Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0009443 (cold)
 92,137 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The activity of hepatic tryptophan pyrrolase in rats exposed to cold increased rapidly and reached a maximum of three-fold at 8 h. On continued exposure up to 48 h stress, the activity partly decreased but remained at a level higher than the initial. Withdrawal from the cold stress reversed the change. Adrenalectomy or treatment with inhibitors of protein synthesis abolished the increase in the enzyme activity during cold stress indicating a possible involvement of corticosteroids and de novo protein synthesis. Treatment with drugs known to block autonomic nervous system failed to inhibit the cold-mediated increase in enzyme activity. The results suggest that the increase in enzyme activity obtained on cold exposure is mediated by corticosteroids and not by either indoleaklylamines or autonomic nervous system. The changes in the enzyme obtained under cold stress with respect to the overshoot phenomenon, relationship to the degree of stress and reversibility on withdrawal from the stress indicate the "adaptate" nature of the response.
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PMID:Nature of induction of tryptophan pyrrolase in cold exposure. 112 Jul 47

The effects of depletion of the serotonin precursor, L-tryptophan, on the threshold and tolerance to cold pressor pain, and the analgesic effect of morphine (10 mg intramuscularly), were tested in a double blind trial on human volunteers. Effects on mood were also assessed using the Profile of Mood States and the Addiction Research Center Inventory (ARCI) Scales. To deplete tryptophan, subjects were fed a tryptophan-deficient amino acid mixture 4.5 h before morphine was administered. Controls received the mixture with tryptophan, which is equivalent to a nutritionally balanced protein. The tryptophan-deficient meal reduced plasma tryptophan more than 70% but had no effect on threshold or tolerance to cold pressor pain. After morphine, tolerance to cold pressor pain increased in controls. Tryptophan depletion abolished this analgesic effect. Pain threshold was not altered by morphine. In subjects with normal tryptophan, the analgesic effect of morphine was predicted by the level of plasma morphine-6-glucuronide, but not by the level of morphine. Morphine increased scores on the LSD scale of the ARCI, but had no effect on other measures of mood. Tryptophan depletion also failed to alter mood in these subjects, who had unusually low depression scores before tryptophan depletion.
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PMID:Acute tryptophan depletion blocks morphine analgesia in the cold-pressor test in humans. 141 Jan 47

Primary hepatocyte cultures have been used to evaluate data concerning hypoxic liver cell injury. To show the suitability of this method in liver preservation studies hepatocyte cultures were incubated under different conditions: warm normoxia (37 degrees C, pO2 greater than 70 mm Hg), warm hypoxia (37 degrees C, pO2 less than 0.1 mm Hg), cold normoxia (4 degrees C, pO2 greater than 70 mm Hg) and cold hypoxia (4 degrees C, pO2 less than 0.1 mm Hg). Incubations were performed in Euro Collins solution (EC), University of Wisconsin solution of Belzer (UW) and histidine ketoglutarat tryptophan solution of Bretschneider (HTK) as well as in Krebs Henseleit buffer (KH) for control incubations. During 12 h of incubation hepatocyte cultures under warm normoxia lost viability continuously in EC, UW and HTK while in KH they remained stable. Under warm normoxia all cultures lost 50% of their viability during 12 h of incubation while in cold normoxia loss of viability was mild but significant. Under cold anoxia which is the standard condition of liver preservation the cultured hepatocytes remained unchanged for 12 h in KH, UW and HTK, while in EC most of the cells were dead after 6 h. It is concluded that incubations of primary hepatocyte cultures under different pO2 and temperatures are well suited to contribute to liver preservation studies on a preclinical level and thus may help to save animal experiments.
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PMID:[Primary hepatocyte cultures as a model of experimental study of liver preservation]. 179 32

This study was designed to assess the effect of chronic dietary administration (2.5 and 5.0% by weight) of the neutral amino acid, L-tryptophan, on the development of hypertension during chronic exposure to cold. In addition, a warm-adapted and cold-treated control group receiving unsupplemented food were used. Chronic administration of the lower dose of L-tryptophan (850 mg/day) prevented the elevation of blood pressure attenuated cardiac hypertrophy, and had no effect on body weight during exposure to cold. The higher dose of L-tryptophan (1,690 mg/day) attenuated the rate of blood pressure increase, did not affect cardiac hypertrophy, attenuated the gain in body weight, and increased the urinary output of epinephrine. Thus, this dose may be associated with some toxicity. Both doses of tryptophan failed to prevent certain other responses characteristically occurring during exposure to cold: i.e. increased weight of the kidneys, adrenal glands and brown adipose tissue; increased food and water consumption; increased dipsogenic responsiveness to angiotensin II, and increased plasma aldosterone concentration. The results indicate that chronic dietary administration of L-tryptophan (850 mg/day) can prevent the development of cold-induced hypertension, as it can in all other models of hypertension tested thus far in rats.
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PMID:Effect of chronic dietary treatment with L-tryptophan on the development of cold-induced hypertension in rats. 194 99

