In this section, we’re diving into how anesthesia drugs manage nerve cell activity to keep the body in a safe, controlled state during surgery. Each drug class plays a unique role in regulating action and resting potentials—the nerve impulses that drive cellular communication. Volatile agents like isoflurane and sevoflurane enhance calming GABA signals while reducing excitatory responses to settle brain activity. IV drugs, such as propofol and etomidate, further quiet the system by promoting hyperpolarization, lowering the likelihood of action potentials. As we explore more, we’ll look at how other agents, like local anesthetics and NMDA blockers, block pain and reduce excitability to achieve precise anesthesia control.
1. Volatile/Inhaled Anesthetics
- Isoflurane, Sevoflurane, Desflurane, Halothane:
- These anesthetics enhance inhibitory GABA signalling and reduce excitatory glutamate activity. Increasing GABA-A receptor activation, helps hyperpolarize the neuron, making it less likely to reach the threshold for an action potential. They also inhibit NMDA receptors, reducing excitatory sodium (Na⁺) and calcium (Ca²⁺) influx, maintaining a low excitatory state in the brain.
2. Intravenous (IV) Anesthetics
- Propofol:
- Propofol enhances GABA-A receptor activity, promoting hyperpolarization and decreasing neuronal excitability, effectively lowering the likelihood of action potential generation.
- Etomidate:
- Like propofol, etomidate increases GABA-mediated inhibition, leading to hyperpolarization and decreased neuronal excitability.
- Thiopental (a barbiturate):
- Additionally, it functions by augmenting GABA activity, hyperpolarizing neurons, and complicating the attainment of the action potential threshold
3. NMDA Receptor Antagonists
- Ketamine:
- Ketamine blocks NMDA receptors, reducing Na⁺ and Ca²⁺ influx, which decreases neuronal excitability and prevents depolarization. This action effectively dampens excitatory signaling, influencing the action potential process.
4. Local Anesthetics
- Lidocaine, Bupivacaine, Ropivacaine:
- These drugs block voltage-gated Na⁺ channels, preventing the influx of Na⁺ ions needed to initiate and propagate action potentials. This action prevents pain signals from being transmitted to the central nervous system.
5. Muscle Relaxants (Neuromuscular Blocking Agents)
- Succinylcholine (Depolarizing muscle relaxant):
- Succinylcholine binds to acetylcholine receptors, causing an initial depolarization but then holds the neuron in a depolarized state (preventing repolarization), leading to muscle paralysis.
- Non-Depolarizing Agents (e.g., Rocuronium, Vecuronium):
- These block acetylcholine receptors at the neuromuscular junction, preventing depolarization necessary for action potential generation in muscle cells.
6. Anti-epileptic drugs Used in Anesthesia
- Phenytoin, Sodium Valproate:
- Occasionally used in anesthesia to stabilize neuronal membranes, these drugs affect Na⁺ channels, prolonging inactivation and reducing repetitive action potential firing.
Each of these drugs influences the excitability of neurons or muscle cells by altering the cell’s resting potential, threshold potential, or response to excitatory and inhibitory inputs, tailoring neuronal activity to achieve the desired anesthetic effect.
