Absence of effect of somatostatin on the guinea pig gallbladder

1980 ◽  
Vol 58 (2) ◽  
pp. 179-182 ◽  
Author(s):  
Pierre Poitras ◽  
Tadataka Yamada ◽  
John H. Walsh
Keyword(s):  
Guinea Pig ◽  
Muscle Contraction ◽  
Inhibitory Effect ◽  
Cholecystokinin Octapeptide ◽  
Direct Inhibitory Effect

The effect of somatostatin (GH-RIH) on cholecystokinin octapeptide (OP-CCK) or acetylcholine (ACh) induced contraction of the guinea pig gallbladder was evaluated in vitro. GH-RIH failed to inhibit the muscle contraction induced by OP-CCK or ACh. To correlate with the in vitro results, the effect of GH-RIH on OP-CCK induced contraction of the gallbladder was evaluated in the guinea pig in vivo. GH-RIH did not affect the OP-CCK induced contraction of the gallbladder. Our results suggest that GH-RIH does not have direct inhibitory effect on the contraction of the guinea pig gallbladder induced by OP-CCK or ACh.

Inhibition of Human and Animal Platelet Adhesiveness to Glass Bead Columns by Adenosine, Dipyridamole, Chlorpromazine and Acetylsalicylic Acid

1976 ◽  
Vol 36 (02) ◽  
pp. 401-410 ◽  
Author(s):  
Buichi Fujttani ◽  
Toshimichi Tsuboi ◽  
Kazuko Takeno ◽  
Kouichi Yoshida ◽  
Masanao Shimizu
Keyword(s):  
Guinea Pig ◽  
Acetylsalicylic Acid ◽  
Guinea Pigs ◽  
Glass Bead ◽  
Animal Species ◽  
Inhibitory Effect ◽  
Rabbit Platelet ◽  
Platelet Adhesiveness

SummaryThe differences among human, rabbit and guinea-pig platelet adhesiveness as for inhibitions by adenosine, dipyridamole, chlorpromazine and acetylsalicylic acid are described, and the influence of measurement conditions on platelet adhesiveness is also reported. Platelet adhesiveness of human and animal species decreased with an increase of heparin concentrations and an increase of flow rate of blood passing through a glass bead column. Human and rabbit platelet adhesiveness was inhibited in vitro by adenosine, dipyridamole and chlorpromazine, but not by acetylsalicylic acid. On the other hand, guinea-pig platelet adhesiveness was inhibited by the four drugs including acetylsalicylic acid. In in vivo study, adenosine, dipyridamole and chlorpromazine inhibited platelet adhesiveness in rabbits and guinea-pigs. Acetylsalicylic acid showed the inhibitory effect in guinea-pigs, but not in rabbits.

Role of endothelial cells in regulating hemoglobin-induced changes in lymphatic pumping

1992 ◽  
Vol 263 (6) ◽  
pp. H1880-H1887 ◽  
Author(s):  
R. M. Elias ◽  
J. Eisenhoffer ◽  
M. G. Johnston
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Inhibitory Effect ◽  
Direct Inhibitory Effect ◽  
Induced Changes ◽  
Lymphatic Pumping ◽  
Pumping Activity

Studies with a sheep isolated duct preparation in vivo demonstrated that the route of administration of hemoglobin was important in demonstrating its inhibitory effect on lymphatic pumping. With autologous oxyhemoglobin administered intravenously (final plasma concentration 5 x 10(-5) M), pumping was not inhibited. However, the addition of oxyhemoglobin (5 x 10(-5) M) into the reservoir (lumen of the duct) resulted in > 95% inhibition of pumping. The extraluminal administration of oxyhemoglobin (10(-5) M) to bovine mesenteric lymphatics in vitro resulted in a 40% inhibition of pumping, whereas the introduction of oxyhemoglobin (10(-5) M) into the lumen of the vessels suppressed pumping 95%. In vessels mechanically denuded of endothelium, intraluminal oxyhemoglobin inhibited pumping 50%. These results suggested that oxyhemoglobin depressed pumping through an effect on both smooth muscle and endothelium. Once pumping was inhibited with oxyhemoglobin administration, stimulation of the duct with elevations in transmural pressure restored pumping activity when endothelial cells were present. However, in the absence of endothelium, pumping decreased with increases in distending pressures. We conclude that oxyhemoglobin has a direct inhibitory effect on lymphatic smooth muscle. The ability of oxyhemoglobin to alter the pressure range over which the lymph pump operates appears to be dependent on an intact endothelium.

