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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuro-effector transmission in the smooth muscle layer of the dog trachea was studied in vitro using the micro-electrode and double sucrose gap methods.1. Electrical field stimulations with short duration (50-100 musec) applied to the whole tissue produced an excitation of the intrinsic nerves, and evoked excitatory junction potentials (e.j.p.s) followed by twitch tension development and subsequent long lasting relaxation of the smooth muscle tissue.2. The effects of field stimulations were abolished by tetrodotoxin (2 x 10(-7)m), and atropine (1.7 x 10(-5)m) selectively blocked both the e.j.p. and twitch tension. On the other hand, propranolol (1.9 x 10(-5)m) suppressed the generation of the prolonged relaxation evoked by the field stimulations.3. E.j.p.s recorded by the double sucrose gap method showed gradual and continuous reduction in amplitude during prolonged exposure in Krebs solution (1-2 hr), and there were no changes in the membrane potential or in the input membrane resistance.4. With application of indomethacin (10(-5)m), a gradual and continuous reduction in the amplitude of e.j.p. was no longer observed, and (after the initial increase in the amplitude) e.j.p.s with a constant amplitude were obtained during 1-1.5 hr. Indomethacin (10(-5)m) modified neither the resting membrane potential nor the input membrane resistance of smooth muscle cells.5. After pre-treatment with indomethacin, low concentrations (10(-11)-10(-8)m) of prostaglandin E(1) or E(2) (PGE series) markedly suppressed the amplitude of e.j.p. with no changes in the resting membrane potential or in the input membrane resistance.6. During the repetitive field stimulation at the stimulus frequency of 0.1-1 Hz, the amplitude of the e.j.p.s was gradually reduced (the depression process). The depression was not affected by applications of prostaglandins, indomethacin or alpha- and beta-adrenoceptor blockers.7. These results indicate that in the dog tracheal smooth muscles, the endogenous PGE series may play an important role in feed-back inhibitory mechanisms, at the nerve terminals related to acetylcholine release.
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PMID:Actions of indomethacin and prostaglandins on neuro-effector transmission in the dog trachea. 627 74

The influence of indomethacin therapy on the circulatory and antianginal effects of nitroglycerin were studied in six patients with stable angina pectoris. Indomethacin 50 mg or identical placebo capsules were administered three times a day for 1 week each in a double-blind, random manner. Heart rate, blood pressure, and ST-segment depression were measured at rest and during exercise before and after the administration of 0.6 mg sublingual nitroglycerin during indomethacin and placebo therapy. Nitroglycerin lowered standing systolic blood pressure by 38 mm Hg during placebo therapy (p less than 0.001) and by 36 mm Hg during indomethacin therapy (p less than 0.001). This was accompanied by a reflex increase in heart rate (p less than 0.001) which was of similar magnitude during placebo and indomethacin therapy. The increase in exercise duration to the onset of angina post nitroglycerin was similar during placebo and indomethacin therapy (128 vs 84 s; NS). Similarly, the increase in the total duration of exercise post nitroglycerin was similar during placebo and indomethacin therapy. Reduction in ST-segment depression post nitroglycerin was more pronounced during placebo than indomethacin therapy, but did not achieve statistical significance. The results show that indomethacin did not modify the circulatory effects of nitroglycerin at rest or during exercise and did not attenuate the increase in exercise tolerance produced by sublingual nitroglycerin. Since indomethacin is a potent prostaglandin inhibitor, the findings indirectly suggest that the vasodepressor and antianginal effects of nitroglycerin are in all probability not mediated by prostaglandins.
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PMID:Interaction of indomethacin and nitroglycerin on hemodynamics and exercise tolerance in patients with angina pectoris. 642 Oct 13

Clonidine (10(-9)-3 X 10(-6) M) produced a concentration dependent inhibition of field stimulation-induced contractions of rat detrusor muscle strip at 0.1 and 1 Hz which were completely abolished by tetrodotoxin (5 X 10(-7) M) but were unaffected by hexamethonium (10(-5) M). Pretreatment with yohimbine (10(-8)-10(-7) M) did not modify the amplitude of contractions but produced a rightward parallel shift of clonidine's cumulative response curve without a depression of the maximal response. The corresponding pA2 value for yohimbine was 8.44 +/- 0.1. Atropine (3 X 10(-6) M) produced a partial inhibition of contractions at both frequencies. In the presence of atropine the cumulative response curve of clonidine was significantly reduced at 1 but not at 0.1 Hz. Indomethacin (5 X 10(-5) M) and theophylline (2 X 10(-4) M) produced a partial inhibition of amplitude of contractions at both frequencies without any interference with the effect of a supramaximal concentration of clonidine. Prazosin (10(-6) M), propranolol (10(-6) M), chlorpheniramine (10(-6) M), ranitidine (10(-6) M), haloperidol (10(-7) M), pizotifen (10(-6) M), naloxone (10(-6) M), quinidine (10(-6) M), strychnine (10(-5) M) or picrotoxin (10(-5) M) neither affected the amplitude of contractions at either frequency nor antagonized clonidine effects. The contractile response of non stimulated strips to acetylcholine (10(-5) M), carbachol (3 X 10(-6) M) and ATP (10(-3) M) were not significantly influenced by pretreatment with clonidine (3 X 10(-6) M). These results suggest that stimulation of prejunctional alpha 2-adrenoreceptors located on postganglionic nerve endings might reduce the output of excitatory neurotransmitter(s) in rat urinary bladder.
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PMID:The effects of clonidine on electrically-induced contractions of rat detrusor strips in vitro. 664 49

