In my thesis-length comment above (below) I said that inflammation is a symptom and not a cause. Some causes are 'good', ie. exercise, and some causes are bad, ie. allergies.
I treat the pain / inflammation from 'good' causes as a well-earned reward (if God exists, this is one of its greatest practical jokes).
Treating inflammation from 'bad' causes (outside of genetic disposition) is probably a bad thing in that it's treating symptoms, not trying to find the cause, and in fact actively supressing the ability find the cause.
Edit: added 'Treating' in front of the last sentence so it makes sense.
This is how I tend to feel about fevers. Fevers are commonly treated with fever suppressants, which doesn't make a lot of sense if you consider that the fever is something that you do to an infection, not something that the infection does to you.
The slight difference here in some cases (few) a fever can go too far and if your body temperature goes too high you can suffer organ failure. Now whilst this isn't overly common for the average cold or flu this is where medication would be required.
For the average person and the average fever, people don't really need to take fever suppressants but they do often allow people to go back to work sooner.
Some inflammation is good to repair damaged stuff, be it muscles, tendons etc. Very often I see this in gym freaks or rock climbers, fighting inflammation at all costs without understanding underlying processes.
Or in case of infection move temperature further away from optimal one for breeding foreign bacteria/viruses, at that scale and numbers its statistics game so any advantage, even by just raising overall temperature is acceptable.
The problem is our bodies sometimes go haywire and don't regulate properly.
Yep, I agree, inflammation is a symptom not a cause. (I also commented on your comment).
My comment just above doesn't describe it as a cause, but a symptom, in this case muscular damage from exercise. In your case, it was due to S1 L5 discs pulling on each other during exercise, which is different.
But nonetheless, inflammation brought upon as a symptom of something else. Which goes for almost everything else in the body when inflammation arises.
Albuterol doesn’t treat inflammation directly, but is absolutely critical for emergency management. And control meds for children seem to (oddly) have zero actual benefit in controlled studies almost every time. But do seem to work.
Which is pretty odd, no?
There is a lot we don’t know about asthma.
Exercise and stress reduction do seem to help, but also not in obvious ways.
Well, asthma is multifaceted. You can have an obstruction caused by muscles contracting, or by mucus from inflammation. In either case, dilating the muscles, which is what albuterol does, can give you better air flow, lessening your perceptible symptoms. You'd still want a corticosteorid-based medicide to treat the inflammation if you have that kind of asthma, though, as the chronic inflammation can worsen your illness over time, hence my original comment.
Generally I assume that holes get larger due to certain muscles tensing and smaller due to certain other muscles tensing. (It's also possible that holes get smaller due to swelling in the tissue surrounding them, and larger when that swelling subsides, but I don't think that's what we're talking about here.)
Are you saying that the muscles that dilate the hole are themselves "dilating" when they tense, while the muscles that contract the hole are not "dilating" when they tense?
Ah, is your objection to the mixed terms, or to the intent of the poster? Or not an objection and a curious question? It can be hard to tell here.
Pretty much all of the bodies sphincters and regulated ‘pipes’ (including circulatory, GI, respiratory) either constrict (muscles tense) or dilate (muscles relax). Often there is minimal/no counter acting structure except perhaps for some ligaments/support structure, and the ‘opening’ force is provided by another means.
Confusingly, the optical pupils are the other way around - the pupillary dilator muscles have to contract to dilate the pupil. They are not the common case.
Albuterol acts directly on bronchial smooth muscle forcing it to relax (and also decreasing any immediate stress response in those cells). Which allows the alveolar duct to dilate during respiration.
I’m not aware of any significant muscular structure that actually would pull open the alveolar ducts - the force to inflate them comes from air inflating the lungs against the slight vacuum in the pleural breathing spaces from the action of the diaphragm and accessory breathing muscles.
The characteristic wheezing of asthma is due to the alveolar ducts (and bronchial in bad cases) muscles contracting excessively, constricting the airway and making it impossible to get adequate tidal volume. Sometimes it’s excessive due to the presence of mucus that isn’t being taken into account, other times even without it.