Homologous and heterologous regulation of somatostatin-binding sites on chicken adenohypophysial membranes

1990 ◽  
Vol 127 (3) ◽  
pp. 417-425 ◽  
Author(s):  
S. Harvey ◽  
J. S. Baidwan ◽  
D. Attardo
Keyword(s):  
Pituitary Gland ◽  
Binding Sites ◽  
Recombinant Dna ◽  
Inhibitory Effect ◽  
Partial Recovery ◽  
Caudal Lobe ◽  
Direct Inhibitory Effect ◽  
Pituitary Glands

ABSTRACT Binding of 125I-labelled [Tyr1]-somatostatin (125I-[Tyr1]-SRIF) to pituitary caudal lobe membranes was suppressed in immature chickens 1 and 2 h after i.v. administration of unlabelled SRIF at concentrations of 1–100 μg/kg. In-vitro preincubation of chicken pituitary glands for 0·5–4·0 h with 0·1 μmol SRIF/l similarly reduced the binding of 125I-[Tyr1]-SRIF to caudal lobe membrane preparations. After a 4-h incubation in 0·1 mmol SRIF/l, the withdrawal of SRIF from the incubation media was accompanied 4 h later by a partial recovery in the binding of 125I-[Tyr1]-SRIF to pituitary membranes. Passive immunoneutralization of endogenous SRIF resulted in a prompt (within 1 h) and sustained (for at least 24 h) suppression of 125I-[Tyr1]-SRIF binding to pituitary membranes. The i.m. administration of cysteamine (300 mg/kg) to 12-week-old birds depleted hypothalamic SRIF stores and decreased the density of 125I-[Tyr1]-SRIF-binding sites in the caudal and cephalic lobes of the chicken pituitary gland. The reduction in SRIF content and in SRIF-binding sites occurred within 1 h of cysteamine administration and was maintained for at least 24 h. In 6-week-old birds, cysteamine (300 mg/kg) administration suppressed pituitary binding of 125I-[Tyr1]-SRIF for at least 5 days. Circulati concentrations of GH were markedly decreased 1 and 4 h after cysteamine injection, but not after 24 h. Pituitary binding sites for 125I-[Tyr1]-SRIF were not affected by pretreatment of pituitary glands for 2–12 h in vitro with thyroxine or oestradiol-17β (1 nmol/l–10 μmol/l) or with ovine GH or recombinant DNA-derived chicken GH (1–100 μg/ml in vitro and 100–1000 μg/kg in vivo). Ovine prolactin, at concentrations of 1–100 μg/ml was also without effect on 125I-[Tyr1]-SRIF binding to pituitary membranes following a 2- or 4-h incubation with pituitary glands. Pituitary binding sites for 125I-[Tyr1]-SRIF were, however, increased after a 24-h incubation with 1 μmol tri-iodothyronine (T3)/l in vitro and 4 and 24 h after the administration of T3 (100–1000 μg/kg) in vivo. Although T3 had no direct inhibitory effect on 125I-[Tyr1]-SRIF binding to pituitary membranes, binding was suppressed 1 and 2 h after the in-vivo administration of T3 at concentrations of 100–1000 μg/kg. These results therefore demonstrate homologous and heterologous regulation of SRIF-binding sites in the chicken pituitary gland. Journal of Endocrinology (1990) 127, 417–425

scholarly journals Selective inhibition by antiflamrnin-2 of thromboxane B2release from isolated and perfused guinea-pig lung

1992 ◽  
Vol 1 (4) ◽  
pp. 251-254
Author(s):  
Lidia Sautebin ◽  
Giuseppe Cirino ◽  
Massimo Di Rosa
Keyword(s):  
Guinea Pig ◽  
Histamine Release ◽  
Calcium Ionophore ◽  
Selective Inhibition ◽  
Inhibitory Effect ◽  
Amino Acid Residues ◽  
A 23187 ◽  
Normal Lungs

