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)

Circulatory and respiratory changes following a mechanical compression of the brainstem of the rabbit were studied. Under light ether anesthesia, the animal was tracheostomized, immobilized by pancuronium bromide, and mechanically ventilated, following which the skull was fixed and suboccipital craniotomy was performed, and finally the brainstem was exposed. The site of compression was selected as (A): 3mm lateral, 3mm rostral, (B): 2mm lateral and (C): 3mm lateral, 3mm caudal, of the obex, respectively. After inhalation of ether was discontinued and elimination of the effect of muscle relaxant was confirmed, the direct compression with glass stick of 0.8mm in diameter was carried out. In each point, vertical compression of 1mm, 2mm and 3mm, was performed stereotaxically. In each depth of the compression, 3 to 4 animals were studied. The blood pressure was measured directly in the femoral artery and the respiratory changes by impedance pneumography. The circulatory changes, biphasic change of arterial pressure and/or transient bradycardia occurred earlier than the respiratory changes in 2mm and 3mm depth of the compression in all 3 points. CO2 response curve with rebreathing method was obtained before and 15 minutes after the compression to evaluate the degree of damage of the medullary respiratory center. The depression of CO2 response curve was observed only in 3mm compression depth at the point (A). It is concluded from this study that excessive invasion of the brainstem during the suboccipital craniotomy under controlled ventilation could be detected through the observation of the changes in circulatory parameters.
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PMID:[Effects of experimental compression of the brainstem on the circulatory and the respiratory parameters in the rabbit]. 273 33

M13 coat protein is a small (50 amino acids) lipid-soluble protein that becomes an integral membrane protein during the infection stage of the life cycle of the M13 phage and is therefore used as a model membrane protein. To study side-chain dynamics in the protein, we have measured individual hydrogen-exchange rates for a primary amide in the side chain of glutamine-15 and for the indole amine of tryptophan-26. The protein was solubilized with the use of perdeuteriated sodium dodecyl sulfate (SDS), and hydrogen-exchange rates were measured by using 1H nuclear magnetic resonance spectroscopy. The glutamine-15 syn proton exchanged at a rate identical with that in glutamine model peptides except that the pH corresponding to minimum exchange was elevated by about 1.5 pH units. The tryptophan-26 indole amine proton exchange was biphasic, suggesting that two populations of tryptophan-26 exist. Approximately one-fourth of the tryptophan-26 resonance intensity exchanged at the same rate as a tryptophan model peptide, whereas three-fourths of the tryptophan-26 resonance intensity exchanged about 1000-fold more slowly. It is suggested that the two populations may reflect protein dimerization or aggregation in the SDS micelles. The pH values of minimum exchange for tryptophan-26 in both environments were also elevated by 1.3-1.9 pH units. This phenomenon is reproduced when small tryptophan- and glutamine-containing hydrophobic peptides are dissolved in the presence of SDS micelles. The electrostatic nature of this phenomenon is proven by showing that the minimum pH for exchange can be reduced by dissolving the hydrophobic peptides in the positively charged detergent micelle dodecyltrimethylammonium bromide. A small hydrophobic effect, which involves the depression of base catalysis to a significantly greater extent than acid catalysis, was observed for some of the peptides solubilized with the neutral detergent octyl glucoside.
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PMID:Side-chain dynamics of a detergent-solubilized membrane protein: measurement of tryptophan and glutamine hydrogen-exchange rates in M13 coat protein by 1H NMR spectroscopy. 279 27

Eleven healthy male volunteers participated in a study comparing the effects of locally and systemically administered cholinoceptor antagonists on the secretory response of sweat glands to intradermally injected carbachol chloride. Atropine sulphate administered locally into the skin antagonised the response to carbachol: the dose-response curve for carbachol was shifted to the right without any depression of the maximum of the curve. The nicotinic receptor antagonists hexamethonium bromide and (+)-tubocurarine chloride, however, had little effect on the response to carbachol. Atropine sulphate, administered systemically by intramuscular injection, caused a non-surmountable antagonism of the response to carbachol: the maximum of the dose-response curve was depressed with little change in the value of ED50. Atropine methonitrate (a mixed muscarinic/nicotinic receptor antagonist), and hexamethonium bromide (a nicotinic receptor antagonist), both with poor access to the central nervous system, were injected intramuscularly: both caused non-surmountable antagonism of the response to carbachol. It is concluded that the response to carbachol is mediated by muscarinic rather than nicotinic receptors. The effect of atropine sulphate on the response to carbachol depends on the route of administration: while locally applied atropine sulphate appears to act as a competitive antagonist, systemically applied atropine sulphate, like atropine methonitrate and hexamethonium bromide, appears to act in a non-competitive manner. It is suggested that the systemically administered cholinoceptor antagonists reduce the response to carbachol by interacting with cholinoceptors in sympathetic ganglia: such an interaction would reduce the impulse flow in sudomotor fibres resulting in decreased sensitivity of the sweat glands to carbachol.
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PMID:Effects of locally and systemically administered cholinoceptor antagonists on the secretory response of human eccrine sweat glands to carbachol. 286 97

