425
SELECTED ABSTRACTS
Immunology UNDER
Experimental S*. .
THE
Evidence
J. A.
M.
A.
117:
DIRECTION OF MATTHEW MURRAY ALBERT, M.D.,
WALZER, BROOKLYN
for Histamine
in
1782,
Release
M.D.,
Allergy.
AND
Katz,
G., and
Cohen,
1941.
The writers investigated t,he role played by histamine humans. It had previously been demonstrated that blood released part of their histamine content into the plasma the related antigen. The quantity of histamine released degree of sensitivity.
in allergic reactions in cells of sensitized animals when mixed in vitro with was proportional to the
In the present experiments venous blood obtained from allergic individuals with circulating atopic reagins was incubated with the specifically related allergen. Plasma histamine determinations were made before and after incubation. An increase in the plasma histamine was observed following incubation of whole blood with the specifically related allergen. Since incubation of plasma alone with the allergen failed to produce a rise in histamine level, the cells were considered to be the source of the increased plasma histamine. The rise in plasma histamine seemed to parallel the degree of clinical sensitivity of the patient rather than the degree of the cutaneous reaction. There was some evidence to indicate that histamine is not the only active substance which is released during the antigen-antibody reaction.
Reversed G. P.,
Passive Skin Sensitization and
Hopkins,
S. J.:
J. Path.
to
Horse Serum in & Bact. 53: 243,
Human 1941.
Beings.
Wright,
The intracutaneous injection of 0.1 ml. of a serum taken from a horse serumsensitive individual into skin sites injected twenty-four to forty-eight hours previousijwith 0.1 ml. of horse serum (tetanus antitoxin) resulted in a positive skin reaction. Normal human serum failed to produce similar reactions. The reversed passive skin reaction occurred with the antiserum in dilutions as high as 1:625. As early as onehalf hour after the skin had been injected with horse serum, it was possible to elicit a positive reaction by injecting the human anti&rum. If a number of hours were permitted to elapse, the antiserum produced a much greater reaction. A comparison of the sensitivity of the reversed reaction with that of the passive transfer reaction (Prausnitz and Kiistner) revealed that the reversed reaction is still strongly positive at levels of antigen and antibody concentration at which the passive transfer reaction begips to fail.
Histamine Exper.
Release Biol.
in the Allergic
& Med.
49:
272,
Skin
Reaction.
Katz,
Gerhard:
Proc.
Sot.
1942.
An ingenious method was devised to demonstrate that histamine is released in the allergic skin reaction. A cantharidss blister was produced on the chest or upper arm of a number of ragweed hay fever patients. The dead skin was removed, and an inverted funnel with the stem cut off was fastened over the denuded area. Locke’s solution, which was introduced into the funnel, was changed at regular intervals and the samples were assayed for their histamine content by biologic and chemical means. After control samples had been taken, from 0.03 to 0.05 ml. of ragweed extract in saline was injected into the denuded skin area. Subsequent samples of the saline bath showed a rise in histamine content when a strong reaction occurred in the denuded area. The histamine content of the saline bath began to rise within ten minutes after the introduction of the allergen into the skin, reached its
Peptone
Shock in Rabbits.
(btzl,
1,‘. W., :tu~l Dragst edt.
(I. A.:
.I. Pharmacol.
&
Tiecause of the similarity I)etweon petrtone shock and :rn:rtrh~-laxis in rahhita, the changes which occur in tlrc c~oncentrntion of histamine in the hlootl and plasma dnaphyl;wtic~ shock in rabbits is characterized hy :I in peptonc shock were stutlietl. marked leucopmia and a dwreasc~ in total hlootl histamine. The addition of antigen to the hlootl of sensitized rahhits, in vitro, pro~luces a wleasr of histamine from the I)lOOtl cells t0 the I)lilS?ll8,. The intravcnour injwtion in hlood lristaminc :1ntl a heparinizrd hlootl of normal cells to tllr platsr11:c. ‘~‘hrrrforr, histamine and upon tltc mhitc following xnaphyluxis in tlw the injection of peptone into anaphylaxis.
Experimental Am.
.I. Path.
In an substances, commonly this type,
of pro1 cases in rahhits pro~luw~l :I tnarlied r,eduction motleratc Ieucopenia. The atltlition of pcptone to rabbits cauwl :I rtlr:n+ of hixtaminc from the blood the etfects of pcptonc sltock upon the total blootl hlootl cell count in rahhits arc similar to ilrosc ohservrrl same animal. H~ww~r, the gcnwrl symptoms following rabbits were not so severe ah those owuwing (luring
Focal Necrosis of the Liver. 18:
323,
lI:Ldley,
Ct., ,Tr., and Lushhaugh,
B. S.:
7942.
effort to ~lrtcrminc whether throtnhosis or both, wrr responsihlc for the f(JGll observed in i nf’wtious and toxic tlirwses, experimentally. in hypersensitive animals.
or
the
(lircct
IlWrOi;iS
the
Of
authow
action liver, inducetl
the'
of toxic which is lesions of
Rabbits and guinea pigs were sensitizwl to crystalline egg alhurnin. Thr antigen was then injected into the mrscnteric veins, tltc m:rrgin:rl ear veins, the abdominal cavity, and the spleen. Thohe animals which survived the an:tphylactic* sltotk wre sacrificed, at rarvinI b7 times , following the injection of the antigen. Hpecimens of liver tissue were taken at the time of the first operation and after the anim:lls were killed. Rabbits sensitized witlt crystalline egg albumin showed large arcas of coagulatetl necrosis of t,lie liver parenchynm, following the injection of the antigen into the peritoneal cavity, into the spleen, or into the mesmteric or marginal ear veins. Control groups treated with nonrelated antigen failed to slrow these lesions. Sensitized guinea pigs, which received injections of crystalline egg albumin into the mrsentoric veins, showed similar hepatic lesions. Vascular thrombosis was rarely present and apparently was second:trg to necrosis of the hepatic cells. The portal veins and the sinusoids ~howrtl ~~olyn~or~~l~onuclear congestion prior to tlw onset of In the interlobular lesions Ihere was no evidence of hemornecrosis of the liver. rhage, edema, or change in the vascular endotlreliurn. It was concluded that focal necrosis of the liver was a direct result of the loc:~l union of antigen and antibody. The coagulative necrosis, the leucocytic response, ant1 the infrequent tluonthosis of the adjacent blood vessels were regarded as secondary to the antigen-antibody reaction.