In Vitro Effects of Ethanol on Rabbit Platelet Aggregation, Secretion of Granule Contents, and Cyclic AMP Levels in the Presence of Prostacyclin

1989 ◽  
Vol 61 (02) ◽  
pp. 254-258 ◽  
Author(s):  
Margaret L Rand ◽  
Peter L Gross ◽  
Donna M Jakowec ◽  
Marian A Packham ◽  
J Fraser Mustard
Keyword(s):  
Cyclic Amp ◽  
Inhibitory Effect ◽  
Rabbit Platelet ◽  
Inhibitory Effects ◽  
Low Concentrations ◽  
Rabbit Platelets ◽  
High Concentrations ◽  
In Vitro Effects ◽  
Aggregation Of Platelets

SummaryEthanol, at physiologically tolerable concentrations, inhibits platelet responses to low concentrations of collagen or thrombin, but does not inhibit responses of washed rabbit platelets stimulated with high concentrations of ADP, collagen, or thrombin. However, when platelet responses to high concentrations of collagen or thrombin had been partially inhibited by prostacyclin (PGI2), ethanol had additional inhibitory effects on aggregation and secretion. These effects were also observed with aspirin- treated platelets stimulated with thrombin. Ethanol had no further inhibitory effect on aggregation of platelets stimulated with ADP, or the combination of ADP and epinephrine. Thus, the inhibitory effects of ethanol on platelet responses in the presence of PGI2 were very similar to its inhibitory effects in the absence of PGI2, when platelets were stimulated with lower concentrations of collagen or thrombin. Ethanol did not appear to exert its inhibitory effects by increasing cyclic AMP above basal levels and the additional inhibitory effects of ethanol in the presence of PGI2 did not appear to be brought about by further increases in platelet cyclic AMP levels.

Ticlopidine Selectively Inhibits Human Platelet Responses to Adenosine Diphosphate

1991 ◽  
Vol 66 (06) ◽  
pp. 694-699 ◽  
Author(s):  
Marco Cattaneo ◽  
Benjaporn Akkawat ◽  
Anna Lecchi ◽  
Claudio Cimminiello ◽  
Anna M Capitanio ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Adenosine Diphosphate ◽  
Inhibitory Effect ◽  
Clot Retraction ◽  
Fibrinogen Binding ◽  
Low Concentrations ◽  
Binding Inhibition ◽  
High Concentrations ◽  
Formalin Fixed

SummaryPlatelet aggregation and fibrinogen binding were studied in 15 individuals before and 7 days after the oral administration of ticlopidine (250 mg b.i.d.). Ticlopidine significantly inhibited platelet aggregation induced by adenosine diphosphate (ADP), the endoperoxide analogue U46619, collagen or low concentrations of thrombin, but did not inhibit platelet aggregation induced by epinephrine or high concentrations of thrombin. Ticlopidine inhibited 125I-fibrinogen binding induced by ADP, U46619 or thrombin (1 U/ml). The ADP scavengers apyrase or CP/CPK, added in vitro to platelet suspensions obtained before ticlopidine, caused the same pattern of aggregation and 125I-fibrihogen binding inhibition as did ticlopidine. Ticlopidine did not inhibit further platelet aggregation and 125I-fibrinogen binding induced in the presence of ADP scavengers. After ticlopidine administration, thrombin or U46619, but not ADP, increased the binding rate of the anti-GPIIb/IIIa monoclonal antibody 7E3 to platelets. Ticlopidine inhibited clot retraction induced by reptilase plus ADP, but not that induced by thrombin or by reptilase plus epinephrine, and prevented the inhibitory effect of ADP, but not that of epinephrine, on the PGE1-induced increase in platelet cyclic AMP. The number of high- and low-affinity binding sites for 3H-ADP on formalin-fixed platelets and their K d were not modified by ticlopidine. These findings indicate that ticlopidine selectively inhibits platelet responses to ADP.