The dose requirement for 95% depression of twitch tension and the time course of the neuromuscular blocking effects of the ED95 of pancuronium bromide and vecuronium bromide were studied during intravenous infusion of glucose, 5%, and nitroglycerin, 1 microgram X kg-1 X min-1, in 20 cats anesthetized with pentobarbital. Nitroglycerin administered continuously starting 1 hr before the administration of the ED95 and maintained during at least five maintenance doses of either pancuronium or vecuronium did not significantly potentiate the action of the neuromuscular blocking drugs, nor did it alter their time course of action. A tendency for a decrease (statistically not significant) rather than an increase in the duration of action of maintenance doses of both pancuronium and vecuronium was apparent during the treatment with nitroglycerin. These findings indicate a lack of interaction between pancuronium or vecuronium and nitroglycerin, provided that moderate doses are used.
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PMID:Does intravenous infusion of nitroglycerin potentiate pancuronium- and vecuronium-induced neuromuscular blockade? 286 18

The interaction of two orally administered Ca-channel blockers, the dihydropyridines nisoldipine and nifedipine, with the non-depolarizing muscle relaxant, vecuronium bromide, was tested in the indirectly stimulated tibialis anterior muscle of anesthetized and ventilated Sprague-Dawley rats. In both the nisoldipine and the nifedipine group, depression of twitch tension and duration of vecuronium-induced neuromuscular blockade was potentiated when compared with a control group. The possible clinical relevance of these findings is discussed.
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PMID:[Interaction of the calcium antagonists nifedipine and nisoldipine with the nondepolarizing muscle relaxant vecuronium bromide in an vivo rat preparation]. 286 75

The muscle-relaxation reactions of Ca-antagonist (nifedipine) pretreated patients and a control group (5 in each group) were observed after administration of vecuronium bromide using the "priming principle." Twitch depression induced by the "priming dose" of vecuronium bromide (20 micrograms/kg body weight and T4/T1 ratio in the Ca-antagonist-treated patients (35 +/- 13% and 0.42 +/- 0.14%, respectively), was significantly different (P less than 0.01) when compared with the control group (1.2 +/- 2.7% and 0.75 +/- 0.15%). Similarly, the onset time to maximum blockade after the intubating dose of vecuronium bromide (60 micrograms/kg body wt.) was significantly shorter in the nifedipine group (40 +/- 21 s) when compared with the controls (100 +/- 17 s). The duration of the effect observed clinically (until 25% recovery) in the nifedipine group 32.9 +/- 7.3 min versus 25 +/- 8.15 min was enhanced; however, the difference between the treated group and the control group was not significant.
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PMID:[Nifedipine and vecuronium bromide. How does a patient treated with calcium antagonists react to nondepolarizing muscle relaxants? Brief scientific communication]. 286 76

Airway mucociliary dysfunction leading to a depression of mucus transport has been demonstrated in patients with acute and chronic bronchitis, cystic fibrosis, and bronchial asthma; use of bronchodilators that might further impair mucociliary function, therefore, generally has been discouraged. Atropine and ipratropium bromide are cholinergic antagonists that are effective bronchodilators in various clinical settings. Atropine has been shown to block the production of respiratory secretions in response to cholinergic stimulation, but to have no effect on baseline secretions. Atropine has also been clearly demonstrated to depress ciliary beat frequency and to slow airway mucociliary clearance, whereas the short-term and long-term administration of ipratropium bromide at higher than clinically recommended doses seems to lack these effects. No satisfactory explanation has thus far been offered for this difference between the two cholinergic antagonists. Nevertheless, with respect to airway mucociliary function, ipratropium bromide appears to be preferable to atropine in the treatment of obstructive airways disease.
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PMID:Effect of ipratropium bromide on airway mucociliary function. 294 58

