from an extract of burn eschar. 183 77

This study was undertaken to investigate the effects of activating dopamine receptors in accumbens and prefrontal cortex on self-stimulation behavior in the medial forebrain bundle. The experiments were carried out in rats chronically implanted with one stimulating electrode in medial forebrain bundle and two bilaterally-placed cannulas for giving injections into accumbens or prefrontal cortex. After completion of training, animals classified as responders and non-responders were given drug tests. The non-responders were tested to determine the effects of the treatment on motor activity. The self-stimulation task involved the depression of a lever to obtain a stimulus of 0.25 s duration, 60 Hz sine waves applied to the medial forebrain bundle. Dopamine receptor activation in accumbens or prefrontal cortex was induced with bilateral injections in these structures of a mixture containing 5 mg dopamine, 10 mg d-amphetamine sulfate and 5 mg pargyline mixed in 0.5 ml saline containing 0.1% ascorbic acid (dopamine + d-amphetamine sulfate + pargyline, the cocktail). Each injection was of 2 microliters/side, yielding a concentration of 20 micrograms of dopamine, 40 micrograms of d-amphetamine sulfate and 20 micrograms of pargyline/injection. The bilateral injections were given immediately before the self-stimulation session which lasted 12 h, starting in late afternoon. The effects of saline containing the ascorbate were determined in control sessions. Saline injected bilaterally in accumbens or prefrontal cortex of self-stimulators or non-self-stimulators had no effects on the response-rate of self-stimulators or on the gross motor activity of non-responders. In contrast, the cocktail of dopamine + d-amphetamine sulfate + pargyline injected in accumbens of self-stimulators induced a complex response which included first a facilitation, then a prolonged suppression and then again one or two episodes of facilitation interspersed with periods of suppression of self-stimulation and then a return to baseline rats. The same cocktail of dopamine + d-amphetamine sulfate + pargyline injected bilaterally in accumbens of non-self-stimulators resulted also in a complex response including as a first component a facilitation of responding, but the complex effect was of shorter duration and lower magnitude, never raising the rate of lever-pressing to levels meeting self-stimulation criteria. The same cocktail of dopamine + d-amphetamine sulfate + pargyline injected in prefrontal cortex of self-stimulators simply attenuated or suppressed responding, and the effect lasted for most of the session. The same effect was seen in non-self-stimulators indicating a decrease in gross motor activity.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Enhanced dopamine receptor activation in accumbens and frontal cortex has opposite effects on medial forebrain bundle self-stimulation. 219 40

The authors studied the respiratory and analgesic effects of nalbuphine (0.21 mg/kg, intravenous), naloxone (0.014 mg/kg, intravenous), and placebo (normal saline) when given after morphine (0.21 mg/kg, intravenous) in a double-blind, randomized fashion. Resting end-tidal CO2 (PETCO2), ventilatory and occlusion pressure responses to CO2 rebreathing, and pain threshold were measured in 12 healthy adult volunteers before, 5 min, and 30 min after morphine. Nalbuphine, naloxone, or saline were administered 55 min after morphine, and the above measurements were repeated 5 min later (60 min after morphine) as well as 90, 120, 180, and 240 min after morphine. Whereas naloxone reversed respiratory depression as measured by all three respiratory parameters, nalbuphine either further depressed (resting PETCO2) or did not affect (ventilatory and occlusion pressure responses to CO2 rebreathing) respiratory drive. Morphine produced a significant elevation of the pain threshold. Significant decreases in the pain threshold were seen only after naloxone. Saline and nalbuphine did not significantly alter the pain threshold. The data indicate that nalbuphine may not reliably antagonize moderate doses of morphine.
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PMID:Failure of nalbuphine to antagonize morphine: a double-blind comparison with naloxone. 308 51

