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)

This study examines the possible role of endogenous prostaglandins (indomethacin; PGF2a; PGE1; PGE2; and prostacyclin or PGI2) on the spontaneous motility of the human ampullar and isthmus deprived of the mesosalpinx. Fallopian tubes were obtained from 12 patients who had hysterectomy and salpingo-oophorectomy. The segments of the tubes were prepared for contractile recordings as previously described and divided into 2 groups: 1) ampullar and isthmic segments were followed by spontaneous variations in motility during 30 minutes; and 2) cumulative close-response curves for PGI2 were constructed for ampullar and isthmic segments 30 minutes after the end of equilibrium. Contractile functions were evaluated in terms of amplitude of isometric developed tension (IDT) and frequency of contraction, and when pertinent, changes in resting basal tone. Student's t-test was used for statistical analysis, and differences between means were considered significantly at P=0.05 or less. Indomethacin significantly enhance the IDT of the isthmic but not the ampullar region. However, a single and identical concentration of 10-6M of PGE1 and PGI2 depressed the ampullar while PGE2 and PGF2a enhanced its contractions. In the isthmus, PGE1, PGE2 and PGF2a augmented while PGI2 diminished the IDI. Both ampullar and isthmic regions exhibited a dose-dependent depression of IDI and contractile frequency. In the isthmus, PGI2 produced a biphasic action on resting basal tone while in the ampulla, only a progressive dose-dependent decline was seen. Prostacyclin may be synthesized by the isthmic region of the human fallopian tubes, but whether it occurs in vivo or what its physiological significance is remains to be seen.
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PMID:Spontaneous motility of isolated mesosalpinx-free isthmic and ampullar segments from human oviducts, and the influences of indomethacin and prostacyclin (PGI2). 4 1

Spleen cells removed from C57Bl/6J mice bearing a methylcholanthrene-induced fibrosarcoma (MC-16) demonstrate suppressed responsiveness of phytohemagglutinin (PHA) and bacterial lipopolysaccharide (LPS) induced mitogenesis as compared to non-tumorous mice. A similar depression of PHA-induced mitogenesis was observed with spleen cells from C3H/HeJ mice bearing syngeneic mammary adenocarcinomas (C3HBA). The administration of indomethacin, a non-competitive irreversible prostaglandin (Pg) synthesis inhibitor, (75 or 100 mug/mouse, IP) on an alternate day basis to groups of tumor-bearing mice of both strains, significantly enhanced immune cell responsiveness to mitogenic stimulation. The addition of indomethacin (10 mug/ml) to cultures of spleen cells from these tumor-bearing mice, as well as to DBA/1J mice bearing the Cloudman S-91 melanoma, enhanced spleen-cell responsiveness to mitogen-induced DNA synthesis by as much as 156%. Indomethacin administration in vivo or in vitro had no significant effect on mitogen-induced DNA synthesis of spleen cells from non-tumor-bearing animals. It is hypothesized that tumors, or tumor-cell antigens, increase Pg production of a population of spleen cells, and that the increased Pg content of the spleen may be important in controlling immune responsiveness in mice.
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PMID:Indomethacin enhancement of spleen-cell responsiveness to mitogen stimulation in tumorous mice. 18 13

Part of the excitatory transmission in rabbit detrusor is noncholinergic and nonadrenergic, and prostaglandins (PGs) and adenosine 5'-triphosphate (ATP) have been implicated in this transmission. The present experiments investigate the possibility of an interaction between PGs and ATP in rabbit detrusor. Indomethacin (2.8 muM) depressed the contraction produced by ATP although it did not antagonize the contraction produced by carbachol. Treatment of detrusor strips with 1.5 mM ATP depressed the frequency response curve in field stimulated tissues. This depression was additive with that produced by atropine. In the present experiments indomethacin did not significantly augment the effect of desensitization with ATP. It is suggested that the atropine-resistant neurotransmission in rabbit detrusor may involve both ATP and PGs acting in cooperation.
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PMID:Interaction of prostaglandins and adenosine 5'-triphosphate in the noncholinergic neurotransmission in rabbit detrusor. 21 89

