10 Matching Annotations
  1. Sep 2021
    1. Salvinorin A was notsoluble in 100% propylene glycol to our surprise. However,solubility increased in propylene glycol by adding increasingconcentrations of DMSO. A 9:1 mixture ended up beingsuitable for our studies

      I'm quite a novice in chemistry. I assume a 9:1 ratio would work with other solvents replacing the 9 parts propylene glycol. That is to say, given that salvinorin A was not soluble in propylene glycol, I'm assuming the propylene glycol plays little to no role.

    1. Exceptionally, chlorophyll b was not found in any of the top phases. The lack of chlorophyll a and chlorophyll b in some ATPSs could be due to low extraction efficiencies or a change in the molecule structure by oxidation. Chlorophyll stability is affected by temperature, light irradiance, acids, bases and oxygen, causing the loss of its magnesium ion and/or phytol group40 and a change in colour to olive‐brown.41

      Which one it is should be possible to determine by running multiple washes and visually assess how much pigmentation is removed. The idea is to dissolve acetone plant extract, add PEG-400, let the acetone evaporate, pour PEG-400 leaving sediment and/or crystals, then repeat. While I'd probably be doing this with salvia divinorum, any leaf should work for testing chlorophyll washing.

    2. Chlorophyll a was recovered by PEG400‐Ch DHp (50.6 ± 2.3%), but it was not detected in the other two systems at 660 nm [Fig. 2(b)].

      They seem to be saying that PEG dissolved 50% of the chlorophyll? I also don't know what what Ch or DHp means. I'm somewhat outside my wheelhouse.

      Assuming PEG-400 does not dissolve salvinorin A, then it may be an excellent option for purification of salvinorin A.

    1. SA was soluble in 25% dimethyl sulfoxide (DMSO)/75% polyethylene glycol 400 (PEG-400) at 4,000 μg/mL and was stable for 6 days, as determined by LC-MS/MS, with only trace amounts of the hydrolysis product salvinorin B (SB) forming.

      As with DMSO and propylene glycol, I suspect that the DMSO is doing the dissolving. Given that it appears to only take 10% DMSO to dissolve salvinorin, naturally the 25% works. Unfortunately, I see no mention of whether salvinorin A is soluble in pure PEG-400. I suspect it is not.

    1. 4. Allow acetone to evaporate in a dark, well-ventilated area. You will be left with a bright green powder – about 1g per 100g of leaf. This powder is about 2 parts chlorophyll to 1 part salvinorin A.

      This is incredibly useful information.

      I noticed my extract had some bitter taste and some earthy notes. I don't know what salvinorin and chlorophyll taste like, but I assume the taste comes from other impurities. However, I extracted for many minutes (10 or so); next time, I should do only the 3 minutes suggested here (3 times 1 minute).

    1. When salvinorin A isolated from leaves of Salvia divinorum was irradiated with 300 nm UV light in ethyl acetate, it degraded from 100 μg/mL to 2.84 ± 0.05 μg/mL in 30 min. The calculated average rate constant k of this degradation was 0.12/min and the half-life was 5.7 min. When authentic salvinorin A was irradiated by UV light in an organic solution or an aqueous solution, it degraded over 90% within 40 min, whereas when it was irradiated by natural sunlight, it took 8 h to degrade 50% both in an organic and an aqueous solution.

      Incredible. I may have destroyed my current batch. I'll have to start over. Good thing I only made a moderate amount.

    1. our Lab. for extracting terpenes and sterols from plant materials, we used petroleum ether (40-60), followed by acetone and finally methanol. Terpenes were found in petroleum ether- and acetone-extract.

      This is the first confirmation I've seen of using acetone as a solvent for terpenes. I'd be surprised had acetone not dissolved them.

      I'm using a method of adding terpenes to my salvia divinorum extract, then evaporating the acetone. This creates an instant e-juice. It's a relatively crude method, containing large amounts chlorophyll. Nonetheless, the contents should be safe for inhalation.

  2. Aug 2021
    1. At lower doses (0.18 mg/kg and 0.32 mg/kg) we observed no prolonged effect on KOR binding but at 0.60 mg/kg salvinorin A induced a sustained decrease in KOR binding (BPND decreased by 40–49%) which persisted up to 2.5 h post administration, long after salvinorin A had been eliminated from the brain. These data point towards an agonist-induced adaptive response by KOR, the dynamics of which have not been previously studied in vivo with PET.

      This may partly represent the salvia "afterglow". It also demonstrates how rapidly tolerance-like mechanism can occur.

      I find it odd that 0.32 mg/kg had little prolonged effect when twice that dose had a very large effect. I'd expect more of a gradient. The graph (figure 4) shows a nonsignificant drop in KOR binding of ~13% at 1 hour at 0.32 mg/kg, which I'm certain would become statistically significant in a larger sample. Still, that's nowhere near the 45% seen at 0.6 mg/kg. At 0.18 mg/kg, we see ~9%.

      I calculated the human equivalent dose to be 6.8mg (0.6mg0.16270). This is an very high dose, so likely does not represent an accurate dose conversion.

  3. May 2021
    1. Salvinorin A, a kappa-opioid receptor agonist hallucinogen: pharmacology and potential template for novel pharmacotherapeutic agents in neuropsychiatric disorders

      I think this may be the best review of salvinorin A that I have ever looked at. I definitely need to sit down and read the full article at some point.

    1. In contrast to its acute administration, repeated salvinorin A administration did not modify dialysate DA levels. Similarly, neither basal extracellular DA levels nor DA uptake was altered. Unlike synthetic KOPr agonists, prior repeated administration of salvinorin A did not attenuate the locomotor activating effects of an acute cocaine (20 mg/kg, i.p.) challenge. However, cocaine-evoked DA overflow was enhanced.

      Fascinating and useful stuff. This is close to what I was expecting. Though, I was expecting chronic exposure to upregulate dopamine beyond baseline. If I'm understanding this correctly, it was upregulated in the sense that it enhanced the dopaminergic effects of cocaine. I've not yet read the full study.