Muscle Relaxants and Reversal Agents

1991 ◽  
Vol 3 (1) ◽  
pp. 151-158 ◽  
Author(s):  
Andrew D. Van Sickel ◽  
Karen Spadaccia
ChemInform ◽  
2010 ◽  
Vol 33 (25) ◽  
pp. no-no
Author(s):  
Kenneth S. Cameron ◽  
Lee Fielding ◽  
Rona Mason ◽  
Alan W. Muir ◽  
David C. Rees ◽  
...  

2002 ◽  
Vol 12 (5) ◽  
pp. 753-755 ◽  
Author(s):  
Kenneth S. Cameron ◽  
Lee Fielding ◽  
Rona Mason ◽  
Alan W. Muir ◽  
David C. Rees ◽  
...  

2006 ◽  
Vol 34 (4) ◽  
pp. 415-415 ◽  
Author(s):  
C. Ball ◽  
R. N. Westhorpe

Author(s):  
Chris Dodds ◽  
Chandra M. Kumar ◽  
Frédérique Servin

The importance of the changes and variability in pharmacology with ageing and the risks these pose in the elderly are emphasized. Detailed descriptions are given of the pharmacokinetic aspects of distribution, initial volume of distribution, and plasma binding; elimination affected by hepatic and renal clearance changes; and effect site variability. The pharmacodynamics changes are then reviewed. Specific anaesthetic agents are then described, covering the induction agents thiopentone, propofol, etomidate, ketamine, and midazolam. The volatile anaesthetics sevoflurane and desflurane, and nitrous oxide are discussed. The opioid analgesics fentanyl, alfentanil, sufentanil, and remifentanil are described followed by the opiate morphine. The much slower onset and offset of muscle relaxants in the elderly is explained, and the differences between steroid and benzylisoquinolinium compounds are described. Finally, the reversal agents, including sugammadex, are reviewed.


1979 ◽  
Vol 41 (03) ◽  
pp. 475-490 ◽  
Author(s):  
Chaoho Ouyang ◽  
Che-Ming Teng

SummaryThe minimal concentration of the platelet aggregation principle (Platelet Aggregoserpen- tin, PAS) necessary to induce platelet aggregation was 10 ng/ml, about one-hundredth of that of the crude venom. PAS induced the release of platelet factors 3 and 4 from platelets, but the released platelet factor 3 was easily inactivated by the anti-phospholipid effect of PAS. Pretreatment of platelets with neuraminidase potentiated PAS-induced platelet aggregation. PAS-induced platelet aggregation was independent on released ADP; it could occur in the ADP-removing systems, such as apyrase or a combination of phosphoenolpyruvate and pyruvate kinase. However, PAS-induced platelet aggregation could be inhibited by adenine nucleotides and adenosine.PAS-induced platelet aggregation was inhibited by some anti-inflammatory agents, antimalarial drugs, local anesthetics, antihistamine and smooth muscle relaxants. After deaggregation of PAS-treated platelets, thrombin and sodium arachidonate could further induce platelet aggregation, but ADP and second dose of PAS could not. It is concluded that PAS-induced platelet aggregation is due to prostaglandin synthesis. Recent literatures on the mechanism of platelet aggregation were surveyed and the actions of PAS were discussed.


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