طخشیقون
بفتح طا و سکون خا و کسر شین معجمه و سکون یاء مثناه تحتانیه و
ضم قاف و سکون واو و نون طفشیقون نیز نامند بمعنی قوسی است
ماهیت آن
دوای سمی است از جملۀ یتوعات که در بلاد ارمن پیکان را بآن آب می
دهند زخم آن کشنده می باشد برک و نبات آن شبیه ببرک کبر و پرشیر و بغایت تند
افعال و خواص آن
ضماد آن جهت قوبا نافع و کویند حلتیت بادزهر آنست شربا و ضماد کردن
بر موضع جراحت آن
مخزن الادویه عقیلی خراسانی
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طخشیقون . [ طَ ] (معرب ، اِ) صاحب برهان
گوید: نام داروئی است بلغت رومی که آنرا از مُلک ارمن آرند و پیکان تیر و بیشتر اسلحه جنگ را بدان زهرآلود سازند - انتهی . ظاهراً اصل
این کلمه طخیقون یا طخسیقون یونانی بمعنی مطلق سم است ، و شاید وقتی این کلمه معنی
خاص سم محصول ارمنیه و مخصوص زهراب دادن پیکان و جز آن میداده است . و طفشیقون نیز
گویند. و تاویل آن قوسی بود، از بهر آنکه آن دوائی است که اهل ارمن پیکان را به وی
زهرآلود کنند و در جنگها بکار برند و حلتیت پادزهر وی است . (اختیارات بدیعی ). دوای
سمی است که بلاد ارمن پیکان را به آن آب داده و زخم آن کشنده باشد، از جمله یتوعات است ، و برگش شبیه به برگ کبر و پرشیر و
بغایت تند، و ضمادش جهت قوبا نافع است . (تحفه
حکیم مومن ). حلتیت پادزهر آن است شرباً، و ضماد بموضع جراحت آن . (مخزن الادویه
). و طخسیقون با سین هم آمده است ، و آن ماده ای است که قدما تیر را بدان زهرآگین میکردند
و این بیشتر معمول مردم ارمینیه بود.
- طخشیقون
معنی :
(طُ) [ معر. ] (اِ.) 1 - نام عمومی سم
ها؛ زهر. 2 - سمی که در قدیم جهت زهرآلود کردن نوک نیزه ها و تیرها به کار می بردند
و امروزه نیز بین قبایل وحشی آفریقای جنوبی و آمریکای جنوبی معمول است و از نوع کورار*
است .
* کورار. (فرانسوی ، اِ) ۞ ماده ای سمی دارای ترکیب شیمیایی
درهم و متفاوت که بومیان آمریکای جنوبی آن را برای زهرآلود ساختن نوک نیزه صید حیوانات به کار می بردند. این ماده از گیاهان
مختلف خصوصاً گونه های مختلف جوزالقی و گیاهان تیره کبابه و تیره
عشقه ها و غیره استخراج می شود. (فرهنگ فارسی معین .(
https://en.wikipedia.org/wiki/Curare
- طفشیقون . [ طَ ] (معرب ، اِ) طخشیقون است و بعضی شوکران
دانسته اند و اصلی ندارد. (فهرست مخزن الادویه ). نام دوایی است به لغت رومی که آن
را از ملک ارمن آورند و پيکان تیر و بیشتر اسلحه
جنگ را بدان زهرآلود سازند. و بجای حرف ثانی ، خاء نقطه دار هم به نظر آمده
است که طخشیقون باشد. (برهان ).
- طقسیقون . [ طُ ] (معرب ، اِ)
۞ ابن البیطار در ضمن شرح «ابن
عرس » از دیسقوریدوس آرد: و ابن عرس پازهر کشنده ای است که آن را طقسیقون گویند. گمان
میکنم این کلمه همان طخشیقون و طفشیقون لغت نامه ها باشد و اصل آن تخیقون یا تکزیکن
یونانی بمعنی مطلق زهر است . واﷲ اعلم .
