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 The effects of calcium and magnesium ions and temperature on the peak amplitude of the nonadrenergic, noncholinergic inhibitory junction potential, evoked by a single stimulus, or paired transmural stimuli, were examined in the circular muscle of guinea-pig small intestine.2 The peak amplitude of the inhibitory junction potential (i.j.p.) could be decreased by lowering the external concentration of calcium or by raising the external magnesium concentration (at 25 degrees C).3 At 25 degrees C, the second of a pair of i.j.ps was larger than the first at short intervals (<0.2 s), but smaller at larger intervals (0.2 to 20 s). Enhancement of the second (test) response decayed exponentially with a time constant of 87 ms. Depression of the test i.j.p. was maximal at 0.4 s and then recovered exponentially with a time constant of 11 s.4 In low calcium or high magnesium solution, depression of the test i.j.p. decreased without any change in the rate of recovery from depression.5 Despite the slow rate of recovery from depression after a single conditioning response, transmitter output could be maintained during low-frequency repetitive stimulation.6 The peak amplitude of the i.j.p. increased as the temperature was raised to 35 degrees C (Q(10) = 1.5).7 In contrast to the neuromuscular junction, the depression of the second of a pair of i.j.ps decreased as the temperature was raised. At 35 degrees C the test i.j.p. was larger than the conditioning i.j.p. for most stimulus intervals (1 to 20 s).8 The results suggest that the rate of replenishment of the store of inhibitory transmitter is sensitive to both temperature and repetitive stimulation.
Br J Pharmacol 1979 Sep
PMID:The effects of calcium and magnesium ions, temperature and repetitive stimulation on inhibitory junctional transmission in smooth muscle of guinea-pig small intestine. 22 7

Endotoxin was shown to depress neutrophil bactericidal activity while enhancing Nitro Blue Tetrazolium reduction and hexose monophosphate shunt activity. Separation of bactericidal action from oxidative metabolism suggests that the effect of endotoxin might involve the formation of reactive oxygen radicals such as superoxide. Chemiluminescence often accompanies metabolic activation of polymorphonuclear neutrophils (PMNs). However, human PMNs did not show chemiluminescence when challenged with endotoxin (lipopolysaccharide; LPS) or lipid A. Superoxide formation was also unaffected by endotoxin. In contrast, preincubation of PMNs with LPS for 30 min produced significant depression of chemiluminescence, oxygen consumption, and superoxide formation. Decreased chemiluminescence was not the result of complement consumption. In a cell-free system, superoxide was not scavenged by LPS, nor did LPS stimulate superoxide dismutase. Oxidase enzymes for reduced nicotinamide adenine dinucleotide or reduced nicotinamide adenine dinucleotide phosphate harvested from broken cells were not affected by LPS. The toxicity of LPS may reside in its ability to activate the PMNs while simultaneously blocking bactericidal capacity.
Infect Immun 1979 Sep
PMID:Endotoxin in vitro interactions with human neutrophils: depression of chemiluminescence, oxygen consumption, superoxide production, and killing. 22 88

Cadmium affects the induction of thymidine and thymidylate kinases in regenerating rat liver. EDTA administered simultaneously with cadmium reverses its inhibitory action on enzyme synthesis, and prevents the depression of thymidine incorporation into DNA observed in cadmium-treated animals. Zinc does not abolish the inhibitory action of cadmium on the synthesis of DNA in regenerating liver, and the incorporation of thymidine into DNA in the testes was inhibited more by intraperitoneal injection of cadmium plus zinc than by injection of cadmium alone. Inhibition of thymidine incorporation into DNA in the liver and testes was proportional to the amount of cadmium administered up to about 2 mg CdCl2/kg body weight, but surprisingly, higher doses of cadmium caused less inhibition.
J Biochem 1979 Sep
PMID:Synthesis of DNA in the liver and testes of cadmium-tested partially hepatectomized rats. 22 99