The effects of alloxan-induced diabetes on uterine decidualization and the associated changes in uterine blood flow (UBF) and corpus luteum activity were evaluated in rats between days 4-9 of pseudopregnancy (day 0 = ovulation). Rats were made diabetic (D) with a 40 mg/kg injection (iv) of alloxan on day 1 of pseudopregnancy. Saline-treated rats served as controls (C). Uterine weights were depressed in D rats between days 6-7 of pseudopregnancy in association with elevated blood glucose levels (greater than 300 mg/dl) relative to control values. UBF rates were also depressed in D rats between days 6-7 of pseudopregnancy compared with control values. Insulin replacement therapy (6 IU bovine/day) effectively normalized both uterine weight and UBF in diabetic rats. Decidual tissue (DT) growth was impaired in D rats between days 7 and 9 of pseudopregnancy (DT induction on day 4 of pseudopregnancy) compared with controls. Tissue blood flow rates were severely depressed throughout pseudopregnancy in D rats, but insulin treatment normalized both uterine parameters to control levels. Serum progesterone levels were lower in D rats than in controls between days 7 and 9 of pseudopregnancy. Daily insulin treatment normalized luteal function to control levels. The depressed DT weights in D rats were mimicked by the experimental reduction of DT blood flow in control rats. These results indicate that the uterine atrophy and poor endometrial decidualization that characterized the D rat are accompanied by impaired UBF and luteal activity. These findings suggest that the D-associated depression in female reproductive performance is related to the lack of proper hormone support of tissue vascular dynamics.
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PMID:Effects of diabetes on uterine condition, decidualization, vascularization, and corpus luteum function in the pseudopregnant rat. 327

Effects of epinephrine (Epi) infusion on the absorption of subcutaneously injected 125I-labeled soluble human insulin (10 U) from the thigh or the abdomen were studied in 16 healthy subjects and from the thigh in 10 insulin-dependent diabetic (IDDM) patients. Epi was infused at 0.3 (high dose) or 0.1 (low dose; healthy subjects) nmol.kg-1.min-1 i.v., resulting in arterial plasma Epi levels of approximately 6 and 2 nM, respectively. Saline was infused on a control day. Insulin absorption was measured as disappearance of radioactivity from the injection site and as appearance of plasma immunoreactive insulin (IRI). Adipose tissue blood flow was measured with the 133Xe clearance technique. First-order disappearance rate constants of 125I from the thigh depot decreased approximately 40-50% during the high dose of Epi compared with control (P less than .001). The corresponding decrease from the abdominal depot was approximately 40% (P less than .001), whereas no significant change was found during the low Epi dose. IRI fell compared with control in all groups at the high Epi dose. The Epi-induced depression of insulin absorption occurred despite unaltered or even slightly increased subcutaneous blood flow. The results indicate that circulating Epi at levels seen during moderate physical stress depresses the absorption of soluble insulin from subcutaneous injection sites to an extent that might be important for glycemic control in IDDM patients. Furthermore, dissociation is found between changes in insulin absorption and subcutaneous blood flow during Epi infusion, suggesting that factors other than blood flow may also influence the absorption of subcutaneously injected insulin.
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PMID:Influence of circulating epinephrine on absorption of subcutaneously injected insulin. 328 90

Normal (N) rats and rats with nephrotoxic serum nephritis (NSN) were used in whole-kidney and micropuncture studies while being kept euvolemic by homologous plasma infusion and after isotonic volume expansion (VE). During euvolemia, whole kidney and single nephron (SN) glomerular filtration rate (GFR), as well as urinary sodium excretion (UNa X V), were significantly lower in NSN rats (GFR = 0.40 +/- 0.06 ml/min; SNGFR = 14.4 +/- 1.9 nl/min; UNa X V = 0.05 +/- 0.02 microEq/min) than in controls (GFR = 1.14 +/- 0.06 ml/min; SNGFR = 32.7 +/- 2.0 nl/min; UNa X V = 0.05 +/- 0.02 microEq/min); fractional proximal and "distal" (beyond the proximal convoluted tubule) sodium reabsorption rates were significantly higher than N, further depressing urinary sodium output. Saline expansion significantly elevated GFR and decreased renal vascular resistance (RVR) in both N and NSN rats. In the latter, however, GFR remained below, and RVR above, levels observed in N rats. Urinary sodium excretion increased markedly with saline expansion in N rats, reaching 26.9 +/- 1.31 microEq/min. NSN rats exhibited a blunted natriuretic response to expansion (UNa X V = 3.85 +/- 1.02 microEq/min); however, despite a still depressed GFR and increased RVR, urinary sodium excretion in NSN rats reached levels well above euvolemic control. Fractional proximal and "distal" tubular sodium reabsorption rates were depressed by VE in both N and NSN rats. However, this depression was less evident in NSN rats, particularly in the "distal" nephron, suggesting that the stimulus for sodium reabsorption in these segments was somehow enhanced in NSN rats. Fractional potassium excretion was increased to a much greater extent in NSN than in N rats. This finding, associated with the small depression of fractional sodium reabsorption in the "distal" nephron of NSN rats, suggests a participation of elevated levels of circulating aldosterone in the sodium retention observed in this model.
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PMID:Sodium handling and renal hemodynamics in euvolemic and volume-expanded nephrotic rats. 359 9