Effects of heavy metals and other trace elements on the fermentative activity of the rumen microflora and growth of functionally important rumen bacteria

1978 ◽  
Vol 24 (3) ◽  
pp. 298-306 ◽  
Author(s):  
C. W. Forsberg
Keyword(s):  
Trace Elements ◽  
Rumen Fluid ◽  
Inhibitory Effect ◽  
Rumen Bacteria ◽  
Inhibitory Effects ◽  
Butyrivibrio Fibrisolvens ◽  
Fermentative Activity ◽  
Rumen Microflora ◽  
High Concentrations

The inhibitory effects of high concentrations of essential and non-essential trace elements were tested on the rumen microflora using the rate of fermentation in vitro as the assay. The elements (and the concentration causing 50% inhibition) in decreasing order of toxicity were Hg2+ (20 μg/ml), Cu2+ (21 μg/ml), Cr6+ (70 μg/ml), Se4+ (73 μg/ml), Ni2+ (160 μg/ml), Cd2+ (175 μg/ml), As3+ (304 μg/ml), and As5+ (1610 μg/ml). The elements tested that were either weak or non-inhibitory at concentrations greater than 400 μg/ml included Zn2+, Cr2+, Fe2+, Mn2+, Pb2+, and Co2+. Methylmercury was as inhibitory as mercuric chloride to the fermentation. When the inhibitory effect of Cd2+ was tested on separated bacterial and protozoal fractions, it was more inhibitory to the bacteria. The inhibitory effects of trace elements were also determined for a number of axenic cultures of rumen bacteria. The bacteria which most frequently exhibited the greatest sensitivity were Bacteroides succinogenes, Ruminococcus albus, Bacteroides amytophilus, and Eubacterium ruminantium. Those often exhibiting intermediate sensitivities included Butyrivibrio fibrisolvens, Selenomonas niminantium, and Megasphera elsdenii, while Streptococcus bovis was very refractory to all elements tested. Rumen fluid provided a modest protective effect for the bacteria.

scholarly journals Effect of aluminium toxicity on the development of poplar (Populus tremula L. x P. alba L.) cultured in vitro

2014 ◽  
Vol 68 (4) ◽  
pp. 245-250 ◽  
Author(s):  
Krystyna Bojarczuk
Keyword(s):  
Aluminium Toxicity ◽  
Inhibitory Effect ◽  
Populus Tremula ◽  
Aluminium Chloride ◽  
Adventitious Bud ◽  
Aluminium Sulphate ◽  
Low Concentrations ◽  
The Media ◽  
High Concentrations

Adventitious bud cultures were established using vegetative buds from selected clones of poplar (<em>Populus tremula</em> L. x <em>P</em>. <em>alba</em> L.) as initial explants. For multiplication of shoots a modified Murashige and Skoog medium (MS) was used. Aluminium salts (aluminium sulphate and aluminium chloride) were added to the media. It was found that the pH of the medium had no effect on the development of cultures at low concentrations of nutrients (1/2 or 1/4 MS). Low concentrations of aluminium (Al 25mg•dm<sup>-3</sup> supplied as aluminium sulphate, Al 15 mg•dm<sup>-3</sup> as aluminium chloride) had no inhibitory effect on shoot development but decreased regeneration of adventitious roots. High concentrations of aluminium inhibited the development of shoots and roots, especially in a medium at pH 4.5. Microcuttings rooted in the highest percentage and formed the strongest rooting system on 1/4 strength MS medium at pH 4.5. It was found that there was no difference between the rooting of shoots excised from cultures cultivated with or without A1 in this medium at pH 5.5.

The Role of Prostaglandins in the ADP-Induced Aggregation of Rabbit Platelets Shown by the Use of 15-Hydroxyprostaglandin Dehydrogenase

1978 ◽  
Vol 39 (03) ◽  
pp. 725-732 ◽  
Author(s):  
Robert B Wallis
Keyword(s):  
Platelet Rich Plasma ◽  
Shape Change ◽  
Rabbit Platelet ◽  
Direct Role ◽  
Initial Shape ◽  
Rabbit Platelets ◽  
Induced Aggregation ◽  
Aggregation Of Platelets

SummaryThe initial shape change and subsequent aggregation of platelets in citrated rabbit platelet-rich plasma caused by ADP in vitro was inhibited by 15-hydroxyprostaglandin dehydrogenase. This inhibition was NAD-dependent and was also seen when shape change and aggregation were initiated by sodium arachidonate or by collagen. The aggregation of gel-filtered rabbit platelets by thrombin was not, however, affected by removal of 15-hydroxyprostaglandins.Indomethacin was found to inhibit ADP-induced aggregation but at a concentration (250 μM) much higher than that required to inhibit collagen-induced aggregation. Moreover the platelet release reaction had not taken place 3 min after ADP stimulation. The direct role 15-hydroxyprostaglandin production in ADP-induced aggregation of rabbit platelets is proposed. The involvement of 15-hydroxyprostaglandins in platelet aggregation caused by other inducers is also discussed.

