ACTION OF PROSTAGLANDIN E2 ON THE RELEASE OF CATECHOLAMINES FROM THE CANINE ADRENAL GLAND AND ITS INTERACTION WITH ACETYLCHOLINE

1978 ◽  
Vol 78 (2) ◽  
pp. 249-254 ◽  
Author(s):  
K. YAMASHITA ◽  
M. MIENO ◽  
T. SHIMIZU ◽  
ER. YAMASHITA
Keyword(s):  
Adrenal Gland ◽  
Prostaglandin E2 ◽  
Adrenal Medulla ◽  
Intravenous Administration ◽  
Catecholamine Secretion ◽  
Prostaglandin E ◽  
Order Of Magnitude ◽  
Dose Dependent Increase ◽  
Dose Dependent

SUMMARY The effect of prostaglandin E2 (PGE2) on the secretion of adrenaline and noradrenaline by the adrenal gland and the interaction between PGE2 and acetylcholine in the adrenal medulla were examined in anaesthetized dogs. In splanchnicotomized dogs, i.v. injection of PGE2 failed to induce any secretion of catecholamines from the adrenal gland, whereas administration of PGE2 into the lumboadrenal artery resulted in a slight, approximately dose-dependent increase in catecholamine secretion within 2 min of the injection. This effect of PGE2 was unaffected by i.v. administration of atropine. Intravenous administration of acetylcholine 1 min after the administration of PGE2 into the lumboadrenal artery of splanchnicotomized atropine-treated dogs had a markedly greater effect on adrenal catecholamine secretion; the resultant output was about twice that evoked by acetylcholine in the absence of PGE2. The effect was more than additive, since the response to acetylcholine was at least one order of magnitude greater than that to PGE2. This indicates that PGE2 and acetylcholine may act synergistically in the adrenal medulla.

Effects of propofol and thiopentone on picrotoxin convulsive threshold in the rabbit

1995 ◽  
Vol 73 (6) ◽  
pp. 714-717 ◽  
Author(s):  
Zyheir Hasan ◽  
Said Khatib ◽  
Ayman Abu-Laban
Keyword(s):  
Intravenous Administration ◽  
Seizure Threshold ◽  
Intravenous Anesthetics ◽  
Threshold Test ◽  
Dose Dependent Increase ◽  
Convulsive Threshold ◽  
Dose Dependent ◽  
Higher Doses

The purpose of the present study was to examine the effect of intravenous administration of propofol and thiopentone on picrotoxin-induced seizures using the picrotoxin convulsive threshold test in the rabbit. Neither propofol nor thiopentone at a dose of 1.25 mg/kg had any significant effect on picrotoxin seizure threshold. However, at higher doses (2.5, 5, 10 mg/kg) both propofol and thiopentone produced a significant and dose-dependent increase in the picrotoxin convulsive threshold. These findings suggest that propofol is an effective anticonvulsant against picrotoxin-induced seizures in the rabbit.Key words: convulsions, intravenous anesthetics, picrotoxin, propofol, thiopentone.

Effect of Tumor Necrosis Factor-α on in vitro Prostaglandin Production in Buffalo Corpus Luteum

2021 ◽  
Author(s):  
M.K. Tripathi ◽  
S. Mondal ◽  
I.J. Reddy ◽  
A. Mor
Keyword(s):  
Mrna Expression ◽  
Corpus Luteum ◽  
Prostaglandin E ◽  
Prostaglandin F ◽  
Important Regulator ◽  
Factor Α ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Necrosis Factor

Background: Corpus luteum plays key role in embryonic survival. Prostaglandins are the important regulator controlling the life span of corpus luteum. The present study investigated the effect of various doses of TNFα on in vitro PGF2α and PGE2 production and expression profiling of PGFS and PGES mRNA in buffalo Corpus Luteum (CL).Methods: Buffalo ovaries with mid-luteal phase CL were collected from the abattoir and CL were enucleated from surrounding tissues. Corpus luteum were finely chopped, rinsed with HBSS (Hanks Balanced Salt Solution) medium; supplemented with gentamycin and 0.1% BSA and incubated at 37°C for 1 hr in HBSS containing 0.1% collagenase. The cell suspension following filtration was washed by HBBS supplemented with gentamycin and 0.1% BSA (bovine serum albumin) and was treated with increasing doses of TNFα (0.1, 0.5 and 1.0 nM) and cultured at 38.5°C, 5% CO2 level for 24 hr. Result: There was dose dependent increase in concentrations of PGF2α and PGE2 with increasing doses of TNFα. The PGFS (prostaglandin F synthase) mRNA expression increased with increasing doses of TNFα. However, there was decrease in PGES (prostaglandin E synthase) mRNA expression at 0.1 nM and 0.5 nM TNFα but PGES mRNA expression increased at 1.0 nM TNFα as compared to control. It can be concluded that TNFα may alter PGES and PGFS mRNA expression and prostaglandin secretion in buffalo CL. 

