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Dental Work, Lidocaine Interaction

Ok so I’m gonna keep this short and sweet iv been in the process of gettin some dental work and vaneers done over the last couple months. I went in today and the lidocaine made my heart go fucking nuts when Injected the dentist said is contains epinephrine and some probably got in my blood.

Just looking and apparently they add epinephrine and it somehow affects androgen receptors. I dont know the scientific lingo is above my knowledge on how to interpret it.

Any thoughts from some of my book guys here.

Only difference between last visit is a shit load of tren
@now_i_care
@readalot
@unreal24278

I do not do any AAS, and know nothing about androgen receptors, but this shit made me feel like my heart was about to explode! Fuck that!

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Its odd the last couple times I was fine but today was bad. My heart was beating so fast I couldn’t breathe and my chest felt like it was caving in. Thankfully it only last about 10-20 seconds.

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The first two visits, made me feel wonky and I mentioned it, but she said, “Pft!” The third time I came out of chair, almost passed out. I told her we would NOT do that again! Then got a lecture about how that has never happened before. After a brief “discussion” we ended our relationship :rage:
Hope you getbit figured out. They do actually make different kinds without the epi.

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Man I feel for you. I am glad you made it. You should not mix vasoconstrictors with nandrolone or even worse tren. Both are potent modulators of beta2-adrenoceptor activity. Some light reading, just see abstracts if too much:

http://www.endoexperience.com/documents/Adversedrugrxs-vasoconstrictorsJADA1999.pdf

Basically with lots of tren as you state, plan to not get startled, watch scary movies, do cocaine, or have an allergic response requiring epi-injection. You hear all this talk of sudden death involving aas use coupled with stress response. The first abstract above puts forth mechanism for how it would work. Heart gets stimulated by epi and nd family of aas potentiates the response. Take care of yourself! Hope this helps.

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https://www.ncbi.nlm.nih.gov/pubmed/15225667

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I am a dentist and this is a fairly common experience. As your dentist stated, the lidocaine solution contains epinephrine, usually in a 1:100000 ratio to constrict the blood vessels in the area to prolong the analgesic effect of the lidocaine. By constricting the blood vessels in the area, it slows down the rate that the circulation removes the lidocaine from the location at which it is acting. If the needle inadvertently injects directly into a vessel in the area, a fair size bolus of epinephrine is carried to the heart and briefly increases the rate and contractile power of the heart. Because the vessels are not visible under the tissue where the injection is occurring, and because everybody’s blood vessels are located in a slightly different location, whether this happens or not has nothing to do with the “skill” or lack thereof of the dentist. It is simply a possible risk assumed anytime such local anesthetic solutions are used. The increase in heart rate and especially the increase in contractile force can be quite a scary experience and can occur to anyone, regardless of AAS use or not. The simplest way to prevent this from happening again is to just ask your dentist to use a non-epinephrine containing anesthetic solution. Every dentist in the world carries these LA solutions which are usually termed “plain” solutions. The most common one is a 3% mepivicaine solution often sold under the brand names of Carbocaine or Polocaine. Mepivicaine tends to produce a more profound anesthesia than lidocaine does anyways and has better penetrating ability also. You may simply need a couple extra shots of it over the course of the appointment if it is a long (1+ hours) appointment because it is removed more quickly than epinephrine containing LA. Hope this helps

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Epinephrines activity on beta 2 adrenergic receptors results in vasodilation, not constriction. Vasoconstriction induced by epinephrine is via alpha receptors.

That being said nandrolone does appear to delay post exercise induced PSN recovery, probably due to upregulation of said beta adrenergic receptors. Extreme stress response + drug use (stimulants typically) high dose AAS could potentially cause an adrenergic storm. But SCD induced by AAS can happen though a variety of avenues

  • One could have a stroke/phat blood clot
  • Myocardial infarction from atherosclerotic plaque buildup
  • structural heart damage predisposing one to lethal arrythmias
  • drug toxicity (catecholamine release + reccy drug use), this doesn’t apply solely to stimulants though

Seriously if you ever drink to the point of intoxication at a dance or something. Check you’re heart rate (even if not at a special event) you’ll notice (depending on how much you drink) a profound increase in RHR, sometimes even to the point of resting tachycardia if you’re active during the night (ones HR can easily hit 200 vigorously dancing while very drunk). This is due to vasodilation and the body trying desperately to metabolise and excrete ethanols (or ethanol + methanol if drinking darker spirits) extremely toxic metabolite acetomaaldehyde and alcohol induced endotheial dysfunction. Then the next day you’ll also notice increased cardiac output, potentially heart palpitations and PVC’s. I don’t ever drink anymore, however the deleterious adverse cardiovascular effects of acute alcohol intake are well documented (both acute and long term)… Interestingly even marijuana has been potentially linked (reports are very flawed, but interesting nonetheless) to acute myocardial infarction and coronary vasospasm, it appears EEEXXXTTRRREEEMEMMEEELY rare, however it does go against the argument “pots never killed anyone” that advocates for legalisation (such as myself) spew out.

Beta adrenergic receptor upregulation isn’t unique to ND, all AAS do it to some degree.

I don’t understand the allure of cocaine, from what I’ve observed (from viewing people take it numerous times), it’s a quick, stimulating rush that aids in productivity and gives the user confidence/mania initially for like 45 mins. However it blocks cardiac sodium channels and depletes the FUUUUCCCKKKK out of you’re amt of dopamine afterwards, therefore what’s the point?

  • extensively cardiotoxic
  • short duration
  • very expensive
  • crash after going off

I’ve never used cocaine and never will because I just don’t see the point, risk/reward ratio is all risk, no reward to me. I’ve just always wondered why people use cocaine as it has (typically) such a short duration of action and the immense level of risk involved makes me think there’s no point. For increased productivity… For 45 minutes… Not gonna get much done in that period of time

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Thanks y’all! Appreciate all the Info

They are indeed 3-4 hour appointments but I think I’d rather have more shots then ever experience what happened the other day. She said the se thing that it was common maybe I just got a large amount in my blood but what I experienced did not seem like it could be considered common lol. It wasn’t a rapid heart beat like when Doing cardio it was rapid like iv never felt and painful to the point I couldn’t breathe. I’m trying to imagine someone of poor cardiovascular health going thru this.

Il def ask for the other stuff!

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