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Curare /kʊˈrɑːri/[1] or /kjʊˈrɑːri/[2] is a common name for various plant
extract alkaloid arrow poisons originating from Central and South America. These poisons function by
competitively and reversibly inhibiting the nicotinic
acetylcholine receptor (nAChR), which is a subtype of acetylcholine
receptor found at the neuromuscular
junction. This causes weakness of the skeletal muscles and,
when administered in a sufficient dose, eventual death by asphyxiation due to paralysis of the diaphragm.
According
to pharmacologist Rudolf Boehm's 1895
classification scheme, the three main types of curare are:[3]
·
tube or bamboo curare (so
named because of its packing into hollow bamboo tubes; main toxin is D-tubocurarine).
·
pot curare (originally
packed in terra cotta pots;
main alkaloid components are protocurarine, protocurine, and protocuridine).
Protocurarine is the active ingredient; protocurine is only weakly toxic, and
protocuridine is not toxic.
·
calabash or gourd curare (originally
packed into hollow gourds; main toxin is curarine).
Of
these three types, some formulas belonging to the tube curare are the most
toxic, relative to their LD50 values.[3]
Contents
[show]
 |
This article is missing information about use of
curare by Central American people. Please expand the article to
include this information. Further details may exist on the talk page. (March 2014)
|
Curare
was used as a paralyzing poison by South American indigenous people. The prey
was shot by arrows or blowgun darts dipped
in curare, leading to asphyxiation owing to the inability of the victim's
respiratory muscles to contract. The word 'curare' is derived from wurari,
from the Carib language of the Macusi Indians of Guyana.[4] Curare is also known among indigenous
peoples as Ampi, Woorari, Woorara, Woorali, Wourali, Wouralia, Ourare, Ourari,
Urare, Urari, and Uirary.
In
1596, Sir Walter Raleigh mentioned
the arrow poison in
his book Discovery of the
Large, Rich, and Beautiful Empire of Guiana (which relates
to his travels in Trinidad and Guayana), though the poison he described
possibly was not curare.[5] In 1780, Abbe Felix Fontana
discovered that it acted on the voluntary muscles rather than the nerves and
the heart.[6] In 1832, Alexander von
Humboldt gave the first western account of how the toxin was
prepared from plants by Orinoco River
natives.[7]
During
1811–1812 Sir
Benjamin Collins Brody (1783–1862) experimented with curare.[8] He was the first to show that curare
does not kill the animal and the recovery is complete if the animal's respiration is maintained artificially.
In 1825, Charles Waterton described
a classical experiment in which he kept a curarized female donkey alive by artificial
respiration with a bellows through a tracheostomy.[9] Waterton is also
credited with bringing curare to Europe.[10] Robert Hermann
Schomburgk, who was a trained botanist, identified the vine as one
of the Strychnos genus
and gave it the now accepted name Strychnos toxifera.[11]
George Harley (1829–1896) showed in 1850
that curare (wourali) was effective for the treatment of tetanus and strychnine poisoning.[12][13] In 1857, Claude Bernard (1813-1878) published the
results of his experiments in which he demonstrated that the mechanism of
action of curare was a result of interference in the conduction of nerve impulses from the motor nerve to the skeletal muscle,
and that this interference occurred at the neuromuscular
junction.[3][14] From 1887, the
Burroughs Wellcome catalogue listed under its 'Tabloids' brand name, tablets of
curare at 1⁄12 grain (price 8
shillings) for use in preparing a solution for hypodermic injection. In
1914, Henry Hallett Dale (1875–1968)
described the physiological actions of acetylcholine.[15] After 25 years, he
showed that acetylcholine is responsible for neuromuscular
transmission, which can be blocked by curare.[16]
The
best known and historically most important (because of its medical
applications) toxin is d-tubocurarine. It was
isolated from the crude drug — from a museum sample of curare — in 1935 by
Harold King (1887–1956) of London, working in Sir Henry Dale's laboratory. He also
established its chemical structure.[17] It was introduced
into anesthesia in the early 1940s as a muscle relaxant for surgery. Curare is
active — toxic or muscle-relaxing, depending on the intended use — only by an
injection or a direct wound contamination by poisoned dart or arrow. It is
harmless if taken orally[9][18] because curare
compounds are too large and highly charged to pass through the lining of the
digestive tract to be absorbed into the blood. For this reason, people can eat
curare-poisoned prey safely. In medicine, curare has been superseded by a
number of curare-like agents, such as pancuronium, which have a similar
pharmacodynamic profile, but fewer side effects.