The purpose of this study was to determine the relative effects of acute hypoxemia on constrictor responses to norepinephrine and angiotensin in two vascular beds, the coronary and skeletal muscle. The left circumflex coronary and gracilis muscle arteries of anesthetized dogs were perfused at constant flow. Practolol or propranolol was administered to block indirect myocardial effects of norepinephrine on coronary resistance. When Po2 of arterial blood perfusing the coronary and muscle beds was reduced from 101 to 44 mm while systemic Pco2 remained normal, constrictor responses to both norepinephrine and angiotensin were inhibited in coronary vessels but not in muscle vessels. When local Po2 was reduced to 27 mm Hg, inhibition of responses was again observed in the coronary circulation with both drugs; in the muscle, responses to angiotensin but not to norepinephrine were depressed significantly. Since intracoronary infusion of adenosine increased, rather than inhibited, vasoconstrictor responses to angiotensin, it is unlikely that release of adenosine during hypoxemia accounts for inhibition of vasoconstriction in the coronary circulation. Indomethacin did not alter the inhibition of coronary vasoconstrictor responses to angiotensin during hypoxemia, which suggests that releease of prostglandins during htpoxemia is not the primary mechanism for inhibition of coronary vascular responses. When contractions in the gracilis muscle were produced by electrical stimulation, vasconstrictor responses to norepinnephrine were inhibited during hypoxemia. We conclude that depression of constrictor responses by hypoxemia is more pronounced in the coronay circulation than in resting muscle, but when muscle is contracting, vasoconstrictor responses are impaired during hypoxemia.
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PMID:Effect of hypoxemia on responses to norepinephrine and angiotensin in coronary and muscular vessels. 23 17

Implants of crystalline PGE2 in the basal preoptic-anterior hypothalamic areas stimulates high levels of sexual receptivity in ovariectomized, estrogen-primed rats. Indomethacin, which blocks the synthesis of PGE2 failed to inhibit either estrogen- or estrogen plus progesterone-induced receptivity. Neither intracerebral nor subcutaneous administration of indomethacin diminished the display of steroid induced reproductive behavior without also causing a depression in open-field activity, and in some cases, causing gastrointestinal problems and even death. These results suggest the prostaglandin synthesis is not a required step in the mechanism by which estrogen and progesterone exert their behavioral effects. The possibility that PGE2 and LH-RH synthesis and/or release might contribute to a collateral mechanism for the induction of sexual receptivity was discussed.
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PMID:Effects of prostaglandin synthesis inhibitor, indomethacin on estrogen- and estrogen plus progesterone-induced sexual receptivity in ovariectomized rats. 67 64

1 Subcutaneous injection of Mycobacterium butyricum suspended in mineral oil into the mouse hind paw caused an oedematous local inflammation. Hind paw swelling was maximum 5 days after injection and was still apparent at day 30. 2 Drug metabolism in vivo (as monitored by ketamine- or pentobarbitone-induced sleeping times) was not affected by the inflammatory disease. However, administration of ketamine or pentobarbitone at day 1 led to significantly elevated sleeping times when the mice showing local inflammation were retested at day 5 with the anaesthetics. 3 Indomethacin inhibited hind paw oedema in the mouse but did not affect ketamine-Mycobacterium butyricum-induced depression of drug metabolism. 4 Prolongation of ketamine-induced anaesthesia by combination with Mycobacterium butyricum at day 5 correlated with the degree of hind paw inflammation at this time. 5 The data suggest that anaesthetics (i.e., ketamine and pentobarbitone) may sensitize hepatic membranes to the effect of Mycobacterium butyricum or some toxic compound elaborated during the active phase of inflammation.
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PMID:Depression of drug metabolism in the mouse by a combination of Mycobacterium butyricum and anaesthetics. 76 Aug 85

The anti-inflammatory drugs, sodium salicylate, indomethacin, hydrocortisone, ibuprofen, and flurbiprofen, were examined for their effects on sulphated glycosaminoglycan synthesis in aged human cartilage in vitro. Cartilage was obtained from femoral heads removed during surgery and drug effects were found to vary significantly from one head to another. Statistical analysis of the results showed that sodium salicylate exhibits concentration-dependent inhibition of glycosaminoglycan synthesis over the concentration range used. Indomethacin, hydrocortisone, and ibuprofen, at concentrations comparable to those attained in man, caused a statistically significant depression of sulphated glycosaminoglycan synthesis in cartilage from some femoral heads but not others, reflecting the variable response of human articular cartilage to anti-inflammatory drugs. Sodium salicylate and indomethacin at higher doses produced significant (Pless than 0-005) inhibition of sulphated glycosaminoglycan synthesis in all femoral heads studied. The results for flurbiprofen were less conclusive; this compound appears not to inhibit glycosaminoglycan synthesis over the concentration range used.
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PMID:Effect of anti-inflammatory drugs on sulphated glycosaminoglycan synthesis in aged human articular cartilage. 100 17

