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| = Introduction = Inhaled narcotics refers to the application of administering agents that can block the sensation of pain, any response to noxious stimuli and cause sleepiness, which allows surgical operations to be carried out without the patient feeling any discomfort. The patient breathes in a mixture of chemicals, and the person will get the state of unconsciousness. Many chemicals with such an effect have been discovered by the scientists. In this essay, we would like to focus on isoflurane and sevoflurane that are very commonly used nowadays for induction and maintenance of general anaesthesia. = Mechanisms of actions = Just as a lot of other anaesthetic drugs, the exact mechanisms of actions of both chemicals that can introduce the state of immobilization have not been completely discovered. However, sevoflurane and isoflurane are known to affect the central nervous system to reduce pain sensation. Both are clear liquids. When it is placed in a vaporizer, it becomes a gas and is ready to be used. Both are in the ether group and their structures are substituted with halogen atoms such as chlorine and fluorine as you can see in the picture. == Sevoflurane == Sevoflurane primarily works on one of the GABA receptors in the central nervous system, termed as GABA-A receptors. GBAA stands for gamma aminobutyric acid As we learn in the class, GABA is the most common neurotransmitter inhibitor in the CNS.. In Figure 3, a GABA-A receptor is shown. GABA-A receptor is a complex that consists of 2 alpha, 2 beta and 1 gamma subunits. These subunits penetrate the membrane, and the extracellular part of GABA-A receptor has the binding site for a couple of ligands including GABA. When GABA binds to the binding site, the receptor opens and Cl ion influx takes place. The Cl ion influx prevents to generate action potential, which in turn makes less excitation. Sevoflurane enhances the affinity of the receptors for GABA. The elevated affinity for GABA is observed in isoflurane as well. Even though there are fewer studies done for sevoflurane than isoflurane, it is safe to assume that they both work almost identically on the four transmembrane domains of GABA alpha subunits to archive its interaction with neurotransmitters (Garcia et al. 2010). Moreover, sevoflurane also bears on presynaptic glutamatergic receptors. It is likely to cause less excitation in presynaptic neurons and elicit the inhibitory interneuron excitation. The inhibition may also be observed in the several cascade processes that create glutamate excitation. Therefore, it successfully works on the presynaptic receptors without affecting the postsynaptic receptors. To our interest, sevoflurane may also work on leaky potassium channels. These K+ channels are pH sensitive, voltage-independent and located in the cerebral nuclei and motoneurons in the brain stem and spinal cord. Sevoflurane promotes the K+ channels to be more active. It then affects another ion channels, which elicits hyperpolarization. This system can depress the phrenic nerve motoneurons (Stuke et al, 2001). == Isoflurane == Isoflurane also has an impact on the glycine receptors and the GABA-A receptors. Similar to sevoflurane, it increases the affinity of the GABA-A receptors for GABA and enhances actions on the glycine receptor. However, in addition to these receptors, isoflurane is said to affect glutamate. Glutamate has three main G-protein ligand-gated channels and they are the NMDA receptors, the AMPA receptors and the Kinate receptors. Isoflurane can reduce the binding of MK-801 or the blocker of the NMDA receptor, which represents less receptor function. This may help produce the state of immobility. However, Sonner et al. (2003) figured out that it does not seem to have any effects on the rest of the receptors. Sodium channel is a voltage-gated receptor. The presynaptic Na+ channels are inhibited by isoflurane, which result in decline of neurotransmitter release including glutamate. This means a reduction of the action potential, and thus the nervous system is depressed (Herold et al. 2012). Although dosage and MAC are different for each chemical, it is clear that the two narcotics work mostly in the same way, probably because they are very similar in terms of the structures. = Effeccts on the organs = |
Itt írjon a(z) inhalation_anestesiology-ról/ről
Introduction
Inhaled narcotics refers to the application of administering agents that can block the sensation of pain, any response to noxious stimuli and cause sleepiness, which allows surgical operations to be carried out without the patient feeling any discomfort. The patient breathes in a mixture of chemicals, and the person will get the state of unconsciousness. Many chemicals with such an effect have been discovered by the scientists. In this essay, we would like to focus on isoflurane and sevoflurane that are very commonly used nowadays for induction and maintenance of general anaesthesia.
Mechanisms of actions
Just as a lot of other anaesthetic drugs, the exact mechanisms of actions of both chemicals that can introduce the state of immobilization have not been completely discovered. However, sevoflurane and isoflurane are known to affect the central nervous system to reduce pain sensation. Both are clear liquids. When it is placed in a vaporizer, it becomes a gas and is ready to be used.
- Both are in the ether group and their structures are substituted with halogen atoms such as chlorine and fluorine as you can see in the picture.
Sevoflurane
Sevoflurane primarily works on one of the GABA receptors in the central nervous system, termed as GABA-A receptors. GBAA stands for gamma aminobutyric acid
As we learn in the class, GABA is the most common neurotransmitter inhibitor in the CNS.. In Figure 3, a GABA-A receptor is shown. GABA-A receptor is a complex that consists of 2 alpha, 2 beta and 1 gamma subunits. These subunits penetrate the membrane, and the extracellular part of GABA-A receptor has the binding site for a couple of ligands including GABA. When GABA binds to the binding site, the receptor opens and Cl ion influx takes place. The Cl ion influx prevents to generate action potential, which in turn makes less excitation. Sevoflurane enhances the affinity of the receptors for GABA. The elevated affinity for GABA is observed in isoflurane as well. Even though there are fewer studies done for sevoflurane than isoflurane, it is safe to assume that they both work almost identically on the four transmembrane domains of GABA alpha subunits to archive its interaction with neurotransmitters (Garcia et al. 2010). Moreover, sevoflurane also bears on presynaptic glutamatergic receptors. It is likely to cause less excitation in presynaptic neurons and elicit the inhibitory interneuron excitation. The inhibition may also be observed in the several cascade processes that create glutamate excitation. Therefore, it successfully works on the presynaptic receptors without affecting the postsynaptic receptors. To our interest, sevoflurane may also work on leaky potassium channels. These K+ channels are pH sensitive, voltage-independent and located in the cerebral nuclei and motoneurons in the brain stem and spinal cord. Sevoflurane promotes the K+ channels to be more active. It then affects another ion channels, which elicits hyperpolarization. This system can depress the phrenic nerve motoneurons (Stuke et al, 2001).
Isoflurane
Isoflurane also has an impact on the glycine receptors and the GABA-A receptors. Similar to sevoflurane, it increases the affinity of the GABA-A receptors for GABA and enhances actions on the glycine receptor. However, in addition to these receptors, isoflurane is said to affect glutamate. Glutamate has three main G-protein ligand-gated channels and they are the NMDA receptors, the AMPA receptors and the Kinate receptors. Isoflurane can reduce the binding of MK-801 or the blocker of the NMDA receptor, which represents less receptor function. This may help produce the state of immobility. However, Sonner et al. (2003) figured out that it does not seem to have any effects on the rest of the receptors. Sodium channel is a voltage-gated receptor. The presynaptic Na+ channels are inhibited by isoflurane, which result in decline of neurotransmitter release including glutamate. This means a reduction of the action potential, and thus the nervous system is depressed (Herold et al. 2012). Although dosage and MAC are different for each chemical, it is clear that the two narcotics work mostly in the same way, probably because they are very similar in terms of the structures.