Definition
A stable, non-explosive inhalation anesthetic, relatively free from significant side effects.
Description
Isoflurane is only found in individuals that have used or taken this drug. It is a stable, non-explosive inhalation anesthetic, relatively free from significant side effects. [PubChem]Isoflurane induces a reduction in junctional conductance by decreasing gap junction channel opening times and increasing gap junction channel closing times. Isoflurane also activates calcium dependent ATPase in the sarcoplasmic reticulum by increasing the fluidity of the lipid membrane. Also appears to bind the D subunit of ATP synthase and NADH dehydogenase. Isoflurane also binds to the GABA receptor, the large conductance Ca2+ activated potassium channel, the glutamate receptor and the glycine receptor.
Top Gene Interactions
Related Pathways
General Information
- Metabolism: Minimal
- Uses/Sources: For induction and maintenance of general anesthesia.
- Health Effects: May lead to cardiac arrhythmias and death (Rarely). In susceptible individuals, Isoflurane anesthesia may trigger a skeletal muscle hypermetabolic state leading to high oxygen demand and the clinical syndrome known as malignant hyperthermia. The syndrome includes nonspecific features such as muscle rigidity, tachycardia, tachypnea, cyanosis, arrhythmias, and unstable blood pressure.(L1471)
- Symptoms: The predicted effects of acute overexposure by inhalation of Isoflurane, USP include headache, dizziness or (in extreme cases) unconsciousness. (L1471)
- Treatment: Stop drug administration, establish a clear airway, and initiate assisted or controlled ventilation with pure oxygen. (L1712)
- Route of Exposure: Inhalation
Toxicity
- Carcinogenicity: No indication of carcinogenicity to humans (not listed by IARC).
- Toxicity: LC50=15300 ppm/3 hrs (inhalation by rat)
Mechanism of Action
Target Name | Mechanism of Action | References |
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GABA-A receptor (anion channel) |
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Calmodulin Calcium-transporting ATPase type 2C member 1 Gamma-aminobutyric acid receptor subunit alpha-1 NADH-ubiquinone oxidoreductase chain 1 Glutamate receptor 1 Potassium voltage-gated channel subfamily A member 1 Glycine receptor subunit alpha-1 ATP synthase subunit delta, mitochondrial |
Isoflurane induces a reduction in junctional conductance by decreasing gap junction channel opening times and increasing gap junction channel closing times. Isoflurane also activates calcium dependent ATPase in the sarcoplasmic reticulum by increasing the fluidity of the lipid membrane. Also appears to bind the D subunit of ATP synthase and NADH dehydogenase. Isoflurane also binds to the GABA receptor, the large conductance Ca2+ activated potassium channel, the glutamate receptor and the glycine receptor. |
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