Pharmacological studies on a plant lectin, Aloctin A. I. Growth inhibition of mouse methylcholanthrene-induced fibrosarcoma (Meth A) in ascites form by Aloctin A

1981 ◽  
Vol 37 (11) ◽  
pp. 1186-1187 ◽  
Author(s):  
K. Imanishi ◽  
T. Ishiguro ◽  
H. Saito ◽  
I. Suzuki
Keyword(s):  
Growth Inhibition ◽  
Plant Lectin ◽  
Pharmacological Studies ◽  
Ascites Form

Light-induced increase in the contents of ferulic and diferulic acids in cell walls of Avena coleoptiles: its relationship to growth inhibition by light

1994 ◽  
Vol 92 (2) ◽  
pp. 350-355 ◽  
Author(s):  
Kensuke Miyamoto ◽  
Junichi Ueda ◽  
Satomi Takeda ◽  
Kazuko Ida ◽  
Takayuki Hoson ◽  
...  
Keyword(s):  
Growth Inhibition ◽  
Cell Walls

Phytochemical and pharmacological studies of Crotalaria madurensis leaves

Planta Medica ◽  
2008 ◽  
Vol 74 (09) ◽  
Author(s):  
SHM Hala ◽  
SAM Mohamed ◽  
TI Magada ◽  
SA El Batran ◽  
DE Omayma
Keyword(s):  
Pharmacological Studies

Phytochemical and pharmacological studies on commercial teas

Planta Medica ◽  
2012 ◽  
Vol 78 (11) ◽  
Author(s):  
HC Rodda ◽  
FKE Rubra ◽  
B Ramya
Keyword(s):  
Pharmacological Studies

Mechanism of the Antiplatelet Action of Dipyridamole in Whole Blood: Modulation of Adenosine Concentration and Activity

1986 ◽  
Vol 55 (01) ◽  
pp. 012-018 ◽  
Author(s):  
Paolo Gresele ◽  
Jef Arnout ◽  
Hans Deckmyn ◽  
Jos Vermylen
Keyword(s):  
Platelet Aggregation ◽  
Adenosine Receptor ◽  
Whole Blood ◽  
Blood Cells ◽  
Inhibitory Action ◽  
Phosphodiesterase Inhibitor ◽  
Inhibitory Effect ◽  
Adenosine Concentration ◽  
Pharmacological Studies

SummaryDipyridamole inhibits platelet aggregation in whole blood at lower concentrations than in plasma. The blood cells responsible for increased effectiveness in blood are the erythrocytes. Using the impedance aggregometer we have carried out a series of pharmacological studies in vitro to elucidate the mechanism of action of dipyridamole in whole blood. Adenosine deaminase, an enzyme breaking down adenosine, reverses the inhibitory action of dipyridamole. Two different adenosine receptor antagonists, 5’-deoxy-5’-methylthioadenosine and theophylline, also partially neutralize the activity of dipyridamole in blood. Enprofylline, a phosphodiesterase inhibitor with almost no adenosine receptor antagonistic properties, potentiates the inhibition of platelet aggregation by dipyridamole. An inhibitory effect similar to that of dipyridamole can be obtained combining a pure adenosine uptake inhibitor (RE 102 BS) with a pure phosphodiesterase inhibitor (MX-MB 82 or enprofylline). Mixing the blood during preincubation with dipyridamole increases the degree of inhibition. Lowering the haematocrit slightly reduces the effectiveness.Although we did not carry out direct measurements of adenosine levels, the results of our pharmacological studies clearly show that dipyridamole inhibits platelet aggregation in whole blood by blocking the reuptake of adenosine formed from precursors released by red blood cells following microtrauma. Its slight phosphodiesterase inhibitory action potentiates the effects of adenosine on platelets.

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