Posted by Miguel (209.42.216.137) on March 09, 2000 at 20:04:02:
I found this info:
"The final line of evidence presented by P&P was from
smooth muscle studies. The guinea pig trachea contracts
when M concentrations of 5-HT are present. The ability
of 5-HT antagonists to inhibit this effect correlates
with the antagonists affinity for the 5-HT2 binding
site. Thus it appears that this muscle contraction is
5-HT2 mediated. It was found that nM concentrations
of LSD did not cause muscle contraction and inhibited
the agonistic effects of M concentrations of 5-HT.
This also is compatible with the actions of an
antagonist."
The above may suggest that if the problem (CH) is in part
due to vascular disfunction, as in dilation/contraction,
the effects of LSD are counterproductive to that side
of the ailment. Clearly, its effects are concetrated
around the RN autoregulating neurons. The effects of
LSD in this manner may decrease the level, or even the
frequency of CH. However, in its absence, if its [LSD's]
vascualr effects are longer lived, or damage to microvasculature's
hemostic process ensues due to its frequent use
(unknow at this point what would constitute "frequent
use"), it is likely that CH could get much worse if LSD
therapy is discontinued. Then again, LSD may be Godsent if
prolonged therapy has not mayor side effects, which I seriously
doubt.
My suggestion would be for LSD "testers" to study the effects
of discontinuing LSD use in CH after several different
lengths of use.