The effects of indomethacin, an inhibitor of prostaglandin synthesis, on rat renomedullary interstitial cells were studied. Indomethacin, 5 mg. per kg. intravenously in divided doses over 48 hours, resulted in reduced granularity of interstitial cells (5.56+/-1.37 versus 9.85+/-1.07 granules per cell, (p is less than 0.001) and, at the same time, inhibited the incorporation of 14C-arachidonate into renomedullary phospholipids (715 + 11 versus 1299 + 42 c.pm.per mug. of lipid orthophosphate; p is less than 0.001) 14C-arachidonate incorporation into cortical phospholipids was not affected by indomethacin. There was a close correlation between individual granule counts and 14C-arachidonate incorporation into medullary phospholipids for both control (r=0.85) and indomethacin-treated animals (r=0.9). Radioactivity in the cytosol fraction was depressed by indomethacin reflecting inhibition of prostaglandin synthesis; cytosol radioactivity correlated closely with individual granule count (r=0.81) in the indomethacin-treated but not in the control rats. Indomethacin given as a single dose 4 hours prior to sacrifice resulted in a significant depression of 14C-arachidonate incorporation but did not affect granularity of interstitial cells. The results suggest that granularity of renomedullary interstitial cells reflects the activity of prostaglandin synthesis and the rate of prostaglandin precursor delivery from microsomal phospholipids.
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PMID:Effects of indomethacin on renomedullary interstitial cells. 127 53

It was aimed to assess if intrathecal (i.t.) injections of acetylsalicylic acid and salicylic acid depress C fibre-evoked activity in the sensory part of the nociceptive system. In rats under urethane anaesthesia, activity was elicited in single neurones in the dorsomedial part of the ventral nucleus (VDM) of the thalamus and in ascending axons of the spinal cord by supramaximal electrical stimulation of the sural nerve. Acetylsalicylic acid and salicylic acid injected i.t. significantly reduced the activity evoked in thalamic neurones. The maximum depression amounted to about 50% of the activity evoked in the controls and was produced by acetylsalicylic acid at a dose of 50 micrograms (0.28 mumol)/rat and by salicylic acid at a dose of 37.5 micrograms (0.27 mumol)/rat. Indomethacin injected i.t. also reduced C fibre-evoked activity in the thalamus in a dose-dependent fashion, 100 micrograms producing a 50% depression. Salicylic acid (37.5 micrograms/rat, i.e.) depressed C fibre-evoked activity in ascending axons but had no effect on A beta fibre-evoked activity. It is concluded that i.t. injection of acetylsalicylic acid selectively inhibits nociceptive impulse transmission in the spinal cord by an action of the salicylic acid moiety. It is possible that prostaglandins are involved in the central action of salicylic acid.
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PMID:Intrathecal injection of acetylsalicylic acid, salicylic acid and indomethacin depresses C fibre-evoked activity in the rat thalamus and spinal cord. 1183 30

The mechanism of pial arteriolar constriction during post-cortical spreading depression (CSD) was examined in anesthetized adult rabbits. Using a closed cranial window and intravital microscopy, the diameter of a pial arteriole was determined. A single CSD was induced by KCl micro-injection and its propagation was monitored by recording slow potential changes accompanying CSD. Prostanoid levels in cortical cerebrospinal fluid (CSF) were determined by radioimmunoassay. Pial arteriolar diameter increased significantly from 76 +/- 6 to a maximum of 119 +/- 5 microns (57%, n = 8) for 1.6 +/- 0.1 min when CSD (velocity, 2.8 +/- 0.1 mm/min) reached the cortex just beneath the vessel irrespective of its location. Shortly after CSD expiration from the cortex, pial arteriolar diameter decreased from the pre-CSD level to a minimum of 67 +/- 5 microns (12%, n = 8) for 19.5 +/- 2.1 min. CSD was elicited again in the same animal while the cortical surface under the window was continuously superfused with artificial CSF at a flow rate of 3.2-4.5 ml/min. Pial arteriolar dilation (from 75 +/- 6 to 115 +/- 3 microns, 53 +/- 9%, for 1.6 +/- 0.1 min, n = 8) was observed again during CSD (velocity, 2.7 +/- 0.2 mm/min), however, no constriction of the vessel was seen after CSD expiration. Indomethacin pretreatment (n = 11) to inhibit prostanoid production enhanced the magnitude of CSD-induced vasodilation from the pretreatment levels of 59 +/- 9% (from 82 +/- 5 to 130 +/- 8 microns for 1.7 min) to the post-treatment levels of 82 +/- 13% (from 78 +/- 5 to 142 +/- 12 microns for 1.8 min).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pial arteriolar constriction following cortical spreading depression is mediated by prostanoids. 161 12


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