![[icon]](https://en.wikipedia.org/wiki/File:Wiki_letter_w_cropped.svg){kind=small} |
The
various components of curare are organic compounds classified as either isoquinoline or indole alkaloids. Tubocurarine is
the major active component in the South American dart poison.[19] As an alkaloid,
tubocurarine is a naturally occurring compound that consists of nitrogenous
bases—though the chemical structure of alkaloids is highly variable.
Like
most alkaloids, tubocurarine consists of a cyclic system with a nitrogen atom
in an amine group.[20] Because of this
structure, tubocurarine can bind readily to the receptors for acetylcholine
(ACh) at the neuromuscular junction, which blocks nerve impulses from being
sent to the skeletal muscles, effectively paralyzing the muscles of the body.
Since tubocurarine binds reversibly to the ACh receptors, treatment for curare
poisoning involves adding an acetylcholinesterase (AChE) inhibitor, which will
stop the destruction of acetylcholine so that it can compete with curare.[21]
Curare
is an example of a non-depolarizing muscle relaxant that blocks the nicotinic
acetylcholine receptor (nAChR), one of the two types of
acetylcholine (ACh) receptors,
at the neuromuscular
junction. The main toxin of curare, d-tubocurarine, occupies the same position on
the receptor as ACh with an equal or greater affinity, and elicits no response,
making it a competitive
antagonist. The antidote for curare poisoning is an acetylcholinesterase
(AChE) inhibitor (anti-cholinesterase), such as physostigmine or neostigmine. By blocking ACh degradation, AChE
inhibitors raise the amount of ACh in the neuromuscular junction; the
accumulated ACh will then correct for the effect of the curare by activating
the receptors not blocked by toxin at a higher rate.
The
time of onset varies from within one minute (for tubocurarine in intravenous
administration, penetrating a larger vein), to between 15 and 25
minutes (for intramuscular
administration, where the substance is applied in muscle tissue).[22]
Curare
has no effect if ingested so the meat of an animal killed by curare does not
become poisonous, and it has no effect on its flavor.[23]
Isolated
attempts to use curare during anesthesia date back to 1912 by Arthur Lawen of
Leipzig,[24] but curare came to
anesthesia via psychiatry (electroplexy).
In 1939 Abram Elting Bennett used
it to modify metrazol induced convulsive therapy.[25] Muscle relaxants are used in modern anesthesia for many reasons, such as
providing optimal operating conditions and facilitating intubation of the
trachea. Before muscle relaxants, anesthesiologists needed to use larger doses
of the anesthetic agent, such as ether, chloroform or cyclopropane to achieve these aims. Such
deep anesthesia risked killing patients that were elderly or had heart
conditions.
The
source of curare in the Amazon was first researched by Richard Evans
Schultes in 1941. Since the 1930s, it was being used in
hospitals as a muscle relaxant.
He discovered that different types of curare called for as many as 15
ingredients, and in time helped to identify more than 70 species that produced
the drug.
In
the 1940s, it was used on a few occasions during surgery as it was mistakenly
thought to be an analgesic or anesthetic. The patients reported feeling the
full intensity of the pain though they were not able to do anything about it
since they were essentially paralyzed.[26]
On
January 23, 1942, Harold Griffith and Enid Johnson gave
a synthetic preparation of curare (Intercostrin/Intocostrin) to a patient
undergoing an appendectomy (to supplement conventional anesthesia). Safer
curare derivatives, such as rocuronium and pancuronium, have superseded d-tubocurarine
for anesthesia during surgery. When used
with halothane d-tubocurarine can cause a
profound fall in blood pressure in some patients as both the drugs are ganglion blockers.[27]However, it is safer to
use d-tubocurarine with ether.
In
1954, an article was published by Beecher and Todd suggesting that the use
of muscle relaxants (drugs
similar to curare) increased death due to anesthesia nearly sixfold.[28] This was refuted in
1956.[29]
Modern
anesthetists have at their disposal a variety of muscle relaxants for use in anesthesia.
