Stimulant used: 3,4-dichloromethylphenidate 10mg/3h x 18h = 60mg tot. at test H+0
Benzodiazepine used: Temazepam 15mg cap po at test H+0
Therapeutic effect onset: test: H+16m
Full therapeutic effect achieved: H+22m
As most among you stimulant users painfully know, vasoconstriction resulting from stimulant
use is a party pooper. Be it "panic attack", "fear of imminent death" or "chest crush" the result is the same: it sucks, it hurts and if you have cardiovascular issues, it can kill you. Beta-blockers can't do much for it; neither will niacin. All other exogenous vasodilator agents won't help either. All but one group: benzodiazepines. Surprised? Up until recently so were we. Up until I, the author of this entry, played rat to his own experiment. As you will see danger was minimal, but results we all but. First a transcript from our source (the least chemically inclined may skip to the last 5 lines):
Although controversial over this off-label purpose, benzodiazepines may play a role in lowering blood pressure. They work as an agonist of the GABA-a receptors in the brain, thus slowing down neurotransmission and dilating blood vessels. GABA is an abbreviation for gamma-aminobutyric acid. It is an inhibitory neurotransmitter among others (glycine, adenosine, etc.) GABA-a receptors are ion channels that are the primary target for benzodiazepines. When an agonist binds to this receptor site, the protein channel opens, allowing negative chloride ions entering the channel and penetrating the voltage-gated ion site. Thus, giving negative feedback in neurotransmission and easing stress, anxiety and tension in patients that can be associated with elevated blood pressure.
In addition to GABA, benzodiazepines inhibit the re-uptake of a nucleoside chemical called Adenosine, which serves as an inhibitory chemical mentioned above. It also serves as a coronary vasodilator, allowing the cardiac muscle to relax and dilating cardiac arteries
Now we got it, the when and the why. Because you see, benzodiazepines have the ability to chill that harpy Adenosine who otherwise would keep pestering and harassing our defenseless heart. Other vasodilators are terrified of that cantankerous shrew so they leave her alone, plain and simple. Despite the biochemistry lingo the conclusion leaves little doubt as to what the original author(s) believe(s), a a belief that I now share.
First's let's take care of the dent in the flimsy armor disguised as the first sentence of the transcribed paragraph: What controversy? None here in any case. The quick-onset benzodiazepine was taken at H+0m, effects were felt at H+16m, full suppression of vasoconstriction was achieved at H+22m. That's 22 minutes from misery to bliss without major interaction between the benzodiazepine used and the positive effects of the stimulant restored. The potent and notoriously vasoconstrictor stimulant 3,4-CTMP, a more potent derivative of methylphenidate, was chosen for the test, along with the quick-onset hypnotic Temazepam at a modest dosage of 15mg po, to avoid inducing hypnosis. Within 22 minutes of ingestion the benzodiazepine had completely removed any perceptible untoward effect of the stimulants effects on the cardiovascular system, namely tachycardia (from 146 to 77) and perceptible signs of HBP (sorry my cellphone can't measure blood pressure).
IMPORTANT NOTICE: This blog entry is not a standard experiment protocol even though it is backed by the personal experience of the author as described. Results published are dose and ratio dependent. Higher stimulant dosage will require ratio recalibration. No other stimulant or benzodiazepine was used but similar results can be projected based on chemical affinities between amphetamine and its congeners, methylphenidate and its congeners, substituted amphetamines and substituted cathinones. Excluded are: psychedelic amphetamine derivatives, methamphetamine, cocaine HCL and its derivatives. Author guarantees veracity of facts reported but accepts no responsibility for any injuries or fatalities resulting from replication of this experiment
Benzodiazepine used: Temazepam 15mg cap po at test H+0
Therapeutic effect onset: test: H+16m
Full therapeutic effect achieved: H+22m
As most among you stimulant users painfully know, vasoconstriction resulting from stimulant
use is a party pooper. Be it "panic attack", "fear of imminent death" or "chest crush" the result is the same: it sucks, it hurts and if you have cardiovascular issues, it can kill you. Beta-blockers can't do much for it; neither will niacin. All other exogenous vasodilator agents won't help either. All but one group: benzodiazepines. Surprised? Up until recently so were we. Up until I, the author of this entry, played rat to his own experiment. As you will see danger was minimal, but results we all but. First a transcript from our source (the least chemically inclined may skip to the last 5 lines):
Although controversial over this off-label purpose, benzodiazepines may play a role in lowering blood pressure. They work as an agonist of the GABA-a receptors in the brain, thus slowing down neurotransmission and dilating blood vessels. GABA is an abbreviation for gamma-aminobutyric acid. It is an inhibitory neurotransmitter among others (glycine, adenosine, etc.) GABA-a receptors are ion channels that are the primary target for benzodiazepines. When an agonist binds to this receptor site, the protein channel opens, allowing negative chloride ions entering the channel and penetrating the voltage-gated ion site. Thus, giving negative feedback in neurotransmission and easing stress, anxiety and tension in patients that can be associated with elevated blood pressure.
In addition to GABA, benzodiazepines inhibit the re-uptake of a nucleoside chemical called Adenosine, which serves as an inhibitory chemical mentioned above. It also serves as a coronary vasodilator, allowing the cardiac muscle to relax and dilating cardiac arteries
Now we got it, the when and the why. Because you see, benzodiazepines have the ability to chill that harpy Adenosine who otherwise would keep pestering and harassing our defenseless heart. Other vasodilators are terrified of that cantankerous shrew so they leave her alone, plain and simple. Despite the biochemistry lingo the conclusion leaves little doubt as to what the original author(s) believe(s), a a belief that I now share.
First's let's take care of the dent in the flimsy armor disguised as the first sentence of the transcribed paragraph: What controversy? None here in any case. The quick-onset benzodiazepine was taken at H+0m, effects were felt at H+16m, full suppression of vasoconstriction was achieved at H+22m. That's 22 minutes from misery to bliss without major interaction between the benzodiazepine used and the positive effects of the stimulant restored. The potent and notoriously vasoconstrictor stimulant 3,4-CTMP, a more potent derivative of methylphenidate, was chosen for the test, along with the quick-onset hypnotic Temazepam at a modest dosage of 15mg po, to avoid inducing hypnosis. Within 22 minutes of ingestion the benzodiazepine had completely removed any perceptible untoward effect of the stimulants effects on the cardiovascular system, namely tachycardia (from 146 to 77) and perceptible signs of HBP (sorry my cellphone can't measure blood pressure).
IMPORTANT NOTICE: This blog entry is not a standard experiment protocol even though it is backed by the personal experience of the author as described. Results published are dose and ratio dependent. Higher stimulant dosage will require ratio recalibration. No other stimulant or benzodiazepine was used but similar results can be projected based on chemical affinities between amphetamine and its congeners, methylphenidate and its congeners, substituted amphetamines and substituted cathinones. Excluded are: psychedelic amphetamine derivatives, methamphetamine, cocaine HCL and its derivatives. Author guarantees veracity of facts reported but accepts no responsibility for any injuries or fatalities resulting from replication of this experiment