The absolute rate of reabsorption by superficial rat proximal tubules was measured by the in situ microperfusion technique under conditions of hydropenia, infusion of saline, and infusion of saline plus aortic constriction sufficient to decrease whole kidney filtration rate below hydropenic levels. Fractional reabsorption was measured in adjacent filtering nephrons by collecting and recollecting tubular fluid from late proximal convolutions during each experimental condition. During hydropenia, the absolute rate of proximal tubular reabsorption averaged 3.56 +/-0.60 nl/min per mm and late proximal tubular fractional reabsorption averaged 0.56 +/-0.10. From these two measurements and measurements of tubule length to the site of micropuncture, a value for filtration rate was calculated for filtering nephrons. During hydropenia this value averaged 32.9 +/-7.1 nl/min. Saline infusion increased sodium excretion to 5.5% of the filtered load as the absolute rate of proximal tubular reabsorption decreased 38% and fractional reabsorption decreased 45%. Calculated superficial nephron filtration rate increased 21% which on the average was identical with the simultaneously measured increase in whole kidney filtration rate. Similar results were obtained in a separate group of animals by the technique of total collection of late proximal tubular fluid. Aortic constriction during saline infusion decreased whole kidney and calculated nephron filtration rate to the same degree and to values lower than those during hydropenia. Fractional reabsorption increased but not to hydropenic values. The persistent natriuresis during aortic constriction was associated with a continued depression of the absolute rate of proximal tubular reabsorption which was sufficient to maintain an increased delivery of filtrate out of the proximal tubule despite the fall in nephron filtration rate. These results indicate that depressed fractional reabsorption in the proximal tubule during acute saline infusion is due predominantly to a decrease in absolute reabsorptive rate and to a lesser extent to an increase in superficial nephron filtration rate which is proportional to the increase in whole kidney filtration. Continued natriuresis when filtration rate is decreased during saline infusion can be accounted for entirely by the persistent large reduction in the absolute rate of proximal tubular reabsorption.
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PMID:The relative contributions of reabsorptive rate and redistributed nephron filtration rate to changes in proximal tubular fractional reabsorption during acute saline infusion and aortic constriction in the rat. 511 9

The effects of extracellular fluid volume expansion on intestinal transport of salts and water were studied in dogs by perfusing loops of bowel in vivo. Saline loading caused depression of duodenal and jejunal absorption with net secretion of salt and water into the lumen. Studies of unidirectional transport of (22)Na(+) revealed that the negative net sodium flux was due primarily, and perhaps exclusively, to increased serosal to mucosal transport, for mucosal to serosal sodium transport was not changed during volume expansion. Net transport of water and potassium paralleled net sodium flux. Administration of deoxycorticosterone did not affect the intestinal response to saline loading. Hemodilution, accomplished by equilibrating the dogs' blood with a reservoir of saline, did not affect intestinal absorption, but isotonic, iso-oncotic expansion of the extracellular fluid produced by reinfusing the saline-blood mixture from the reservoir resulted in negative net transport of water, sodium, and potassium by the duodenum. It is suggested that the small bowel is capable of secreting salts and water through intercellular spaces, and that this process is stimulated by extracellular fluid volume expansion.
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PMID:Intestinal transport of water and electrolytes during extracellular volume expansion in dogs. 512 9


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