Atropine Inhibition

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The hypotheses given were greatly supported during the experiment. Three of the four drugs; Lignocain, Hexamethonium, and Atropine, all showed a decline of inhibition of peristalsis. Nicardipine showed to have complete inhibition of peristalsis. It showed to have a 0 au drug amplitude. There were two standard pressures for this experiment. This was due to the two groups having to compensate for the differences in the two tissues used. Pressures used for Hexamethonium and Nicardipine was 2 cm/H2O. Whereas Atropine and Lignocaine, were tested in 3 cm/H2O ( Table 1). All four drugs showed a decrease in contractional response when they were compared to their control.
Lignocaine is a widely used local anaesthetic. This drug shows inhibition of peristalsis due to its ability to block sodium ion protein channels in the nerves of the body. This prevents the initiation and rapid increase of nerve action potentials, this allows for its use as a local anaesthetic by acting on nociceptive neurons (Dale et al., 2015). This will then result in diminished amplitudes of contractions and indicates that only partial inhibition was occurring.
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Both of these drugs are antagonists. Atropine has an antagonising effect on the muscarinic acetylcholine receptors caused prevention of acetylcholine (Ach) release from excitatory motor neurons (Dale et al., 2015). Hexamethonium on the other hand is a nicotinic cholinergic antagonist. It is also often referred to as a prototypical ganglionic blocker. Finally we had Nicardipine. Nicardipine is a calcium entry blocker, also known as a calcium ion antagonist. It inhibits the calcium channels from providing the necessary calcium to the smooth muscle for contraction. It does this by inhibiting the muscle contractibility. By doing so, this inhibits

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