The ability to produce muscle relaxation irrespective of sedation has permitted
anesthetists to adjust the two effects independently and on the fly to ensure
that their patients are safely unconscious and sufficiently relaxed to permit
surgery. The use of neuromuscular
blocking drugs carries with it a very small risk of anesthesia awareness.
There
are dozens of plants from which isoquinoline and indole alkaloids with
curarizing effects can be isolated, and which were utilized by indigenous
tribes of Central and South America for the production of arrow poisons. Among
them are:
In
family Menispermaceae:
Other
families:
·
several species of
the Strychnos genus of family Loganiaceae including toxifera, guianensis, castelnaei, usambarensis
·
at least three members of
the Artanthe genus of family Piperaceae
Some
plants in the Aristolochiaceae family
have also been reported as sources.
 |
This section does not cite any sources. Please
help improve this section by adding citations to reliable sources.
Unsourced material may be challenged and removed.(February 2016) (Learn
how and when to remove this template message)
|
The
toxicity of curare alkaloids in man hasn't been established. Administration
must be parenterally, as
gastro-intestinal absorption is ineffective.
LD50 (mg/kg)
man:
0.735 est. (form and method of administration not indicated)
mouse:
pot:0.8-25; tubo: 5-10; calabash: 2-15.
|
|
In
the Amazon there is such a bounty of plants so rich in alkaloids that an
effective curare can be made by boiling down several kilos of any combination
of 20 different species of jungle leaves. Once it becomes a thick syrupy tar it
will most likely be able to bring down anything from a monkey to a man.[citation needed]
 |
This article contains weasel
words: vague phrasing that often accompanies biased or unverifiable information. Such
statements should be clarified
or removed. (December
2014)
|
It
is known[citation needed] that the final
preparation is often more potent than the concentrated principal active
ingredient. Various irritating herbs, stinging insects, poisonous worms, and
various parts of amphibians and reptiles are added to the preparation. Some of
these accelerate the onset of action or increase the toxicity; others prevent
the wound from healing or blood from coagulating.
Curare
poisoning can be indicated by typical signs of neuromuscular-blocking
drugs such as paralysis including respiration but not directly
affecting the heart.
Curare
poisoning can be managed by artificial
respiration such as mouth-to-mouth
resuscitation. In a study of 29 army volunteers that were paralyzed
with curare, artificial respiration managed to keep an oxygen saturation of
always above 85%,[31] a level at which
there is no evidence of altered
state of consciousness.[32] Yet, curare
poisoning mimics the total locked-in
syndrome in that there is paralysis of every voluntarily
controlled muscle in the body (including the eyes), making it practically
impossible for the victim to confirm consciousness while paralyzed.[33]
Spontaneous
breathing is resumed after the end of the duration of action of
curare, which is generally between 30 minutes[34] to 8 hours,[35] depending on the
variant of the toxin and dosage. Cardiac muscle is not directly affected
by curare, but if more than four to six minutes has passed since respiratory
cessation the cardiac muscle may stop functioning by oxygen-deprivation,
making cardiopulmonary
resuscitation including chest compressions necessary.[36]
Muscle
paralysis can be reversed by administration of a cholinesterase
inhibitor such as pyridostigmine.[37]
3. ^ Jump up to:a b c Gray, TC (1947). "The Use of D-Tubocurarine Chloride in
Anæsthesia" (PDF). Ann R Coll Surg
Engl. 1 (4): 191–203. PMC 1940167
. PMID 19309828.
. PMID 19309828.
7. Jump up^ [1]Personal
Narrative of Travels to the Equinoctial Regions of America, During the Year
1799-1804 — Volume 2, Humboldt, Alexander von
14. Jump up^ Bernard, C (1857). "Leçons sur les effets des substances toxiques et
médicamenteuses" (in French). Paris: J.B. Baillière:
369–80. |chapter= ignored (help)
21. Jump up^ Saladin, Kenneth S. Anatomy and
Physiology The Unity of Form and Function. 7th ed. New York: McGraw Hill
Education, 2015. Print.
23. Jump up^ From the Rainforests of South America to The Operating
Room: A History of Curare, By Daniel Milner, BA, CD, Summer 2009.
