scholarly journals An in vitro investigation of the inhibitory effect of methysergide on the spinal monosynaptic reflex discharge

1981 ◽  
Vol 31 ◽  
pp. 264
Author(s):  
Koji Saito ◽  
Shigeo Ito ◽  
Takio Kitazawa ◽  
Akira Ohga
Keyword(s):  
Inhibitory Effect ◽  
Monosynaptic Reflex ◽  
In Vitro Investigation ◽  
Reflex Discharge

Ba2+ inhibition of electrogenic Cl- secretion in vitro frog and piglet gastric mucosa

1980 ◽  
Vol 239 (3) ◽  
pp. G151-G160 ◽  
Author(s):  
W. L. McLennan ◽  
T. E. Machen ◽  
T. Zeuthen
Keyword(s):  
Short Circuit ◽  
Short Circuit Current ◽  
Inhibitory Effect ◽  
Surface Charges ◽  
Inhibitory Effects ◽  
Cl Secretion ◽  
High K ◽  
In Vitro Investigation ◽  
Newborn Pigs

Gastric mucosae from frogs and newborn pigs were used for in vitro investigation of the effects of Ba2+ (10 microM to 7 mM) on transepithelial potential difference (PD), resistance and conductance (G), short-circuit current (Isc), H+ secretion, and transepithelial fluxes of 36Cl-. Ba2+ in the serosal, but not the mucosal, solution of both preparations caused PD, G, Isc, and Cl- secretion (JnetCl, Isc conditions) to decrease, while H+ secretion remained constant. Because the oxyntic cells were most likely the site of action for Ba2+, these cells must have the capacity to secrete Cl- in excess of H+ ions. The inhibitory effect of Ba2+ was not due to competition in the serosal membrane by Ba2+ for surface charges, Ca2+ sites, Na+ sites, or Cl- sites. When [K+] in both the mucosal and serosal solutions or in just the serosal solution ([K+]s) alone was increased to 10 mM, the inhibitory effects of low [Ba2+] were reduced; however, at higher [Ba2+], Isc was stimulated. At least part of the Ba2+ effect seems to be due to blockage of K+ channels in the serosal membrane of oxyntic cells. High [K+]s also caused decreased PD and Isc (but increased G) with no change in H+ secretion. It is proposed that during Isc conditions, JnetCl involves a neutral Na+-dependent accumulation of Cl- within oxyntic cells and a passive, conductive efflux fromthe cells into the mucosal solution. Ba2+ and high [K+] may alter this transport by depolarizing and, under certain conditions, hyperpolarizing intracellular voltage.

scholarly journals An in vitro Investigation into the Cytotoxicity of Methyl Methacrylate Monomer

2012 ◽  
Vol 13 (6) ◽  
pp. 838-841 ◽  
Author(s):  
AV Sreekumar ◽  
Nishna Pradeep
Keyword(s):  
Cell Growth ◽  
Methyl Methacrylate ◽  
Inhibitory Effect ◽  
Control Group ◽  
Dead Cell ◽  
Type I ◽  
In Vitro Investigation ◽  
Methacrylate Monomer ◽  
Methyl Methacrylate Monomer

ABSTRACT Aim of this study was to assess the cytotoxicity of monomer. An in vitro study was designed to study the growth inhibitory effect of monomer (Stellon, Denture Material Improved, Type I, Class I, Dental Products of India Limited) on cells seeded in petri dishes and maintained in an incubator with 5% carbon dioxide at 37°C. The growth of V79 cells (fibroblast cells) maintained in a culture medium to which monomer was added was studied for a period of 5 days. Results of this study pointed out that even at a concentration of 1 μl of monomer, the cell growth was significantly inhibited, when compared to the control group. The number of viable cells decreased dramatically whereas dead cells increased in the culture groups treated with the monomer. The cytotoxic effect was dose dependent. As the concentration increased from 1 to μl there was a marked inhibition of cell growth and a corresponding increase in dead cell count. Results of this study proved beyond doubt that monomer is indeed cytotoxic even in very low concentrations. Thus, it becomes imperative to adopt every possible means to minimize residual monomer content in heat cured resins. Also precautions to minimize tissue contact should be taken while handling monomer by the dentist and dental personnel in the laboratory. How to cite this article Pradeep N, Sreekumar AV. An in vitro Investigation into the Cytotoxicity of Methyl Methacrylate Monomer. J Contemp Dent Pract 2012;13(6):838-841.