The effects of intravitreally injected prostaglandins (PGs) and arachidonic acid (AA) on the electrical activity of the retina were studied by monitoring the electroretinogram (ERG) of rabbits. In normal rabbits, intravitreal injection of PGE1, PGE2, or AA caused a gradual depression of b-wave amplitude as measured either in low (2 lux) or normal (300 lux) background illumination: up to 45% depression was observed within 1 hr and no recovery was noted during 4 hr of monitoring. The depression of the b-wave amplitude after the intravitreal injection of AA and PGs was similar in time course. Bromcresol green, an inhibitor of PG transport, significantly potentiated the effects of low doses of PGE1 and PGE2 and, to a lesser extent, that of AA. Indomethacin, a known inhibitor of cyclooxygenase activity, prevented the AA-induced, but not the PG-induced depression of the b-wave amplitude. It is concluded that PGs can have a direct effect on the retina and that this region of the eye contains sufficient cyclooxygenase activity to produce pathophysiologically significant amounts of PGs and/or related autacoids.
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PMID:The effects of prostaglandins and arachidonic acid on the electroretinogram: evidence for functional cyclooxygenase activity in the retina. 680 28

E. Coli endotoxin was injected by i.v. route to rats at a dose immediately lower than the minimal lethal dose. Assays were performed on anesthetized rats (urethane 1 g/kg i.p.). The carotid arterial pressure was recorded 1, 2, 4, 16 and 24 hours after endotoxin administration, and hypertensive responses to three successive doses of phenylephrine (2; 5 or 10 micrograms/kg i.v.) was measured until return to initial values. Compared to control rats the hypertensive responses in the endotoxin-treated rats were depressed. This depression was evident at the first hour following endotoxin administration and was maintained at least for four hours. This lower response was improved by a treatment of the rats with indomethacin (10 mg/kg i.v.) when this drug was administered half an hour before, or concomitantly with endotoxin. When indomethacin (10 mg/kg) was given two hours after endotoxin the improvement was less marked. So did indomethacin at 5 mg/kg dose level. Indomethacin alone did not potentiate the pressive responses to phenylephrine. These results show that the endotoxin-induced decrease in the hypertensive responses to phenylephrine does not appear to depend on its hypotensive or lethal effects. It can be brought together with the low cardiovascular responses to different drugs found in animals under endotoxin shock. These results show moreover that an early increase in prostaglandin synthesis under the influence of endotoxin may be involved in this depressant effect.
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PMID:[Decrease of the hypertensive responses to phenylephrine in the rat submitted to a sublethal dose of E. coli endotoxin. Restoration by indomethacin (author's transl)]. 704 7

Attempts were made to demonstrate release of vasoactive substances from the heart during coronary occlusion (for 60 min) and reperfusion (for 60 min), and to clarify the pathophysiological significance of them. Vasoactive substances were detected by superfusion of rabbit aortic and dog coronary arterial strips with great coronary venous blood. Plasma thromboxane (TX) B2 was radioimmunologically assayed. Gradually developing, sustained contraction of both vascular strips was noted during coronary occlusion and reperfusion, while a transient contraction in rabbit aortic and relaxation in dog coronary arterial strips were seen immediately after reperfusion. The TXB2 released into the great coronary venous blood significantly increased during occlusion and reperfusion. Indomethacin treatment of the dog abolished the sustained contraction of both vascular strips and TXB2 release. The transient contraction of rabbit aorta after reperfusion was inhibited by phenoxybenzamine. Reactive hyperaemia following a 60 min occlusion was significantly depressed, as compared with that following 30 s to 30 min occlusion, and the depression was alleviated by indomethacin and imidazole. These results suggest that catecholamine(s) and TXA2 are released during coronary occlusion and reperfusion, and that the latter might be responsible for the coronary circulatory failure during reperfusion of irreversibly damaged myocardium.
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PMID:Coronary circulatory failure and thromboxane A2 release during coronary occlusion and reperfusion in anaesthetised dogs. 707 70