The interaction of surfactants with the vesicle membrane of the negatively charged lipid, dilauroylphosphatidic acid, was investigated through their effect on the gel-to-liquid-crystalline phase transition of the lipid bilayer. Three types of surfactants (anionic, cationic and non-ionic) with different hydrocarbon chain length were examined. (i) Anionic sodium alkylsulfates affected the phase transition temperature, Tm, only weakly. (ii) Non-ionic alkanoyl-N-methylglucamides decreased Tm monotonously with increasing concentration. The depression of Tm induced by these surfactants was analyzed by applying the van't Hoff model for the freezing-point depression, and the partition coefficients of the surfactants between bulk water and lipid membrane were estimated. (iii) Cationic alkyltrimethylammonium bromides affected Tm in a complex manner depending on the hydrocarbon chain length of the surfactants. Octyl-/tetradecyl-trimethylammonium bromide depressed/elevated Tm monotonously with increasing concentration, whereas the change in Tm induced by decyl- and dodecyltrimethylammonium bromides was not monotonous but biphasic. This complex behavior of the phase transition temperature was well explained, based on the statistical mechanical theory presented by Suezaki et al. (Biochim. Biophys. Acta, 818 (1985) 31-37), which takes into account the interaction between surfactant molecules incorporated in the lipid membrane.
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PMID:Interaction of surfactants with bilayer of negatively charged lipid: effect on gel-to-liquid-crystalline phase transition of dilauroylphosphatidic acid vesicle membrane. 324 47

Excessive maternal bromide exposure during pregnancy from drugs and occupation have been reported to have adverse effects on the fetus and newborn, including central nervous system depression at birth and possible teratogenicity. To define further fetal bromide exposure during pregnancy, we determined the cord serum bromide concentration in 1267 newborn babies born in Rochester, New York, during the 6-month period from January 1, 1984 to June 30, 1984. There was a normal distribution of the cord serum bromide concentration values (mean +/- SD = 8.6 +/- 2.6 mg/L; range 3.1 to 28.5 mg/L). The highest concentration was still significantly below the minimal bromide concentration associated with toxic effects (720 mg/L). There was no association between the cord serum bromide concentration and indices of fetal health including Apgar scores, presence of congenital malformations, and neonatal disposition. No mothers were taking significant amounts of bromide-containing drugs during pregnancy. The second highest cord serum bromide concentration (21.4 mg/L) was in a woman who was an amateur photographer and developed her own film, which required her to use chemicals containing bromide. Our results indicate that excessive fetal bromide exposure is rare and probably occurs only in the setting of maternal use of bromide-containing drugs or occupational exposure during pregnancy.
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PMID:Cord serum bromide concentration: variation and lack of association with pregnancy outcome. 367 53

Neuropathological and biochemical effects of neonatal exposure to the alkyl metal triethyltin were examined in juvenile male Long Evans rats. Rats were injected intraperitoneally on postnatal day 5 with 6 mg/kg of triethyltin bromide and sampled on day 20. The brains of tin-treated animals weighed significantly less than either saline or starved controls and exhibited a marked caviation of the ventrolateral surfaces. Histologically, neuronal necrosis was noted in the entorhinal and transitional cortex, an observation confirmed by immunocytochemical staining of astrocytes. Hippocampal involvement was further evidenced by a protrusion of the molecular layer of the dentate gyrus, and an abnormal histochemical staining pattern of acetylcholinesterase in this layer. Sections stained by the Timm's method for the deposition of heavy metals showed a marked reduction in the staining of the hippocampal CA4,3,2 sectors and an absence of stained laminae in the outer molecular layer of the dentate gyrus. Receptor binding assays indicated a selective depression of the benzodiazepine receptor in the hippocampus of tin-treated pups compared to starved controls. Taken in concert, these data indicate that neonatal exposure to triethyltin produces severe neuronal damage in the posterior cortex and a derangement of hippocampal afferent circuitry.
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PMID:Triethyltin-induced neuronal damage in neonatally exposed rats. 371 27


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