scholarly journals L-ascorbyl 6-palmitate as lead compound targeting SphK1: an in silico and in vitro investigation

2021 ◽  
pp. 174751982110018
Author(s):  
HaiJiao Chen ◽  
Xinmei Yang ◽  
Peng Sun ◽  
Ying Zhi ◽  
Qingqiang Yao ◽  
...  
Keyword(s):  
Ascorbyl Palmitate ◽  
Inhibitory Effect ◽  
Lead Compound ◽  
22Rv1 Cell ◽  
In Vitro Investigation ◽  
Anti Cancer ◽  
Sphingosine Kinases ◽  
Lipid Kinases ◽  
Strong Inhibitory Effect

Sphingosine kinases (SphKs) are a class of lipid kinases, that have received extensive attention as important rate-limiting enzyme in tumor. Inhibition of the activity of SphK1 can lead to an anticancer effect. Herein, we describe the discovery process and biological characteristics of a new SphK1 inhibitor, ascorbyl palmitate, discovered through computer-aided drug design. Biochemical experiments show that ascorbyl palmitate has a strong inhibitory effect on SphK1, with an IC50 value of 6.4 μM. The MTT experiment showed that ascorbyl palmitate had anti-cancer effects toward the U87, A549, 22RV1, and A375 cell lines. Among them, ascorbyl palmitate has prominent inhibitory activity against the 22RV1 cell line, with an IC50 value of 41.57 μM. To explore the structure–activity relationship, four ascorbyl palmitate derivatives were synthesized and tested for kinase activity. The outstanding effect of ascorbyl palmitate toward SphK1 and its known non-toxicity suggest that ascorbyl palmitate may be a lead compound for the development of effective SphK1 anti-cancer inhibitors.

Inhibitory effect of gap junction blockers on cerebral vasospasm

2008 ◽  
Vol 108 (3) ◽  
pp. 551-557 ◽  
Author(s):  
Tao Hong ◽  
Yang Wang ◽  
Hai-tao Wang ◽  
Huan Wang
Keyword(s):  
Gap Junctions ◽  
Gap Junction ◽  
Cerebral Vasospasm ◽  
Therapeutic Efficacy ◽  
Morphological Changes ◽  
Inhibitory Effect ◽  
In Vitro Investigation ◽  
Basilar Arteries

Object The gap junction is important in the propagation of dilation/constriction signals along vessels for coordinated behavior in control of vascular tone. The authors hypothesized that gap junctions might play a role in cerebral vasospasm following subarachnoid hemorrhage (SAH). The aims of the present study were to investigate the role of gap junctions and to observe the potential therapeutic efficacy of gap junction blockers in cerebral vasospasm in vitro and in vivo. Methods For the in vitro investigation, the effect of heptanol on the oxyhemoglobin (HbO2)-induced contraction of isolated rabbit basilar arteries (BAs) was observed by using an isometric tension-recording method. For the in vivo experiments, the potential therapeutic efficacy of heptanol and carbenoxolone was surveyed after it was given intravenously in the rabbit double-hemorrhage model. Light microscopy was performed to assess the morphological changes in the arteries examined. Results For the in vitro method, heptanol significantly inhibited the sustained contraction induced both by HbO2 and K+ in the BA rings. The magnitude of the heptanol-induced relaxation was dose dependent. The inhibitory effect of heptanol on the K+-induced vasoconstriction was weaker than that on the HbO2-induced constriction. After arterial rings were pretreated for 10 minutes, heptanol significantly decreased their responses to the HbO2-induced contraction. For the in vivo method, heptanol and carbenoxolone significantly decreased the narrowing of BAs when given intravenously in the rabbit double-hemorrhage model. In both treated groups, the diameters of the arteries had not changed significantly on Day 7 compared with those of the arteries in the SAH + vehicle and the SAH-only group. Conclusions Heptanol and carbenoxolone significantly inhibited the experimental cerebral vasospasm both in vitro and in vivo. Blockage of gap junctions is a probable candidate for a new approach in the treatment of cerebral vasospasm. Gap junctions may play a pathophysiological role in cerebral vasospasm.