EFFECT OF PROSTAGLANDIN E2 AND A2 ON STEROID SYNTHESIS BY THE RAT ADRENAL GLAND

1975 ◽  
Vol 65 (1) ◽  
pp. 55-63 ◽  
Author(s):  
A. SPÄT ◽  
SARA JÓZAN
Keyword(s):  
Adrenal Gland ◽  
Prostaglandin E2 ◽  
Adrenal Glands ◽  
Prostaglandin E ◽  
Sodium Restriction ◽  
Aldosterone Secretion ◽  
Steroid Synthesis ◽  
Aldosterone Production ◽  
Hypophysectomized Rats

SUMMARY Prostaglandin E2 increased aldosterone output by superfused capsular adrenal glands obtained from sodium-repleted, hypophysectomized rats but corticosterone did not show a statistically significant increase. Prostaglandin A2 increased corticosterone but not aldosterone production by incubated capsular glands obtained from sodium-repleted, hypophysectomized rats. Both aldosterone and corticosterone production rates were increased by PGA2 after previous sodium restriction. Corticosterone production rate of the decapsulated adrenal gland was not significantly modified by prostaglandin A2 in a concentration effective on the capsular adrenal gland. A possible role of prostaglandins in the regulation of aldosterone secretion is discussed.

Flow- and agonist-mediated nitric oxide- and prostaglandin-dependent dilation in spinal arteries

1997 ◽  
Vol 273 (5) ◽  
pp. H2217-H2223 ◽  
Author(s):  
Yasuaki Yashiro ◽  
Toshio Ohhashi
Keyword(s):  
Nitric Oxide ◽  
Constant Pressure ◽  
Marked Decrease ◽  
Additional Treatment ◽  
Prostaglandin E ◽  
Arterial Diameter ◽  
Small Arteries ◽  
Triton X ◽  
Dose Dependent Increase ◽  
Dose Dependent

Isolated rabbit spinal resistance-sized arteries (∼100 μm in diameter and ∼3 mm long) were cannulated at both ends with glass micropipettes and perfused at constant pressure (60 mmHg). An increase of flow rate corresponding to a change of pressure gradient (ΔP) ranging from 0 to 20 mmHg produced a flow-dependent vasodilation. Treatment with 50 μM aspirin or 10 μM indomethacin produced a significant reduction of the flow-dependent vasodilation only at ΔP of 5 mmHg. In contrast, treatment with N ω-nitro-l-arginine methyl ester (l-NAME, 30 μM) produced no significant change. In the presence of 10 μM indomethacin, however, 30 μMl-NAME caused a marked decrease in the arterial diameter at ΔP of 5 mmHg, which was completely reversed with additional administration of 1 mMl-arginine. Acetylcholine (ACh) produced a dose-dependent increase in the arterial diameter. The ACh-induced vasodilation was significantly reduced by 10 μM indomethacin or 50 μM aspirin and partially suppressed by 30 μMl-NAME. Pretreatment with both indomethacin and l-NAME completely reduced the ACh-induced vasodilation. In the presence of 10 μM indomethacin, additional treatment with 1 mMl-arginine significantly reversed the l-NAME-induced inhibition of the ACh-mediated vasodilation. Endothelial removal with Triton X-100 significantly reduced the ACh-induced vasodilation. Isocarbacyclin (a stable prostaglandin I2 analogue), prostaglandin E2, and arachidonic acid caused a dose-dependent dilation in the small arteries. These findings suggest that prostanoids play a major role in the flow- or ACh-induced vasodilation in the rabbit spinal resistance-sized small arteries.