Regulation of Thromboplastin Synthesis in Mouse Placental Cells In Vitro

1983 ◽  
Vol 50 (04) ◽  
pp. 831-834 ◽  
Author(s):  
Knut Dalaker ◽  
Hans Prydz
Keyword(s):  
Cyclic Amp ◽  
Phosphodiesterase Inhibitor ◽  
Inhibitory Effect ◽  
Low Concentrations ◽  
Placental Cells ◽  
Dose Dependent ◽  
Higher Doses ◽  
Dose Dependent Effect ◽  
Methyl Xanthine

SummaryMouse placental cells are probably constitutive producers of the thromboplastin apoprotein in vitro. The effect of cyclic AMP- elevating compounds on their expression of thromboplastin activity has been studied. Dibutyryl cyclic AMP, the phosphodiesterase inhibitor Ro 20-1724 and the adenyl cyclase stimulator forskolin all decrease the synthesis of thromboplastin. Prostaglandin E2 and the phosphodiesterase inhibitor butyl-methyl-xanthine have a biphasic dose dependent effect. A stimulation was observed at low concentrations, whereas higher doses decreased the synthesis of thromboplastin. Adrenaline had no effect. Combination of two compounds, each at maximally inhibiting concentration gave no significant additive inhibitory effect, showing that they probably act via the same pathway.

HIGH CONCENTRATIONS OF HEPARIN ARE MORE INHIBITORY TO PLATE- AGGREGATION IN-VITRO THAN ARE LOW MOLECULAR WEIGHT HEPARINS AND HEPARINOIDS AT THE SAME CONCENTRATION

1987 ◽  
Author(s):  
H Messmore ◽  
B Griffin ◽  
J Seghatchian ◽  
E Coyne
Keyword(s):  
Molecular Weight ◽  
Heparan Sulfate ◽  
Dermatan Sulfate ◽  
Platelet Rich Plasma ◽  
Inhibitory Effect ◽  
Low Molecular Weight ◽  
Low Concentrations ◽  
High Concentrations ◽  
Induced Aggregation

Other investigators have shown that heparin in the usual therapeutic range (0.1-0.5 units/ml) has an enhancing effect on ADP aggregation and an inhibitory effect on collagen and thrombin induced aggregation. The effects of low molecular weight heparin (LMWH)and heparinoids (dermatan sulfate, heparan sulfate) on platelet aggregation have not been as extensivelystudied. We have utilized citrated platelet rich plasma (3.2%citrate-whole blood 1:9) drawn in plastic and adjusted to a final platelet count of 250,000/ul. A Bio-Data 4 channgl aggregometer was utilized with constantstirring at 37 C. The reaction was allowed to run for 20 minutes. Platelet rich plasma was supplemented 1:9 with saline or heparin and various agonists were then added ifno aggregation occurred. ADP, collagen, thrombin, ristocetin and serum from patients with heparin inudced thrombocytopenia (HIT) were utilized as agonists. Heparin was substituted at concentrations of 0.1 to 500 units per ml and various LMWH and heparinoids were substituted in equivalent anti-Xa or gravimetric concentrations. At low concentrations no inhibitory effect on any ofthe agonists was observed with any of the heparins or heparinoids. At concentrations of heparin of 100 u/ml or greater, all agonists were inhibited. At equivalent concentrations of five different LMWH (Cy 216, Cy 222, Pk 10169, Kabi 2165 and pentasaccharide) inhibition did notoccur at all or at very high concentions only. Dermatan sulfate and heparan sulfate inhibited only at high concentrations. HIT serum could not aggregate platelets with dermatan sulfate or pentasaccharide atany concentrations, but it was a good agonist with the other heparins and heparinoids.