University of Ottawa Faculty of Medicine.
26. Jump up^ Dennett, Daniel C. Brainstorms:
Philosophical Essays on Mind and Psychology (1978), Cambridge, MA : MIT
Press, p209
27. Jump up^ Mashraqui S. Hypotension induced with
d-tubocurarine and halothane for surgery of patent ductus arteriosus. Indian Journal
of Anesthesia. 1994 Oct; 42(5): 346-50
28. Jump up^ Beecher H. K.; Todd D. P.
(1954). "A Study of the Deaths Associated with Anesthesia
and Surgery : Based on a Study of 599,548 Anesthesias in Ten Institutions
1948-1952, Inclusive". Annals of Surgery. 140 (2):
2–35. PMC 1609600. PMID 13159140. (reprinted
in "Classical File", Survey of Anesthesiology 1971, 15 ,
394, 496)
. PMID 13159140. (reprinted
in "Classical File", Survey of Anesthesiology 1971, 15 ,
394, 496)
29. Jump up^ Albertson HA, Trout HH, Morfin E
(June 1956). "The Safety of Curare in Anesthesia'". Annals
of Surgery. 143 (6): 833–837. doi:10.1097/00000658-195606000-00012. PMC 1465152. PMID 13327828.
. PMID 13327828.
30. Jump up^ Curare, a South American Arrow Poison, from
"Plants and Civilization" by Professor Arthur C. Gibson, at UCLA
Mildred E. Mathias Botanical Garden.
31. Jump up^ Page 520 in: Paradis, Norman A.
(2007). Cardiac arrest: the science and practice of resuscitation
medicine. Cambridge, UK: Cambridge University Press. ISBN 0-521-84700-1.
32. Jump up^ Oxymoron: Our Love-Hate Relationship with Oxygen,
By Mike McEvoy at Albany Medical College, New York. 10/12/2010
33. Jump up^ Page 357 in: Damasio, Antonio R.
(1999). The feeling of what happens: body and emotion in the making of
consciousness. San Diego: Harcourt Brace. ISBN 0-15-601075-5.
34. Jump up^ For therapeutic dose of tubocurarine
by shorter limit as given at page 151 in: Rang, H. P.
(2003). Pharmacology. Edinburgh: Churchill Livingstone. ISBN 0-443-07145-4. OCLC 51622037.
35. Jump up^ For 20-fold paralytic dose of
toxiferine ("calabash curare"), according to: Page 330 in: The Alkaloids: v. 1:
A Review of Chemical Literature (Specialist Periodical Reports). Cambridge,
Eng: Royal Society of Chemistry. 1971. ISBN 0-85186-257-8.
36. Jump up^ "four to six minutes" given
from: Cardiopulmonary Resuscitation (CPR) in
Farlex medical dictionary, in turn citing Gale Encyclopedia of
Medicine. Copyright 2008.
37. Jump up^ Page 153 in: Thomas Morgan III;
Bernadette Kalman (2007). Neuroimmunology in Clinical Practice.
Wiley-Blackwell. ISBN 1-4051-5840-9.
·
strychnine, a related alkaloid poison that
occurs in some of the same plants as curare
·
arrow poison, what curare was originally used
for
·
poison dart frog, another source of arrow
poison
·
Foldes, F.F. "Anesthesia
before and after curare", Anasthesieabteilung des
Albert-Einstein-College of Medicine. Anaesthesiol Reanim, 1993,
18(5):128-31. (retrieved June 20, 2005)
·
James, Mel. "Harold Griffith",Heirloom
Series, Volume 6. (retrieved June 20, 2005)
·
"Curare", Blue
Planet Biomes, 2000. (retrieved September 27, 2005)
·
Smith, Roger. "Cholernergic Transmission",
(retrieved March 13, 2007)
·
Strecker G J et al. "Curare binding and the curare-induced
subconductance state of the acetylcholine receptor channel.", Biophysical
Journal 56: 795-806 (1989). (retrieved May 12, 2007)
 |
Wikisource has the text of the
1921 Collier's
Encyclopedia article Woorali Poison.
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·
LCCN: sh85034841
·
BNF: cb11957231d (data)
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