Gastric alkaline response to mucosa-damaging agents: effect of 16,16-dimethyl prostaglandin E2

1981 ◽  
Vol 241 (6) ◽  
pp. G509-G515
Author(s):  
J. S. Swierczek ◽  
S. J. Konturek
Keyword(s):  
Prostaglandin E2 ◽  
Sodium Taurocholate ◽  
Potential Difference ◽  
Mucosal Barrier ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Stimulation Of ◽  
Bathing Fluid ◽  
Related Increase

We investigated the effects of luminal application of graded concentrations of conventional mucosal barrier breakers such as ethanol, aspirin (ASA), and sodium taurocholate (TCh), as well as 16,16-dimethyl prostaglandin E2 (DMPGE2) on gastric alkaline output (GAO) and transmucosal potential difference (PD). The Lucite chamber stomach-flap preparation was used in 50 dogs whose basal H+ secretion was inhibited by intravenous cimetidine. Graded concentrations of ethanol, and TCh at pH 5.0, and acidified solutions of ASA (at pH 5.0--2.0) were found to produce a dose-dependent increase in GAO accompanied by a stepwise decline in PD. Increasing concentrations of DMPGE2 above 1.0 microgram/ml caused a dose-related increase in GAO and a reduction in PD. The combination of DMPGE2 with ethanol aggravated the PD changes, whereas GAO induced by these agents was decreased. Alterations in GAO and PD evoked by the ASA solutions varying in pH were not significantly affected by the addition of 1.0 microgram/ml DMPGE2 to the bathing fluid. These results indicate that stimulation of gastric alkalinization with concomitant fall in PD is a common feature for various mucosa-irritant substances, and pretreatment with DMPGE2 does not prevent these effects.

scholarly journals Systemic Immune Challenge Activates an Intrinsically Regulated Local Inflammatory Circuit in the Adrenal Gland

Endocrinology ◽  
2008 ◽  
Vol 149 (4) ◽  
pp. 1436-1450 ◽  
Author(s):  
Linda Engström ◽  
Khadijah Rosén ◽  
Anna Angel ◽  
Anna Fyrberg ◽  
Ludmila Mackerlova ◽  
...  
Keyword(s):  
Adrenal Gland ◽  
Prostaglandin E2 ◽  
Receptor Antagonist ◽  
Immune Cell ◽  
Cortical Layer ◽  
Cyclooxygenase 2 ◽  
Prostaglandin E ◽  
Autocrine Signaling ◽  
Immune Cell Population

There is evidence from in vitro studies that inflammatory messengers influence the release of stress hormone via direct effects on the adrenal gland; however, the mechanisms underlying these effects in the intact organism are unknown. Here we demonstrate that systemic inflammation in rats elicited by iv injection of lipopolysaccharide results in dynamic changes in the adrenal immune cell population, implying a rapid depletion of dendritic cells in the inner cortical layer and the recruitment of immature cells to the outer layers. These changes are accompanied by an induced production of IL-1β and IL-1 receptor type 1 as well as cyclooxygenase-2 and microsomal prostaglandin E synthase-1 in these cells, implying local cytokine-mediated prostaglandin E2 production in the adrenals, which also displayed prostaglandin E2 receptors of subtypes 1 and 3 in the cortex and medulla. The IL-1β expression was also induced by systemically administrated IL-1β and was in both cases attenuated by IL-1 receptor antagonist, consistent with an autocrine signaling loop. IL-1β similarly induced expression of cyclooxygenase-2, but the cyclooxygenase-2 expression was, in contrast, further enhanced by IL-1 receptor antagonist. These data demonstrate a mechanism by which systemic inflammatory agents activate an intrinsically regulated local signaling circuit that may influence the adrenals’ response to immune stress and may help explain the dissociation between plasma levels of ACTH and corticosteroids during chronic immune perturbations.

Increased Expression of u-PA and u-PAR on Monocytes by LDL and Lp(a) Lipoproteins – Consequences for Plasmin Generation and Monocyte Adhesion

1999 ◽  
Vol 81 (04) ◽  
pp. 594-560 ◽  
Author(s):  
Florence Ganné ◽  
Marc Vasse ◽  
Jean-Louis Beaudeu ◽  
Jacqueline Peynet ◽  
Arnaud François ◽  
...  
Keyword(s):  
Fold Increase ◽  
Surface Expression ◽  
Cell Surface Expression ◽  
Atheromatous Plaque ◽  
Monocyte Adhesion ◽  
Blood Monocytes ◽  
Proteolytic Cascade ◽  
Ecm Degradation ◽  
Dose Dependent Increase ◽  
Dose Dependent