In vitro investigation of Varizella zoster virus as an oncolytic virus in glioblastoma therapy

2008 ◽  
Vol 35 (S 01) ◽  
Author(s):  
H Leske ◽  
A Baiker ◽  
C Schichor ◽  
J.C Tonn ◽  
R Goldbrunner ◽  
...  
Keyword(s):  
Oncolytic Virus ◽  
In Vitro Investigation ◽  
Varizella Zoster Virus

Effect of Dipyridamole on Spontaneous Platelet Aggregation in Whole Blood Decreases with the Time After Venepuncture: Evidence for the Role of ADP

1987 ◽  
Vol 58 (02) ◽  
pp. 744-748 ◽  
Author(s):  
A R Saniabadi ◽  
G D O Lowe ◽  
J C Barbenel ◽  
C D Forbes
Keyword(s):  
Platelet Aggregation ◽  
Correlation Coefficient ◽  
Whole Blood ◽  
Blood Platelet ◽  
Inhibitory Effect ◽  
Time Interval ◽  
Adp Receptor ◽  
Spontaneous Platelet Aggregation

SummarySpontaneous platelet aggregation (SPA) was studied in human whole blood at 3, 5, 10, 20, 30, 40 and 60 minutes after venepuncture. Using a whole blood platelet counter, SPA was quantified by measuring the fall in single platelet count upon rollermixing aliquots of citrated blood at 37° C. The extent of SPA increased with the time after venepuncture, with a correlation coefficient of 0.819. The inhibitory effect of dipyridamole (Dipy) on SPA was studied: (a) 10 μM at each time interval; (b) 0.5-100 μM at 3 and 30 minutes and (c) 15 μM in combination with 100 μM adenosine, 8 μM 2-chloroadenosine (2ClAd, an ADP receptor blocker) and 50 μM aspirin. There was a rapid decrease in the inhibitory effect of Dipy with the time after venepuncture; the correlation coefficient was -0.533. At all the concentrations studied, Dipy was more effective at 3 minutes than at 30 minutes after venepuncture. A combination of Dipy with adenosine, 2ClAd or aspirin was a more effective inhibitor of SPA than either drug alone. However, when 15 μM Dipy and 10 μM Ad were added together, the inhibitory effect of Dipy was not increased significantly, suggesting that Dipy inhibits platelet aggregation independent of Ad. The increase in SPA with the time after venepuncture was abolished when blood was taken directly into the anticoagulant containing 5 μM 2ClAd. It is suggested that ADP released from the red blood cells is responsible for the increased platelet aggregability with the time after venepuncture and makes a serious contribution to the artifacts of in vitro platelet function studies.

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.

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.

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.

Inhibition of Platelet Function by Antiarrhythmic Drugs, Verapamil and Disopyramide

1982 ◽  
Vol 47 (02) ◽  
pp. 150-153 ◽  
Author(s):  
P Han ◽  
C Boatwright ◽  
N G Ardlie
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Antiarrhythmic Drugs ◽  
Adenosine Diphosphate ◽  
Inhibitory Effect ◽  
Second Phase ◽  
Ionophore A23187 ◽  
High Concentrations ◽  
Artery Disease

SummaryVarious cardiovascular drugs such as nitrates and propranolol, used in the treatment of coronary artery disease have been shown to have an antiplatelet effect. We have studied the in vitro effects of two antiarrhythmic drugs, verapamil and disopyramide, and have shown their inhibitory effect on platelet function. Verapamil, a calcium channel blocker, inhibited the second phase of platelet aggregation induced by adenosine diphosphate (ADP) and inhibited aggregation induced by collagen. Disopyramide similarly inhibited the second phase of platelet aggregation caused by ADP and aggregation induced by collagen. Either drug in synergism with propranolol inhibited ADP or collagen-induced platelet aggregation. Disopyramide at high concentrations inhibited arachidonic add whereas verapamil was without effect. Verapamil, but not disopyramide, inhibited aggregation induced by the ionophore A23187.

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