Endothelial cell damage caused by myocardial cardioplegic solutions (Bretschneider HTK and St. Thomas' Hospital No. 2) or renal and hepatic cold storage solutions (modified Collins and University of Wisconsin solution) was assessed in monolayer cultures of adult human venous endothelial cells at 4 degrees to 10 degrees C with phase-contrast microscopy. St. Thomas' Hospital solution caused the cells to contract, resulting in disruption of monolayer integrity and opening of intercellular gaps, and resulted in a 24-hour postexposure survival of 51.0% +/- 2.4%. Bretschneider HTK solution altered cellular morphology less and produced the best postexposure survival (80.2% +/- 2.6%; p less than 0.001). Although morphology was altered the least with University of Wisconsin solution, postexposure survival with this solution, which was similar to that with modified Collins solution, was superior to that with St. Thomas' (p less than 0.01) but inferior to that with Bretschneider HTK (p less than 0.05). The superior protection provided by Bretschneider HTK was due to its additives histidine, tryptophan, and KH-2-oxygluterate (p less than 0.005), and to its low chloride content (p less than 0.005). Furthermore, modifying St. Thomas' solution by decreasing its chloride content improved cell survival to 71.2% +/- 2.3% (p less than 0.001). Normothermic (37 degrees C) exposure to Bretschneider HTK, modified Collins, and University of Wisconsin solution was cytotoxic, whereas normothermic exposure to St. Thomas' cardioplegia was not. In conclusion, the preservation solution that is the least harmful to endothelial cells at hypothermia is Bretschneider HTK cardioplegic solution.
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PMID:Endothelial cell toxicity of solid-organ preservation solutions. 212 22

The ischemic damage following liver transplantation (LTX) is predominantly located at the endothelial cell level and is a major cause for a disturbance of microcirculation. The present study was designed to test the hypothesis that changes in the quality of organ preservation are correlated with changes in microcirculation: 16 pigs underwent LTX, preservation by Bretschneider's HTK-solution (Histidin, Tryptophan, alpha-Ketoglutarat) complemented by indomethacin (50 mumol/L). Cold ischemia times were 9 hr (n = 8) and 18 hr (n = 8), respectively. Using the H2-clearance technique, hepatic microcirculation was measured before, 30 min, and 20 hr after LTX. Normal tissue perfusion was 107 +/- 16 ml/100 g/min, at 30 min posttransplantation 91 +/- 13 ml/100 g/min in the short-term and 48 +/- 7 ml/100 g/min in the long-term preservation group. Whereas no animal of the long-term preservation group survived longer than 8 hr, all animals of the short-term preservation group survived, and tissue perfusion could be measured 20 hr postoperatively (101 +/- 19 ml/100 g/min). At 30 min postoperatively, all surviving animals had tissue perfusion rates greater than 70, and all nonsurvivors had values below 60 ml/100 g/min. We conclude therefore that the extent of decrease of microcirculation after LTX may be a useful predictor of organ function and survival.
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PMID:Evaluation of preservation damage after porcine liver transplantation by assessment of hepatic microcirculation. 225 66

A rodent model of neurovisceral toxic syndrome induced by the neuroexcitant amino acid, domoic acid, is described, along with the activity of a putative antidote, the nonselective excitotoxin antagonist, kynurenic acid. Both an extract of contaminated mussels and pure domoic acid induced a characteristic syndrome including: sluggishness, scratching stereotypy, convulsions and death. Autopsy revealed gastric and duodenal lesions and peritoneal ascites. Kynurenic acid significantly obtunded these behavioral and physiological effects, particularly when given 60-75 min after the toxic insult. Probenecid, a blocker of organic acid transport, and tryptophan, a precursor of endogenous brain kynurenic acid, increased the time frame in which kynurenic acid exerted its protective effects. Kynurenic acid alone, in nontoxin-challenged animals significantly blocked cold-stress gastric lesions, significantly reduced basal gastric acid secretion and was protective to a lesser degree against ethanol-induced gastric mucosal injury. The murine model of domoate toxicity represents an inexpensive, reliable and sensitive biological assay for screening commercial shellfish for excitotoxin contamination. We are currently exploring kynurenic acid and other compounds for possible therapeutic use in both current and any future victims of neuroexcitant amino acid toxicosis.
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PMID:Domoic acid-induced neurovisceral toxic syndrome: characterization of an animal model and putative antidotes. 235 97

