Oxygen and carbon dioxide travels to and from tiny air sacs in the lungs, through the walls of the capillaries, into the blood. Blood leaves the heart through the pulmonic valve, into the pulmonary artery and to the lungs. Blood leaves the heart through the aortic valve, into the aorta and to the body.
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Numerous antiepileptic medications, such phenytoin, have been designed to block voltage-gated sodium channels (VGSC) in neuronal membrane. In addition, multiple toxins and pharmacological modulators work by attaching to various biophysical states of the VGSC to cause their effects. Depending on how modulatory agents act, some VGSC states are stabilized or destabilized, altering the channel's biophysical properties. The first anticonvulsant to successfully treat epileptic disorders without causing undesirable side effects such as brain drowsiness was phenytoin.
Phenytoin has been indicated to block high-frequency neuronal activity potentials from the inner vestibule of the pore, as demonstrated by electrophysiological research and site-directed mutation.
Frequency and voltage both affect phenytoin binding.
There are theories that phenytoin interferes with the late sodium current that sustains depolarizations in epilepsy by blocking non-inactivated channels.
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