scholarly journals New Coumarinic Azo-Derivatives of Metoclopramide and Diphenhydramine: Synthesis and In Vitro Testing for Cholinesterase Inhibitory Effect and Protection Ability Against Chlorpyrifos

2020 ◽  
Vol 13 (1) ◽  
Author(s):  
Mahmood AAJ ◽  
Mustafa YS ◽  
Abdulstaar M
Keyword(s):  
Inhibitory Effect ◽  
Azo Compounds ◽  
Inhibitory Effects ◽  
High Concentration ◽  
Low Concentrations ◽  
Maximum Protection ◽  
Coumarin Compounds ◽  
New Compounds ◽  
Derivatives Of

Introduction: This study aims to synthesize new coumarin azo compounds of metoclopramide and diphenhydramine and to evaluate their in vitro cholinesterase inhibitory effects and protection abilities against chlorpyrifos. Methods: Two series of azo coumarin compounds were synthesized. Series I compound resulted from the diazotization of metoclopramide and then coupling with coumarin and 4-methyl coumarin to give compounds 1 and 2 respectively. Series II compound resulted from the diazotization of 7-aminocoumarin and 7-amino 4-methyl coumarin and then coupling with diphenhydramine to give compounds 3 and 4 respectively. The new compounds were tested for their in vitro cholinesterase inhibitory effect and protection ability against chlorpyrifos using the modified Elman electrometric method. Results: Metoclopramide derivatives with coumarin show selectivity protection for ChE against chlorpyriphos inhibitory effect as protect BChE and increase the inhibition of the AChE, or the opposite. Conclusion: Diphenhydramine derivatives with coumarin show more protective ability for both BChE and AChE as one of them shows the maximum protection for all concentration. However, the other derivative shows different manner as the low concentrations act as metoclopramide derivatives while the high concentration act as first diphenhydramine derivative (protect both AChE and BChE).

scholarly journals A proteinaceous organic matrix regulates carbonate mineral production in the marine teleost intestine

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Kevin L. Schauer ◽  
Christophe M. R. LeMoine ◽  
Adrian Pelin ◽  
Nicolas Corradi ◽  
M. Danielle McDonald ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Organic Matrix ◽  
Magnesium Content ◽  
Inhibitory Effect ◽  
Marine Teleost ◽  
Low Concentrations ◽  
The Matrix ◽  
Mineral Production ◽  
High Concentrations

AbstractMarine teleost fish produce CaCO3in their intestine as part of their osmoregulatory strategy. This precipitation is critical for rehydration and survival of the largest vertebrate group on earth, yet the molecular mechanisms that regulate this reaction are unknown. Here, we isolate and characterize an organic matrix associated with the intestinal precipitates produced by Gulf toadfish (Opsanus beta). Toadfish precipitates were purified using two different methods, and the associated organic matrix was extracted. Greater than 150 proteins were identified in the isolated matrix by mass spectrometry and subsequent database searching using anO. betatranscriptomic sequence library produced here. Many of the identified proteins were enriched in the matrix compared to the intestinal fluid, and three showed no substantial homology to any previously characterized protein in the NCBI database. To test the functionality of the isolated matrix, a micro-modifiedin vitrocalcification assay was designed, which revealed that low concentrations of isolated matrix substantially promoted CaCO3production, where high concentrations showed an inhibitory effect. High concentrations of matrix also decreased the incorporation of magnesium into the forming mineral, potentially providing an explanation for the variability in magnesium content observed in precipitates produced by different fish species.