Counterintuitively, the difficulty breathing is generally because the air already inhaled cannot escape easily enough to allow room for more air. The wheezing is strongest on exhalation, and when responding to calls in the past, I’ve personally heard so bad it was clearly audible through multiple interior walls and the exterior wall - and outside the building. With an ambulance and fire truck running outside.
That is for adults who have stronger muscles. Pediatric patients are usually much more subtle.
Inadequate respiratory tidal volume is of course an immediate life threatening emergency, and very high on the ‘kills ya faster’ list. Time wise, potentially similar to hypovolemic shock or cardiac arrest.
It seems saying the ‘muscle dilates’, while not being technically exacting, isn’t misleading in this situation.
> Pretty much all of the bodies sphincters and regulated ‘pipes’ (including circulatory, GI, respiratory) either constrict (muscles tense) or dilate (muscles relax). Often there is minimal/no counter acting structure except perhaps for some ligaments/support structure, and the ‘opening’ force is provided by another means.
> Confusingly, the optical pupils are the other way around
There is no muscular action involved in constricting the pupil?
My understanding is based on what I was taught about how muscles work - specifically, that they can be in one of two behavioral states:
1. The muscle is trying to tense.
2. The muscle is not trying to tense.
Along with a continuum of physical states:
A. The muscle is fully contracted.
B. The muscle is fully extended.
As far as I was taught, muscles cannot extend themselves; some external force, most commonly another muscle, needs to draw them away from their (perhaps partially) tensed state. (And in the case of a cramp, this process fails because the muscle is still actively tensing.) Hence, as you just noted, the opening of the alveolar ducts is driven by tensing in the diaphragm. Or, when food passes from the esophagus into the stomach, what's happening is that muscles in the esophagus are tensing above the food to force it downward.
> Albuterol acts directly on bronchial smooth muscle forcing it to relax
So the immediate question prompted by my model here would be "does albuterol force the muscle to lengthen [a change in the physical state of the muscle], or does it stop the muscle from resisting as other processes lengthen it? [A change in the behavioral state.]"
> Ah, is your objection to the mixed terms, or to the intent of the poster? Or not an objection and a curious question? It can be hard to tell here.
My objection is to the fact that if you tell me a muscle is dilating, I have no idea what that means. Dilation isn't a concept that applies to muscles, whether in a direct or a metaphorical sense. Muscles, to the best of my knowledge, do not have any behaviors that it would make sense to describe as "dilating". Dilation refers to a hole getting larger, while muscles are unlike a hole in that they exist and occupy space, and they can't get larger, only smaller.
I didn’t say the muscle was dilating, fyi. That was another poster.
I’m just pointing out that while it’s not technically correct, you can figure out what they mean if you look at the actual details.
The iris does have a sphincter and dilator muscle, unlike most of these because unlike most there is no common counter pressure to expand them. Well, no safe one anyway.
For examples of ‘normal’ sphincters and controlled tubes in the body, for instance, the rectal sphincter vs feces (propelled via the smooth muscle in the colon or pressurized in various ways), esophageal sphincter vs various ways stuff gets pushed or propelled through it, blood pressure against the arterial smooth muscles, air pressure via the esophagus into the lungs vs the negative pressure pleural space, the small and large intestine, etc.
If they relax, they no longer resist those forces, and hence the sphincter or tube will dilate.
This is also why various things tend suddenly leak out upon death. No ennervation, no tensing, sphincter dilates. At least until rigor mortis sets in.
Albuterol forces smooth muscle to no longer tense - aka relax. So any sphincter, tube, or duct that muscle controls will dilate if there is any force present, which there generally is - or the patient is already dead.
I treat the pain / inflammation from 'good' causes as a well-earned reward (if God exists, this is one of its greatest practical jokes).
Treating inflammation from 'bad' causes (outside of genetic disposition) is probably a bad thing in that it's treating symptoms, not trying to find the cause, and in fact actively supressing the ability find the cause.
Edit: added 'Treating' in front of the last sentence so it makes sense.