The intravenous injection of ketamine in the human arm with isolated circulation, using the same technique as for intravenous regional anesthesia, produces a dose-related depression of neuromuscular transmission, as evidenced by the evoked response to supramaximal stimulation of the ulnar nerve with a nerve stimulator. The dose range of ketamine was 200, 25, 10, 5, 1, 0.5 and 0.25 mg, in 20 ml of 5% dextrose in water. The exact mechanism of this effect is discussed. This depression may have clinical significance under certain circumstances.
Acta Anaesthesiol Belg 1979 Sep
PMID:Regional ketamine-induced depression of neuromuscular transmission in man. 23 85

The local graft-versus-host reaction in F1 hybrid rats, assayed by popliteal lymph node enlargement, is specifically depressed by pretreating the host with parental lymphocytes. The conditions for demonstrating specific depression are injection of a small dose of parental lymphocytes and assay 7 days later. Pretreatment with cells from thymus and bone marrow is ineffective, as is pretreatment with purified B lymphocytes. The structures which stimulate the suppressed response of F1 hybrids are not present on parental B lymphocytes.
Transplantation 1975 Sep
PMID:Modification of hybrid responsiveness in the local graft-versus-host reaction by injection of parental lymphocytes. 24 Feb 24

Three patients with aortitis syndrome ehibited paroxysmal hypertension which seemed to result from baroreceptor dysfunction. All of the patients had signs of active inflammation of aortitis syndrome and stenotic carotid and subclavian arteries. During the attacks, the blood pressure rose to at least 230 mm. Hg systolic and the heart rate exceeded 100. However, with prolonged administration of steroid hormones, the attacks ceased. In two patients with dilated thoracic aortas and aortic regurgitation, the attacks of paroxysmal hypertension occurred without apparent precipitating factors and were followed by anginal pain with marked ST depression. The sympathicotonic state resulting from the disturbance of the baroreceptors was considered to be responsible for the attacks. In another patient, the attacks occurred in the course of treatment with a steroid hormone and were provoked only by voluntary micturition. This post-micturition hypertension was presumed to be an expression of abnormal overshooting following a fall in blood pressure after voiding.
Am Heart J 1975 Sep
PMID:Paroxysmal hypertension in aortitis syndrome. 24 Feb 66

Insulin was adsorbed to a strongly acidic ion exchanger and incubated with pepsin. The digestion of the matrix-bound insulin was found to be restricted to the cleavage of the peptide bond between phenylalanine-B25 and tyrosine-B26. Factionation of the reaction products was achieved by gel filtrationon Sephadex G-50 at pH 8 where des-pentapeptide(B26-30)-insulin does not aggregate. Another way to purify this compound was ion-exchange chromatography, which was easy due to the loss of one positive charge on the modified insulin. Crystallization could be achieved in a phenol-containing buffer. Des-pentapeptide(B26-30)-insulin was found to be molecularly uniform by electrophoresis at pH 2.2 and 8.6, thin-layer chromatography, performic acid oxidation, end group analysis and amino acid analysis. The CD-spectrum indicated conformational changes compared to insulin. The biological activity was considerably reduced: fat cell assay 20%, blood sugar depression 30%.
Hoppe Seylers Z Physiol Chem 1975 Sep
PMID:[B-chain shortening of matrix-bound insulin by pepsin, I:Preparation and properties of bovine des-pentapeptide(B26-30) insulin (suthor's transl)]. 24 Jul 71