A biphasic effect of noradrenaline on renin release from rat juxtaglomerular cells in vitro is mediated by α1- and β-adrenoceptors

1992 ◽  
Vol 132 (1) ◽  
pp. 133-140 ◽  
Author(s):  
M. Takagi ◽  
K. Atarashi ◽  
H. Matsuoka ◽  
T. Sugimoto
Keyword(s):  
Dynamic Balance ◽  
Inhibitory Effect ◽  
Renin Release ◽  
Dependent Manner ◽  
Adrenergic Stimulation ◽  
Cortical Cells ◽  
Adrenoceptor Antagonist ◽  
Low Concentrations ◽  
High Concentrations

ABSTRACT The direct effect of noradrenaline on renin release from juxtaglomerular (JG) cells in vitro were investigated in a dynamic superfusion system of dispersed rat renal cortical cells. At low concentrations (1–100 nmol/l), noradrenaline stimulated renin release in a dose-dependent manner, while at higher concentrations (0·1–1 mmol/l) it inhibited renin release. The stimulatory effect of 0·1 μmol noradrenaline/l was completely blocked by a β-adrenoceptor antagonist, propranolol (0·1 μmol/l). When applied at concentrations of 1 μmol/l or 10 μmol/l, noradrenaline had no consistent effect on renin release, although 10 μmol noradrenaline/l had an inhibitory effect in the presence of propranolol (0·1 μmol/l). The inhibitory effect of noradrenaline (0·1 mmol/l) was converted to a stimulatory effect by the addition of an α1-adrenoceptor antagonist (bunazosin, 1 μmol/l), but was not altered by the addition of an α2-adrenoceptor antagonist (yohimbine, 1 μmol/l). These results indicate that low concentrations of noradrenaline directly stimulate renin release from JG cells by the activation of β-adrenoceptors, while high concentrations of nor-adrenaline inhibit renin release by the activation of α1-adrenoceptors. Accordingly, a dynamic balance may exist between β-adrenergic stimulation and α1-adrenergic depression of renin release. Journal of Endocrinology (1992) 132, 133–140

Regional release of [3H]dopamine from rat brain in vitro: effects of opioids on release induced by potassium, nicotine, and L-glutamic acid

1983 ◽  
Vol 61 (1) ◽  
pp. 43-60 ◽  
Author(s):  
Marc Marien ◽  
James Brien ◽  
Khem Jhamandas
Keyword(s):  
Glutamic Acid ◽  
Rat Brain ◽  
Brain Regions ◽  
Inhibitory Effect ◽  
Significant Inhibition ◽  
Endogenous Opioid ◽  
Low Concentrations ◽  
In Vitro Effects ◽  
The Brain

Previous studies have suggested that the release of dopamine (DA) in the rat brain may be sensitive to modulation by opioid agents, including the endogenous opioid peptides (enkephalins and endorphins). The present study examined the effects of morphine and the enkephalin analogue D-Ala2-Met5-enkephalinamide (DALA) on the release of radiolabeled DA from superfused slices of rat brain regions. The release of preloaded [3H]DA was evoked from slices of the caudate–putamen (CP) by application of potassium (K+), nicotine (NIC), or L-glutamic acid (L-GLU). The release of [3H]DA from slices of the nucleus accumbens (NA), olfactory tubercle (OT), and substantia nigra (SN) was evoked by L-GLU. Both K+ and NIC evoked a concentration-related release of [3H]DA from CP slices. K+-induced release was only partially dependent on calcium (Ca2+), while NIC-evoked release was completely Ca2+ independent. Neither morphine nor DALA influenced the release of [3H]DA evoked by K+ or NIC. L-GLU produced a concentration-dependent release of [3H]DA from slices of CP, NA, OT, and SN. In all four brain regions, this release was (a) Ca2+-dependent, (b) strongly inhibited by low concentrations of magnesium (Mg2+), (c) greater than the release evoked by D-GLU, (d) attenuated by the putative L-GLU receptor antagonist glutamic acid diethylester (GDEE), and (e) insensitive to tetrodotoxin (TTX) except in the SN. Morphine produced a significant inhibition of L-GLU-evoked [3H]DA release from all four regions. Naloxone, which by itself had no significant effect on the L-GLU-evoked release of [3H]DA, blocked the inhibitory effect of morphine on this release in the CP but not in the other regions. Levorphanol and dextrorphan were equipotent in reducing the glutamate-stimulated release of [3H]DA from CP slices. DALA had no effect on L-GLU-induced release in any of the brain regions examined. The results indicate that L-GLU provokes regional release of DA by acting at a Mg2+-sensitive glutamate receptor. This release is selectively modified by morphine through a mechanism which is insensitive to naloxone.

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