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

In isolated strips of canine mesenteric vein prostacyclin (PGI2) causes a dose-dependent depression of the amplitude of the spontaneous rhythmic contractions without influencing their frequency. This suggests that prostacyclin affects the events leading from the depolarization of the smooth muscle cells to their contractions, rather than the induction of the myogenic activity itself. Furthermore, prostacyclin reduces the noradrenaline-induced contraction of the canine saphenous vein without affecting the electrically induced responses, suggesting a possible dual effect of the drug: at the smooth muscle it causes depression of the responsiveness to noradrenaline whereas at the adrenergic nerve endings it enhances the evoked release of the adrenergic transmitter.
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PMID:Effect of prostacyclin on myogenic activity and adrenergic neuroeffector interaction in canine isolated veins. 21 44

Pregnant hamsters were administered (SC) prostaglandin or vehicle on the morning of the 4th day of pregnancy. Serum progesterone was significantly depressed (p less than .01) at 0.5, 2, and 6 hours after treatment with 100 microgram PGF2alpha. Serum progesterone levels were unchanged 2 hours and 6 hours after treatment with 100 microgram PGF2beta and 2 hours after treatment with 1 mg PGF2beta. Progesterone levels were depressed to less than 1 ng/ml 6 hours after treatment with 1 mg PGF2beta. The specific uptake of 3H-PGF2alpha in whole hamster corpora lutea was significantly depressed 2 hours and 6 hours following 100 microgram PGF2alpha treatment. A 15% depression in specific uptake occurred 0.5 hour post-treatment. Treatment with 100 microgram PGF2beta resulted in no change. Administration of 1 mg PGF2beta resulted in depressed 3H-PGF2alpha uptake at both 2 and 6 hours post-treatment. Prostacyclin (PGI2) treatment resulted in no change in either 3H-PGF2alpha specific uptake or serum progesterone 2 hours after 100 microgram treatment SC. These parameters were both reduced approximately 30% 6 hours post-treatment. Treatment with 6-keto-PGF1alpha resulted in a complete lack of measurable 3H-PGF2alpha uptake and serum progesterone levels less than 1 ng/ml at both 2 and 6 hours after treatment with 1 mg SC.
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PMID:Effect of in vivo prostaglandin treatment on 3H-PGF2alpha uptake in hamster corpora lutea. 36 47

Prostacyclin is a new prostaglandin first demonstrated as a product of arterial microsomes and prostaglandin endoperoxide intermediates. The potential to form prostacyclin has now been demonstrated in many organs. It inhibits platelet aggregation, inhibits gastric acid secretion, stimulates the monkey but not the rat uterus in vivo, is a bronchodilator, is a vasodepressor on both systemic and pulmonary circulation, increases cardiac output and markedly decreases peripheral resistance. It reduced progesterone in pregnant hamsters but is not luteolytic in non-pregnant monkeys. In rats, i. v. infusion of 0.56 but not 1 mg/kg/day was tolerated without overt central nervous system depression. The depressor effect of i. v. infusions of prostacyclin in anesthetized rats was partially antagonized by a pressor reaction eliminated by nephrectomy, an effect not seen during infusions of prostaglandin.
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PMID:The general pharmacology of prostacyclin PGI2, (PGX): a new prostaglandin especially active on the cardivascular system. 36 53

Physiological roles have been suggested for prostacyclin in the cardiovascular system. Prostacyclin was administered by intravenous infusion to unanesthetized rats. Over a 24 hr period, 0.32 mg/kg/day caused only flushing of the ears. Larger doses (0.56 and 1 mg/kg/day) caused hypothermia, behavioral depression, and swelling of the paws. Cumulative dose-response curves for its depressor action were determined in both unanesthetized and anesthetized, vagotomized, ganglion-blocked rats. In unanesthetized rats, the threshold dose was about 0.1 ug/kg/min. Respiratory depression precluded doses larger than 1 ug/kg/min. In anesthetized rats, the threshold dose was about 0.001 ug/kg/min, and the maximally effective dose was about 0.1 micrograms/kg/min. At 0.032 ug/kg/min, blood pressure first fell and then rose slightly. This compensatory rise did not occur in nephrectomized rats, suggesting renin release as the mechanism. Intravenous infusion of 0.1 but not 0.01 ug/kg/min in unanesthetized rats doubled plasma renin activity. In saline-loaded unanesthetized rats, urine volume and urinary sodium excretion were decreased by 0.1 ug/kg/min of prostacyclin.
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PMID:The cardiovascular pharmacology of prostacyclin (PGI2) in the rat. 37 17

The profile of spontaneous contractions as well as the influences of prostacyclin (PGI2) on the motility of human ovarian veins obtained during the estrogenic phase of the sex cycle were explored. The preparations exhibited a distinct phasic activity, which progressively decreased as isolation time progresses, dissapearing almost completely following more than two hours. PGI2 produced a biphasic influence on quiescent preparations. After the threshold is attained lower concentrations caused depression of tone whereas higher ones enhanced the basal tone and induced phasic contractile cycles. Phentolamine reduced markedly the stimulating influence of PGI2 but had no action on the inhibitory effects, whereas propranolol failed to alter either the excitatory of the depressive action. The results suggest a participation of alpha-adrenoceptive-mediated mechanisms in the stimulatory effect of PGI2. On the other hand, PGI2 may be of importance in the regulation of venous flow and the spontaneous or PGI2-induced contractions could play a role in the counter current mechanism between veins and arteries in the ovarian pedicle.
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PMID:Spontaneous contractile activity of isolated ovarian human vein. A dual influence of prostacyclin (PGI2). 39 50