Ascitic fluids and sera from patients with malignant tumors were tested for their ability to modulate the mitogen-induced blastogenic responses of normal subjects' peripheral blood mononuclear cells in vitro. The addition of either ascitic fluid or serum to cultures of normal blood cells greatly enhanced the blastogenic response of cells to phytohemagglutinin P, and markedly depressed the responses to concanavalin A and succinyl-concanavalin A. The blastogenic response of the cells to pokeweed mitogen was unaffected by the addition of serum and depressed by the addition of ascitic fluid. Autologous normal serum also enhanced the response to phytohemagglutinin P but had no effect on the response to the other mitogens. These activities were concentration-dependent and heat-stable (56 degrees C, 60 min) and could be detected even if the ascitic fluid or serum was added as late as the second day of culture. Cells that had been preincubated with serum or ascitic fluid and washed well before culturing with the mitogens responded in the same manner as cells cultured in the presence of serum or ascitic fluid. The mitogen-induced blastogenic responses of mononuclear cells were not affected by the addition of autologous cells that had been preincubated with either serum or ascitic fluid, washed, and treated with mitomycin C. Indomethacin (2 X 10(-7)M) did not prevent the ascitic fluid-mediated depression of blastogenic responses of normal cells. The ascitic fluid and serum of these cancer patients appeared to contain a specific immunoinhibiting substance which exerted its effects by a direct action on the responding mononuclear cells and not by the induction of suppressor cells.
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PMID:Effect of immunomodulating factors present in ascitic fluids and sera from cancer patients on the responses of cultured mononuclear cells from normal subjects. 709 91

Salmonella anatum was given orally to 8 horses on 11 occasions in doses ranging from 9.5 X 10(6) to 8.8 X 10(11) organisms. Four distinct syndromes were induced based upon clinical, laboratory and pathological findings: (1) asymptomatic; (2) moderate clinical signs with or without changes in faecal consistency; (3) fever, depression, anorexia with unstructured or diarrhoeic faeces; and (4) septicaemia with or without diarrhoea, and peripheral circulatory failure. All animals excreted the organism. The peak temperature preceded the onset of diarrhoea by 1 or 2 days. Changes in faecal consistency were associated with direct isolation of the organism. The degree of neutropaenia increased with the dosage. Blood cultures were unsatisfactory, only 1 of 33 samples being positive. The serological responses were not significant although one animal displayed a significant seroconversion consistent with the clinical reaction. Indomethacin was not of value in moderating intestinal fluid secretion in one animal. The distribution and quantitation of positive cultures at autopsy closely reflected the type of syndrome induced. The invasiveness of the organism was confirmed by frequent direct recoveries from intestinal wall and draining lymph node samples. S. anatum appears to be of similar pathogenicity to S. typhimurium in the horse, at least under experimental conditions.
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PMID:Experimental Salmonella anatum infection in horses. 713 42

To determine the local effects of cigarette smoke on the pulmonary vasculature, we measured pulmonary artery pressure--flow curves in isolated, blood-perfused pig lungs before and after 4 exposures to cigarette smoke. During each exposure, smoke was administered into the trachea for 3 to 4 min at a rate of 20 to 25 puffs/min and a puff volume of 35 to 50 ml with a smoking machine. During hypoxia (inspired PO2, 50 mmHg), when baseline vasomotor tone was high, cigarette smoke caused an acute transient vasodilation. During control (inspired PO2, 200 mmHg), when baseline tone was low, no significant effect was observed. In addition to this acute effect, cigarette smoke caused a depression of the pulmonary pressor response to hypoxia, which developed gradually during the course of the experiment. Indomethacin, at perfusate concentrations of 20 and 100 micrograms/ml, did not significantly alter the acute vasodilating effect of smoking, suggesting that prostaglandins synthesized by cyclooxygenase were not the mediators of this response. Indomethacin did, however, prevent the gradual depression of the pulmonary vasoconstrictor response to hypoxia.
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PMID:Vascular effects of cigarette smoke in isolated pig lungs. 730 9

The actions of NO synthase inhibitors and indomethacin, a cyclooxygenase inhibitor, on the nonadrenergic noncholinergic (NANC) mechanical responses of cat distal colon were studied in vitro using muscle strips orientated in the axis of the longitudinal muscle layer with pelvic nerves attached. Electrical field stimulation (EFS) or pelvic nerve stimulation (PNS) caused inhibition of spontaneous contractions followed by off-contractions. Indomethacin (10-30 microM) caused concentration-dependent reductions in amplitude and duration of EFS- and PNS-evoked off-contractions but not latency. The NO synthase inhibitors, N omega-nitro-L-arginine (L-NNA), N omega-nitro-L-arginine methyl ester (L-NAME) and NG-monomethyl-L-arginine (L-NMMA) (each at 100 microM) significantly reduced latency, amplitude, and duration of off-contractions evoked by EFS and PNS. This inhibition was partially reversed by L-arginine (120 microM) but not by D-arginine. Incubation of colonic strips with alpha-chymotrypsin (2 U/ml) decreased latency, amplitude, and duration of NANC off-contractions. L-NNA reduced amplitude, duration, and latency of off-contractions in preparations pretreated with alpha-chymotrypsin. Hydroquinone (10-30 microM), a generator of superoxide anions, caused significant depression of amplitude, duration, and latency of off-contractions which was completely reversed by superoxide dismutase (200 U/ml). These data suggest that the components of NANC off-contractions evoked by EFS and PNS involve peptides, NO, and prostaglandins.
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PMID:A nitric oxide and prostaglandin-dependent component of NANC off-contractions in cat colon. 750 99


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