SummaryMonocyte-derived foam cells figure prominently in rupture-prone regions of atherosclerotic plaque. As urokinase/urokinase-receptor (u-PA/u-PAR) is the trigger of a proteolytic cascade responsible for ECM degradation, we have examined the effect of atherogenic lipoproteins on monocyte surface expression of u-PAR and u-PA. Peripheral blood monocytes, isolated from 10 healthy volunteers, were incubated with 10 to 200 µg/ml of native or oxidised (ox-) atherogenous lipoproteins for 18 h and cell surface expression of u-PA and u-PAR was analysed by flow cytometry. Both LDL and Lp(a) induced a dose-dependent increase in u-PA (1.6-fold increase with 200 μg/ml of ox-LDL) and u-PAR [1.7-fold increase with 200 μg/ml of ox-Lp(a)]. There is a great variability of the response among the donors, some of them remaining non-responders (absence of increase of u-PA or u-PAR) even at 200 μg/ml of lipoproteins. In positive responders, enhanced u-PA/u-PAR is associated with a significant increase of plasmin generation (1.9-fold increase with 200 μg/ml of ox-LDL), as determined by an amidolytic assay. Furthermore, monocyte adhesion to vitronectin and fibrinogen was significantly enhanced by the lipoproteins [respectively 2-fold and 1.7-fold increase with 200 μg/ml of ox-Lp(a)], due to the increase of u-PAR and ICAM-1, which are receptors for vitronectin and fibrinogen. These data suggest that atherogenous lipoproteins could contribute to the development of atheromatous plaque by increasing monocyte adhesion and trigger plaque weakening by inducing ECM degradation.

The Effect of Adrenaline Infusions on Blood Coagulation in Normal and Haemophilia B Dogs

1966 ◽  
Vol 15 (03/04) ◽  
pp. 349-364 ◽  
Author(s):  
A.H Özge ◽  
H.C Rowsell ◽  
H.G Downie ◽  
J.F Mustard
Keyword(s):  
Body Weight ◽  
Factor Viii ◽  
Factor Ix ◽  
Clotting Factor ◽  
Blood Ph ◽  
Order Of Magnitude ◽  
Dose Dependent ◽  
Generation Test ◽  
Plasma Activity

SummaryThe addition of trace amounts of adrenaline to whole blood in plasma in vitro increased factor VIII, factor IX and whole plasma activity in the thromboplastin generation test. This was dose dependent.Adrenaline infusions less than 22 (μg/kg body weight in normal dogs accelerated clotting, increased factor IX, factor VIII and whole plasma activity in the thromboplastin generation test and caused a fall in blood pH. In a factor IX deficient dog, there was no increase in factor IX activity. After adrenaline infusions, however, the other changes occurred and were of the same order of magnitude as in the normal. Adrenaline in doses greater than 22 μg/kg body weight did not produce as great an effect on clotting in normal or factor IX deficient dogs. The platelet count in the peripheral blood was increased following the infusion of all doses of adrenaline. These observations suggest that the accelerating effect of adrenaline on clotting is not mediated through increase in activity of a specific clotting factor.

LH-RH TEST IN 100 PATIENTS WITH OVARIAN INSUFFICIENCY

1974 ◽  
Vol 75 (3) ◽  
pp. 428-434 ◽  
Author(s):  
P.-J. Czygan ◽  
M. Breckwoldt ◽  
F. Lehmann ◽  
R. Langefeld ◽  
G. Bettendorf
Keyword(s):  
Intravenous Injection ◽  
Functional State ◽  
Clear Correlation ◽  
Normal Range ◽  
Ovarian Insufficiency ◽  
Lh Rh ◽  
Dose Dependent Increase ◽  
Dose Dependent

ABSTRACT The effect of synthetic LH-RH was studied in 100 patients with various types of ovarian insufficiency by following up the FSH- and LH-levels in plasma. LH-RH was administered in doses of 12.5, 25 and 100 μg as a rapid intravenous injection. The patients were classified according to the endocrine state of the pituitary as evidenced by the urinary gonadotrophin levels. A clear correlation between the functional state of the pituitary and its responsiveness to exogenous LH-RH was demonstrated. Most of the patients with undetectable low urinary gonadotrophin levels failed to respond. The majority of patients with gonadotrophin excretion in the normal range and those with elevated levels reacted with a dose dependent increase in circulating LH. The amount of liberated FSH however was related to the injected dose only in patients with high gonadotrophic excretion. The present study indicates that synthetic LH-RH provides a useful tool in the evaluation of the pitutiary function particularly in patients with low and with undetectable gonadotrophin excretion. The data presented in this paper also demonstrate that the functional state of the pituitary is clearly reflected by the urinary gonadotrophin levels.

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