The use of antiarrhythmie drugs in combination has been limited because of possible side effects secondary to myocardial depression in the acute myocardial infarction patient. Therefore, we investigated in intact dogs (group I) the hemodynamic interaction of propranolol plus procainamide (subgroup A) or quinidine (subgroup B) and in dogs after experimental myocardial infarction produced by coronary artery ligation (group II). Infusion of procainamide (30 mg/kg over 5 min) in animals of group IA produced a significant (P less than 0.05) decrease of 30% in mean aortic pressure, a decrease of 40% in left ventricular dp/dt and 29% in cardiac output. When procainamide was reinfuse after propranolol (1 mg/kg), its hemodynamic effects were not significantly different from those observed before propranolol in both groups IA and IIA. Infusion of quinidine (10 mg/kg over 5 min) in animals of group IB (intact dogs) also produced significant decreases of 24% in mean aortic pressure and 38% in dp/dt while cardiac output was unchanged. However, these hemodynamic changes were seen only after beta-blockade and were significantly different from those obtained before propranolol, where heart rate increased by 14%, dp/dt by 30%, and cardiac output by 35%. These changes occurred despite a similar reduction in mean aortic pressure. This drug combination produced similar response in animals after coronary artery ligation (group IIB). In conclusion, we feel that the administration of propranolol does not prevent the depressive circulatory effects of procainamide. The combined use of quinidine and propranolol also has a negative circulatory effect although not as marked as the effects observed after procainamide with propranolol.
Proc Soc Exp Biol Med 1975 Sep
PMID:Hemodynamic effects of procainamide and quinidine and the influence of beta-blockade before and after experimental myocardial infarction. 24 Oct 83

1 An electrophysiological study has been made of the effects of either blocking noradrenaline (NA) uptake or alpha-adrenoceptors on conduction in adrenergic preterminal axons and on NA release. 2 The excitatory junction potential (e.j.p.) evoked by a single stimulus increased slightly in duration (maximum 20%) in the presence of high concentrations of desipramine or cocaine (larger than or equal to 1 mug/ml) but there was no change in the spontaneous miniature excitatory junction potential (m.e.j.p.s); the single compound preterminal action potential was decreased in amplitude by a maximum of 10%. The e.j.p., m.e.j.p. and the terminal action potential were not altered by lower concentrations of these drugs (less than mug/ml). 3 The increased decline of the e.j.p. amplitude observed during the first few hundred impulses at high frequencies (10 Hz) in the presence of desipramine or cocaine was accompanied by a similar decline in the amplitude of the preterminal compound action potential, suggesting that the latter gave rise to the former. 4 These observations suggest that the action on post-synaptic alpha-adrenoceptors of NA released by single impulses is terminated by diffusion, and that any NA which is subsequently taken up into nerves is metabolized. 5 All the alpha-adrenoceptor blocking drugs tested reversed the normal depression in e.j.p. amplitude observed during the first few hundred impulses at high frequencies to facilitation; this was unaccompanied by any changes in the preterminal compound action potential. 6 Alpha-Adrenoceptor blocking drugs did not alter the potentiating effect which a conditioning impulse had on the amplitude of the e.j.p. evoked by a subsequent test impulse. The facilitated release of NA during trains of impulses was quantitatively predicted in terms of the addition of the individual potentiations introduced by each impulse in the train. 7 It is suggested that if there is an auto-inhibition of NA release, then it is unlikely that the pre- and post-synaptic alpha-adrenoceptors are identical.
Br J Pharmacol 1975 Sep
PMID:An electrophysiological analysis of the effects of amine-uptake blockers and alpha-adrenoceptor blockers on adrenergic neuromuscular transmission. 24 45

Yohimbine injected intravenously or intracerebroventricularly in conscious dogs produced behavioural excitation accompanied by a rise in blood pressure and heart rate. The cardiovascular effects were reduced or abolished by hexamethonium, phenoxybenzamine and reserpine. In conscious cats intravenously administered yohimbine was depressor but intracerebroventricular administration in these animals caused a rise in blood pressure accompanied by behavioural depression. In anaesthetized or decerebrate cats yohimbine was always depressor. Yohimbine injected intracerebroventricularly produced a rise in blood pressure and heart rate in both conscious and anaesthetized rats. When administered intravenously to these animals there was a fall in blood pressure. It was concluded that the pressor action of yohimbine in conscious dogs was central in origin via the sympathetic nervous system. The different pattern of cardiovascular responses in the dog, cat and rat may be related to differences in the balance between medullary effects and effects on higher brain centres of the three species.
Arch Int Pharmacodyn Ther 1975 Sep
PMID:The role of the central nervous system in the cardiovascular responses to yohimbine. 24 88


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