1 Rabbit hearts were perfused with a solution containing [14C]-arachidonic acid (AA) and various concentrations of nicotine (3 x 10(-8) to 3 x 10(-5) M). The venous effluent was collected and extracted for lipid acid material, which was subsequently subjected to thin layer radiochromatography. 2 Human platelets were incubated with nicotine (10(-8) to 10(-4) M), in the absence or presence of unlabelled AA. The amount of smooth muscle stimulating activity resulting from 30s of incubation was tested on a rabbit aortic strip. 3 In hearts perfused with [14C]-AA; nicotine induced a dose-related depression of the release of [14C]-6-keto-prostaglandin F1alpha, and a parallel increase of [14C]-prostaglandin E2. 4 Nicotine neither induced synthesis of thromboxane in human platelets, nor affected the platelet synthesis of thromboxane induced by AA. 5 It is suggested that nicotine affects the metabolism of prostaglandin endoperoxides in the heart by inhibiting their conversion to prostacyclin and facilitating, directly or indirectly, the formation of prostaglandin E2.
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PMID:Effects of nicotine on cardiac prostaglandin and platelet thromboxane synthesis. 72 84

The effects of iloprost, a chemically stable analog of prostacyclin, on motor activity, pentylenetetrazol (PTZ)- and strychnine (ST)-induced seizures were studied in rats. Depression on motor activity was observed after a 500 ng/icv dose. Thus, both spontaneous locomotor activity and exploratory behavior were significantly reduced. While iloprost was ineffective against ST-induced seizures, it produced dose-dependent inhibition of PTZ-induced seizures. ED50 (95% confidence limits) value of iloprost for the suppression of clonic convulsions induced by PTZ was 224.96 (100.43-504.00) ng/icv. Anticonvulsive effect of iloprost was significantly potentiated by clonazepam pretreatment. In this case ED50 of iloprost was 39.40 (23.88-65.01) ng/icv. Unilateral iloprost injections into substantia nigra pars reticulata in a relatively lower dose range (0.5-2.0 ng/ic) also dose-dependently inhibited PTZ-induced seizures. In comparison to other prostanoids iloprost seems to have more potent and selective anticonvulsive activity against PTZ-induced seizures without marked motor depressant action in rats. It is further suggested that antiseizure effect of iloprost might be mediated by GABAergic inhibitory mechanisms.
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PMID:Effects of intracerebral iloprost injections on motor activity and chemically-induced seizures in rats. 128 72

Defibrotide (DEF), a compound previously found to stimulate vascular prostacyclin (PGI2) formation, has been investigated in an experimental model of septic shock. Anesthetized pigs were subjected to i.v. infusion of lipid A (1.5 mg/kg per hr for 4 hr). DEF (50 mg/kg per hr) or vehicle were infused i.v. throughout the experiments, starting 1 hr prior to lipid A. Two out of 7 pigs receiving vehicle survived lipid A infusion for 4 hr, whereas 6 out of 7 DEF treated animals survived this period (P less than 0.05). DEF delayed the shock-induced depression of platelet count and preserved platelet secretory function (collagen-induced ATP-secretion). DEF increased plasma PGI2 by 45% (P less than 0.05) during lipid A infusion and tended to reduce thromboxane levels. DEF did not change eicosanoid formation in sham-shock pigs (n = 4 per group). In vivo treatment with DEF significantly increased the stimulatory effect of bradykinin (1 microM) and arachidonic acid (100 microM) on PGI2 formation ex vivo of mesenteric and iliac artery segments. The improvement of survival in lipid A-induced shock by DEF may be related to an enhancement of vascular PGI2 generation, potentially due to a reduction of shock-induced platelet activation and microcirculatory dysfunction.
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PMID:Favourable effect of defibrotide in lipid A-induced shock in pigs. 142 20

Agonist challenged aortic prostacyclin production was examined in copper-adequate, -marginal and -deficient rats fed AIN-based diets providing 6.7, 1.7 and 0.8 micrograms Cu/g, respectively. Aortic rings were incubated in Krebs-Henseleit salts, 10 mmol/L HEPES buffer, pH 7.4, 95%:5% O2:CO2, 37 degrees C, and equilibrated for 1 h. Equilibrated rings were challenged with buffer (basal), 273.0 nmol/L thrombin and angiotensin II at 84.6 pmol/L and 846.0 pmol/L. Prostacyclin production, determined at 10 minutes by RIA as 6-keto prostaglandin F1 alpha, in basal and 84.6 pmol/L angiotensin II ring incubations was significantly reduced by 28 to 48% in copper-deficient rats. With thrombin or 846.0 pmol/L angiotensin II prostacyclin production was significantly reduced by 18 to 55% in copper-marginal and copper-deficient rats. Copper-dependent superoxide dismutase activity was significantly depressed by 30 and 57% in aortae of copper-marginal and copper-deficient rats. Lipid peroxidation, estimated by the thiobarbituric acid test, was significantly increased by 85% in copper-deficient rats, with a nonsignificant 40% increase in aortae from copper-marginal rats. The results suggest that the decreases in aortic prostacyclin production in aortae from both copper-deficient and copper-marginal rats are associated, in a dose-dependent manner, with copper-dependent superoxide dismutase depression and increases in aortic lipid peroxidation.
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PMID:Copper-marginal and copper-deficient diets decrease aortic prostacyclin production and copper-dependent superoxide dismutase activity, and increase aortic lipid peroxidation in rats. 143 51


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