Antiflammin-2 (AF2) is a nonapeptide corresponding to the amino acid residues 246–254 of lipocortin-1 showing anti-inflammatory activity both in vitro and in vivo. The effect of AF2 on the thromboxane B2(TXB2) and histamine release from isolated and perfused guinea-pig lungs has been studied. AF-2 (10–100 nM) inhibited leukotriene C4- (LTC4) (3 ng) and antigen-induced (ovalbumin, 1 mg) TXB2release in normal and sensitized lungs, respectively. In contrast AF-2 (100 nM) did not modify TXB2release induced by histamine (5 μg) or bradykinin (5 μg) in normal lungs. Antigen-induced histamine release was not affected by 100 nM AF-2 infusion. When tested in chopped lung fragments AF-2 (0.1–25 μM) did not modify the release of histamine and TXB2induced by antigen (ovalbumin, 10 μg ml−1) or calcium ionophore A 23187 (1 μM). Our results show that the inhibitory effect of AF-2 on TXB2release is selective and depends on the stimulus applied. In this respect AF-2 mimics, at least in part, the actions of both glucocorticoids and lipocortin-1.

scholarly journals Bronchodilatory effect of Myxopyrum serratulum in animal model

2017 ◽  
Vol 12 (1) ◽  
pp. 84
Author(s):  
Vijayalakshmi Maruthamuthu ◽  
Ruckmani Kandasamy
Keyword(s):  
Guinea Pig ◽  
Methanolic Extract ◽  
Relaxation Effect ◽  
Inhibitory Effect ◽  
Chlorpheniramine Maleate ◽  
Relaxant Effect ◽  
Significant Inhibitory Effect ◽  
Guinea Pig Model

<p class="Abstract">The plant <em>Myxopyrum </em>serratulum is traditionally claimed to relieve asthma and cough. The present study was undertaken to evaluate the bronchodilatory effect of the methanolic extract of <em>M. </em>serratulum on histamine-induced bronchospasm by <em>in vivo</em> and the inhibitory effect of the extract on histamine-contracted tracheal chain and ileum by <em>in vitro</em> guinea pig model. Additionally, the relaxant effect of four cumulative concentrations of the extract (0.25, 0.5, 0.7 and 1.0 g%) was assessed using precontracted tracheal chain under different conditions. The extract (400 mg/kg) prolonged the preconvulsive time to 102.3 ± 3.8 sec when compared to saline and standard chlorpheniramine maleate as 121.3 ± 4.5 sec (p&lt;0.05). The extract also possessed significant inhibitory effect on histamine-contracted guinea pig ileum and tracheal chain and also exhibited significant relaxation effect on precontracted tracheal chain of guinea pig models contracted by 60 mM KCl (p&lt;0.001) and 10 µM methacholine (p&lt;0.001) when compared with standard theophylline.</p>

Thyroidal inhibition of chicken pituitary growth hormone: alterations in secretion and accumulation of newly synthesized hormone

1991 ◽  
Vol 131 (1) ◽  
pp. 39-48 ◽  
Author(s):  
R. J. Denver ◽  
S. Harvey
Keyword(s):  
Thyroid Hormone ◽  
Mammalian Species ◽  
Inhibitory Effect ◽  
Stimulatory Action ◽  
Thyrotrophin Releasing Hormone ◽  
Gh Secretion ◽  
Direct Inhibitory Effect ◽  
Hormone Exposure

ABSTRACT Hypothyroidism reduces GH synthesis and release in several mammalian species, in which thyroid hormone directly stimulates GH gene transcription. In contrast, hypothyroidism stimulates GH secretion in birds, in which thyroid hormone directly inhibits pituitary GH release. We have, therefore, investigated the effects of thyroid status on the accumulation of newly synthesized GH in the pituitaries of 8- to 10-week-old Leghorn cockerels in vitro and in vivo. The incorporation of [35S]methionine into immunoprecipitable GH ([35S] GH) was increased, over a 4-h incubation period, in glands from birds made hypothyroid by injections of methimazole (50 mg/kg day for 10 days) in comparison with glands from vehicle-injected controls. Treatment with tri-iodothyronine (T3, 100 μg/kg per day for 10 days) in vivo did not significantly alter the accumulation of [35S]GH in vitro but did block the release of [35S]GH in response to a GH secretagogue (thyrotrophin-releasing hormone; exposure to 280 nmol/l for 30 min) and reduced immunoassayable pituitary GH content. Pretreatment of glands from euthyroid birds with T3 (100 nmol/l) in vitro (for 20 h) reduced the basal accumulation of [35S]GH as well as that induced by another GH secretagogue (GH-releasing factor; 100 nmol/l) during a 6-h labelling period. These results show that, unlike the generally stimulatory action of thyroid hormone in mammals, in birds, T3 exerts a direct inhibitory effect on the accumulation of newly synthesized pituitary GH. Journal of Endocrinology (1991) 131, 39–48

