1 Ondansetron: By preventing the binding of serotonin to its receptor sites through blockage of the 5HT3 receptors, ondansetron ends up preventing the vomiting reflex.
Midazolam: Neural inhibition is caused by the indirect activation of GABA A receptors by midazolam. This occurs through enhancement of GABA on the receptors. This increases the opening of the chloride channels. Consequently, the effects of midazolam are felt i.e. anti-convulsant effects.
Ipratropium: Ipratropium causes relaxation of smooth muscles of the airways. The secretions of the airways are also dried up. This occurs through inhibition of vagally-mediated reflexes. At the same time, acetycholine is antagonized due to increase in cyclic-GMP.
Atropine: It acts antagonistically to acetycholine on the muscarinic receptors. When the vagal effects on the SA node are blocked, tachycardia ensues. The heart rate is increased by the hyperpolarization of the SA node by the acetycholine.
Adenosine: The drug causes short-lived blockage of the heart at the AV node. This is through increased efflux of the K+ due to hyperpolarization of the cells. The hyperpolarization is often due to reduction in cAMP since the adenylyl cyclase is inhibited by the action of adenosine on A1 receptor.
Ketamine: Analgesia results due to inhibition of calcium influx. This is through PCP binding of ketamine within the NMDA channel. In the dorsal horn neurons, sensitization is prevented as a result of antagonism of the NMDA receptor. By inhibiting NO synthesis, ketamine ends up inhibiting the enzyme nitric oxide synthase, thus pain perception is greatly reduced.
Naloxene: Naloxene competitively binds on opioid receptors leading to relaxation of the respiratory as well as the nervous systems.
Aspirin: The enzyme prostaglandin cyclo-oxygenase is inhibited by aspirin in a non-reversible manner such that the thromboxane factor A2 is not formed, thus platelet aggregation is prevented.