Propofol acts on GABA receptors as an agonist, GABA is an inhibitory neurotransmitter, stimulating its receptors inhibits excitory neurotransmitters like dopamine and serotonin, so yeah, it puts the brain in a sedated state. The brain works somewhat like a biological analog computer, it's networking of cells, nerves communicating to each other through electrical action potentials and chemical messengers across synapses from cell to cell, in patterns and different pathways, a memory is pretty much a communication pathway to different parts of the body and different parts of the brain. If you alter the signals by stimulating different receptors, you alter a person's state of consciousness itself. Ketamine is an NMDA receptor (a type of glutamate receptor) inhibitor. Glutamate is another excitory neurotransmitter, you block the brain's ability to send those glutamate signals and it alters your brain's ability to function and consequently, alters consciousness.
The heart races in response to stimuli because of signals sent to it from the brain telling it to do so. Cardiac rhythm is controlled in the brain stem as far as I know. If the brain stem is damaged, the heart can stop.
My friend, you are still reading medical metaphor and assuming them real. I in fact, invoked the 'brain is a computer' as another example of a metaphor falsely assumed true earlier. Take receptor and neurotransmitter - we are invoking metaphors taken from Radio or so. Receptors don't receive 'signals' as much as being altered by the molecules. When activated, proteins alter and thus render membranes less or more permeable to ion exchange, for instance.
Similarly, neurons act by complex membrane potentials and electrochemical gradients regulating ion exchange. This is not an electrical signal being conducted, much less a circuit; but is crudely likened to wiring for ease of understanding. Circuits are closed loops, while nerves are one way depolarisations of membranes. Take the various forms of nerve conduction, such as myelinated nerves conducting via nodes of Ranvier - why do demyelinating conditions then disrupt nerves, if they are only 'conducting an impulse'? The metaphor breaks down. There is a broad equivalence in speed of the impulse between myelination and axon thickness, but not wholely so - and further, no nerve merely propogates an action potential, but subtly modifies it. This is why we can run a lignocaine infusion intra-operatively for pain, even though we are using a sodium channel blocking agent that should in fact be completely disrupting all nerve function in the classic sense.
When we get to the Anaesthetic agents, I would ask you if you are aware what GABA receptors do? It is all fine and well to label it inhibitory, but it really isn't so. What is it inhibiting, I ask you? Where are we locating this system, pray? Did you know Propofol and Benzodiazepines may invoke a paradoxical excitatory state? Why is Sodium Thiopentone not anti-emetic if we have similar arm-brain circulatory times for induction of Anaesthesia? Why does Propofol's lipid solubility make such a difference then? What of the Volatiles? Are we invoking 5-angstrom theory, or lipid solubility as absolutes to maintaining Anaesthetic depth? You are aware we have not shown how volatiles induce any neural change, only aware that it does. We even use the alveolar concentration as surrogate, assuming this corresponds to brain levels we have not been able to measure. How does this correspond to Total IV Anaesthesia? Ketamine is in fact excitatory, but creates a dissociative Anaesthetic, yet the end result looks deceptively similar on EEG. We are not merely dealing with 'dirsupting signals', but a dynamic response. If you take the latters ability to modulate wind-up phenomenon in pain, or morphine to limit opiate hyperanalgesia, this is even more plain. The factors are far more complex than you realise, I am afraid.
Let us get to brass tacks. Why do you think we know Propofol acts on GABA receptors? GABA receptors were identified in crayfish and muscle tissue specimens, and shown to be susceptible to chloride solutions and termed inhibitory accordingly and assumed a chloride-gated ligand at play. From this, we extrapolated to in-vivo nerve tissue. We then labelled drugs like Benzodiazepines or used radioligand binding to try and identify them, and later established subtypes. Now we have actually never demonstrated that Propofol actually does bind GABA receptors, but have shown that a mutation in GABA(A) subunit impacts its functioning in mice, and that in vitro albumin solutions identified potential binding sites using x-ray crystallography. Not that I am doubting that propofol acts on GABA related systems in some way, and probably does bind it - but the relation of receptor and substance and calling it merely 'inhibitory' or 'disrupting signals' is utterly facile and substantially flawed. There is debate on what an Anaesthetic even means, and whether or not the states induced by Propofol vs Volatiles vs Ketamine vs Etomidate are even really equivalent.
I am sorry for getting technical here, as I assume you have no medical background. Sufficed to say, just because a physiology textbook labels something an 'inhibitory neurotransmitter', don't assume you know what that necessarily means based on the metaphorical equivalence of 'transmitter' or take that 'inhibitory' at face value. We don't know where Consciousness arises. We cannot demonstrate when Consciousness is present or not, as many studies in awareness under Anaesthesia have demonstrated; or recent Australian trials in BiS monitoring (a form of EEG) and muscle relaxants showed, where we had aware subjects that appeared 'sedated' on EEG. Neural correlates have been found, but nothing even close to causation has been demonstrated. Neural pathways similarly are not so simplistic to label them merely communication pathways and an 'biological computer'. Nerves don't just take input, then run functions and present output, on the most basic level. We are not dealing with a computer except on the level of metaphor, anymore than the heart is a pump.
The heart is controlled by the vagus nerve for parasympathetic responses and the sympathetic chain otherwise, but has its own automaticity foci running from the SA node to the AV node down to the final purkinye fibres. If the brainstem is damaged, the heart takes over itself, dropping its rate lower and lower. The fact that it doesn't need nerve supply absolutely, is why we can transplant it. The heart will race, or not, depending on nerve signals sent to it - but likewise, if I stimulate the heart directly, I can directly impact nerves and the central nervous system. A good example is the Bezold Jarisch reflex from stimuli in the heart, or a vaso-vagal response in general. Again, the body's systems cannot be fully separated, nor do we face an 'act upon/acted by' dynamic, rather a series of complex interactions with usually some form of negative feedback. If the brain is damaged the heart will eventually die, and vice versa. Don't confuse metaphor with reality, no matter how fond we doctors are of describing things by the mechanical metaphors lifted from plumbing or electrics or such.