Effects of Dipyridamole and Aspirin on Platelet camp Levels and Prostaglandin Biosynthesis in vivo in Patients with Diabetes Mellitus

1979 ◽  
Author(s):  
L.C. Best ◽  
M.B. McGuire ◽  
J.D. Ward ◽  
T. Holland ◽  
F. E. Preston ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Cyclic Amp ◽  
Microvascular Complications ◽  
Inhibitory Effect ◽  
Slight Reduction ◽  
Patients With Diabetes ◽  
Direct Inhibitory Effect ◽  
Pre Treatment

Platelets from diabetics with microvascular complications were shown to have lowered aggregation thresholds to ADP, epinephrine and collagen. They also produced more malonyl dialdehyde (MDA) than normal controls. In eight diabetic subjects, administration of dipyridamole (100mg tds)raised platelet aggregation thresholds and increased cyclic AMP levels, presumably as a result of inhibition of phosphodiesterase activity. It also caused a slight reduction of MDA production. This latter effect could be due to the rise in cyclic AMP, although we have found an apparently direct inhibitory effect to dipyridamole on MDA and thromboxane B2 production by intact platelets and platelet microsomes in vitro. On withdrawal of the drug, platelet cyclic AMP and MDA levels and aggregation thresholds returned toward pre-treatment levels. The administration of aspirin (120) plus dipyridamole markedly inhibited platelet aggregation, particularly in response to arachidonic acid and collagen and strongly inhibited MDA production. However, the rise in platelet cyclic AMP levels produced by dipyridamole alone was not present when aspirin and dipyridamole were given together, Aspirin may influence platelet cyclic AMP metabolism directly or by inhibiting prostacyclin formation. Thus, under appropriate conditions, basal platelet cyclic AMP may provide an index of PGI2 production in vivo.

The Effect of Barbituric Acid Derivatives on Platelet Function in Vitro and in Vivo

1973 ◽  
Vol 30 (02) ◽  
pp. 315-326
Author(s):  
J. Heinz Joist ◽  
Jean-Pierre Cazenave ◽  
J. Fraser Mustard
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Barbituric Acid ◽  
Platelet Rich Plasma ◽  
Inhibitory Effect ◽  
Primary Response ◽  
Sodium Pentobarbital ◽  
Barbituric Acid Derivatives

SummarySodium pentobarbital (SPB) and three other barbituric acid derivatives were found to inhibit platelet function in vitro. SPB had no effect on the primary response to ADP of platelets in platelet-rich plasma (PRP) or washed platelets but inhibited secondary aggregation induced by ADP in human PRP. The drug inhibited both phases of aggregation induced by epinephrine. SPB suppressed aggregation and the release reaction induced by collagen or low concentrations of thrombin, and platelet adherence to collagen-coated glass tubes. The inhibition by SPB of platelet aggregation was readily reversible and isotopically labeled SPB did not become firmly bound to platelets. No inhibitory effect on platelet aggregation induced by ADP, collagen, or thrombin could be detected in PRP obtained from rabbits after induction of SPB-anesthesia.

Phenolic Acids Exert Anticholinesterase and Cognition-Improving Effects

2018 ◽  
Vol 15 (6) ◽  
pp. 531-543 ◽  
Author(s):  
Dominik Szwajgier ◽  
Ewa Baranowska-Wojcik ◽  
Kamila Borowiec
Keyword(s):  
Phenolic Acids ◽  
Ex Vivo ◽  
Amyloid Β ◽  
Inhibitory Effect ◽  
In Vivo Studies ◽  
Amyloid Β Peptide ◽  
Beneficial Effects ◽  
Aβ Fibrils

Numerous authors have provided evidence regarding the beneficial effects of phenolic acids and their derivatives against Alzheimer's disease (AD). In this review, the role of phenolic acids as inhibitors of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) is discussed, including the structure-activity relationship. In addition, the inhibitory effect of phenolic acids on the formation of amyloid β-peptide (Aβ) fibrils is presented. We also cover the in vitro, ex vivo, and in vivo studies concerning the prevention and treatment of the cognitive enhancement.

Sign in / Sign up

Export Citation Format

Share Document