Final answer:
Elevated extracellular K+ levels disrupt the normal function of the Na+/K+ pump and K+ leakage channels, leading to a reduced repolarization phase, which can impair the ability of neurons and muscle cells to fire action potentials effectively and potentially cause irreversible damage.
Step-by-step explanation:
The effect of a large dose of extracellular K+ on the transmission of the action potential in the sarcolemma is significant because potassium (K+) is the major intracellular cation responsible for establishing the resting membrane potential after depolarization and action potentials. A disruption in K+ concentration affects the membrane potential. Normally, the concentration of K+ is higher inside the neuron than outside. After the repolarization phase of an action potential, K+ leakage channels and the Na+/K+ pump help to return the ions to their original locations, supporting the refractory period and restoring the resting membrane potential.
However, when extracellular K+ levels are elevated, such as after an ischemic event like a stroke, this balance is disrupted. High levels of extracellular K+ can result in decreased efflux of K+ from the cell during the action potential, leading to a reduced repolarization phase. This can affect the neuron's or muscle cell's ability to fire subsequent action potentials effectively, potentially leading to irreversible neuronal damage or dysfunction.
Glial cells, especially astrocytes, are typically responsible for clearing excess K+ to support the Na+/K+ pump in maintaining the chemical environment and ionic balance crucial for proper functioning of the CNS tissue. In cases where extracellular K+ is too high, these cells may not be able to compensate, leading to drastic outcomes such as neuronal excitability alterations and increased risk of seizures or arrhythmias.