Effects of Alpha and Beta Receptor Stimulating and Blocking Agents on Experimental Disseminated Intravascular Coagulation

Moriau, M; Noel, H; Masure, R

doi:10.1055/s-0038-1647682

Cited by 15 publications

(3 citation statements)

References 20 publications

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“…The rise in the negative charge [5] and aggregation was reversed in vitro with -blocking agents, particularly with PRO, in a dose-dependent way (6,7). There were no species differences in the inhibition of platelet aggregation induced by -blockers in vitro.…”

Section: In Vitro Studies Bab Drugs and Platelet Aggregationmentioning

confidence: 82%

Antiplatelet and Antileukocyte Effects of Cardiovascular,Immunomodulatory and Chemotherapeutic Drugs

Nosáľ¹

2006

CHAMC

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In vitro and ex vivo interactions of betaadrenoceptor blocking drugs, antihistamines and chloroquine with blood platelets and polymorphonuclear leukocytes resulted in different alterations of regulatory functions of these blood cells. Inhibition of platelet aggregation, arachidonate regulatory pathway, 5-hydroxytryptamine transportation, removal of platelet membrane receptors, inhibition of second messenger pathways at subcellular level and suppression of phagocytosis are indicative of nonreceptor rather than specific receptor interactions. Binding of drugs with biomembranes is reversible depending on the ionic charge of the molecule and hydrophobicity of the bilayer, partition coefficient, pH and pKa of the amphiphilic molecules and other physico-chemical properties of amphiphilic drugs. Alterations in the drug molecule structure alters the drug-phospholipid binding profile. Any change in the metabolism of membrane phospholipids directly or indirectly influences one or more of the important components of the phospholipid-signalling pathway. In addition to changes in phospholipase A, C and D activities, protein kinase C, calmodulin-phosphodiesterase, Ca2+,Mg2+-ATPase, Na+,K+-ATPase and other messengers were found to be changed in cells and tissue after cationic amphiphilic drug (CAD) administration. Although not much has been understood of the mechanism by which some CAD affect immune functions, there are good reasons to suggest that these effects might occur. CADs share sufficient similarities in their structure even though they come from diverse pharmacological classes. CADs affect ion transport, immune functions, tumour growth, serotonin metabolism and several other functions in the body. Extensive therapeutic use and associated side effects have generated a great deal of interest in understanding the nonreceptor interactions with CADs.

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Section: In Vitro Studies Bab Drugs and Platelet Aggregationmentioning

confidence: 82%

Antiplatelet and Antileukocyte Effects of Cardiovascular,Immunomodulatory and Chemotherapeutic Drugs

Nosáľ¹

2006

CHAMC

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“…More than the α-receptor sites may be involved, however. Moriau et al [158] observed an enhancement of artificial DIC (intra venous thrombin to rabbits) when either the alpha or the beta receptor sites were stimulated by metaraminol and isoproterenol, respectively, and more so still if both stimulators were used. Further, if the receptor sites were blocked-alpha by phentolamine and beta by practolol, singly or especially together-the DIC was minimized.…”

Section: Causes Of Icf Syndromesmentioning

confidence: 99%

Chronic Intravascular Coagulation and Fibrinolysis (ICF) Syndromes (DIC)

Owen¹,

Bowie²

2008

Semin Thromb Hemost

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“…In thromboembolic diseases accom panied by an elevated catecholamine level in blood, adrenaline-mediated platelet reactions may enhance the risk of thrombosis. As shown in animal experiments, catecholamines promote platelet aggregation in the microvasculature and increase experimental disseminated intra vascular coagulation (11,15,16,18,25). Therefore, tire pharmacological influence on adrenaline-induced changes in platelets pro vokes growing interest.…”

mentioning

confidence: 90%

Studies on the Inhibition of Adrenaline-Induced Aggregation of Blood Platelets

Glusa¹,

Markwardt²,

Barthe³

1979

Pharmacology

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α-Adrenoceptors of platelets seem to differ from those of other cell types. The inhibitory effect of α-adrenoceptor-blocking agents on adrenaline-induced aggregation of human platelets does not parallel that on adrenaline-induced contraction of rabbit aortic strips. The most potent inhibitors of adrenaline-induced platelet aggregation are the dihydrogenated ergot alkaloids of the peptide type. Among the other ergoline derivatives tested, only lisuride has a stronger inhibitory effect than those of natural ergot alkaloids.

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Effects of Alpha and Beta Receptor Stimulating and Blocking Agents on Experimental Disseminated Intravascular Coagulation

Cited by 15 publications

References 20 publications

Antiplatelet and Antileukocyte Effects of Cardiovascular,Immunomodulatory and Chemotherapeutic Drugs

Antiplatelet and Antileukocyte Effects of Cardiovascular,Immunomodulatory and Chemotherapeutic Drugs

Chronic Intravascular Coagulation and Fibrinolysis (ICF) Syndromes (DIC)

Studies on the Inhibition of Adrenaline-Induced Aggregation of Blood Platelets

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