The initial rate of L-tryptophan uptake into human red cells as a function of its concentration in the medium was measured in a group of 8 depressed patients hospitalized included 2 bipolar disorders (296.5x, DSM III), 3 major depressions, single episode or recurrent (296.3x and 296.2x, DSM III) and 3 dysthymic disorders (300.40x, DSM III), which were out of antidepressive treatment, with age ranging from 34 to 64 years compared to a group of 11 healthy volunteers with age ranging from 23 to 54 ans. Kinetic constants were measured at 37 degrees C on red cells incubated with tritiated L-tryptophan and cold L-tryptophan over the concentration range 0.1 to 10 mM. The maximum velocity (Vmax) of the saturable transport is severely lowered in a significant manner in the patients compared to controls (mean +/- s.e.m. = 48.9 +/- 5.5 mumol/l cells/min and 92.0 +/- 14 which represents 47% in decrease). In return, the Michaelis constant is unaffected. The linear component of tryptophan transport, which corresponds to the participation of nonspecific transport systems, is not modified. The possible incidence of such a deficit in the plasmatic reserve of tryptophan in depressed patients on the central availability of serotonin synthesis precursor is postulated.
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PMID:[Changes in the kinetics of erythrocyte membrane transport of tryptophan in depression]. 275 58

The cold agglutinin isolated from the albumin gland of the snail Achatina fulica was modified with various chemical reagents in order to detect the amino acids and/or carbohydrate residues present in its carbohydrate-binding sites. Treatment with reagents considered specific for modification of lysine, arginine and tryptophan residues of the cold agglutinin did not affect the carbohydrate-binding activity of the agglutinin. Modification of tyrosine residues showed some change. However, modification with carbodiimide followed by alpha-aminobutyric acid methyl ester causes almost complete loss of its binding activity, indicating the involvement of aspartic acid and glutamic acid in its carbohydrate-binding activity. The carbohydrate residues of the cold agglutinin were removed by beta-elimination reaction, indicating that the sugars are O-glycosidically linked to protein part of the molecule. Removal of galactose residues from the cold agglutinin by the action of beta-galactosidase indicated that the galactose molecules are beta-linked. These carbohydrate-modified glycoproteins showed a marked change in agglutination property, i.e. they agglutinated rabbit erythrocytes at both 10 degrees C and 25 degrees C, indicating that the galactose residues of the glycoprotein play an important role in the cold-agglutination property of the glycoprotein. The c.d. data showed the presence of an almost identical type of random-coil conformation in the native cold agglutinin at 10 degrees C and in the carbohydrate-modified glycoprotein at 10 degrees C and 25 degrees C. This particular random-coil conformation is essential for carbohydrate-binding property of the agglutinin.
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PMID:Studies on chemical modification of cold agglutinin from the snail Achatina fulica. 311 67

The effects of alpha-neoendorphin, kyotorphin, melatonin or diphenylhydantoin (DPH) on thyrotropin-releasing hormone (TRH) and thyrotropin (TSH) release in rats were studied. alpha-neoendorphin (1.0 mg/kg), kyotorphin (1.0 mg/kg), melatonin (2.5 mg/kg) or DPH (75 mg/kg) was injected iv or ip, and the rats were serially decapitated. TRH, TSH and thyroid hormone were determined by radioimmunoassay. The hypothalamic immunoreactive (ir-TRH) contents decreased significantly after melatonin injection, but not after alpha-neoendorphin, kyotorphin or DPH. The plasma ir-TRH concentrations decreased significantly after DPH injection, but not after alpha-neoendorphin, kyotorphin or melatonin. The plasma TSH levels decreased significantly in a dose-related manner with a nadir at 10 min. after melatonin, at 30 min. after DPH and at 40 min. after alpha-neoendorphin or kyotorphin injection. The plasma thyroid hormone levels did not change significantly after these drugs injection. The plasma ir-TRH and TSH responses to cold were inhibited by these drugs, but the plasma TSH response to TRH was not influenced. In the L-DOPA- or 5-hydroxy-tryptophan (5-HTP)-pretreated group, the inhibitory effect of alpha-neoendorphin or kyotorphin on TSH levels was prevented, but not in the haloperidol- or para-chloprophenylalanine (PCPA)- pretreated group. In the haloperidol- or PCPA-pretreated group, the inhibitory effect of melatonin on TSH levels was prevented, but not in the L-DOPA- or 5-HTP-pretreated group. These drugs alone did not affect plasma TSH levels in terms of the dose used. The inactivation of TRH immunoreactivity by hypothalamus or plasma in vitro after these drugs injection did not differ from that of the control.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of various drugs on thyrotropin secretion in rats. 316 12


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