The antigenic effect of intravenous injection of diphtheria toxin

1925 ◽  
Vol 28 (2) ◽  
pp. 273-278 ◽  
Author(s):  
A. T. Glenny ◽  
C. G. Pope
1915 ◽  
Vol 22 (3) ◽  
pp. 292-303 ◽  
Author(s):  
Francis R. Fraser

1. In rabbits transient and also permanent enlargements of the heart occur as the result of the intravenous injection of adrenalin, spartein and adrenalin, diphtheria toxin, and streptococci. 2. Transient and permanent enlargements of the heart to the left are associated with decrease in the size of the upwardly directed waves of the Q, R, S group in Lead II of the electrocardiograms and increase in the downwardly directed. Transient enlargement to the right is associated with changes in the opposite direction. 3. The stages in the process of enlargement have been observed and are associated with gradual changes in the size of these waves. 4. A diminution in the size of all the waves of the Q, R, S group was observed in degenerative conditions of the heart muscle. 5. Extreme degeneration of the structures of the heart was associated with slowing of the heart's action, lengthening of conduction time (P-Q), and lengthening of the time occupied by the individual waves of the electrocardiogram. 6. Ectopic ventricular contractions were seen in rabbits injected intravenously with suspensions of living streptococci.


1927 ◽  
Vol 46 (4) ◽  
pp. 609-614 ◽  
Author(s):  
C. W. Jungeblut

1. The minimum amount of diphtheria toxin which killed normal mice of from 24 to 30 gm. in weight upon intravenous injection, was found to be between 75 and 100 times the M.F.D. for the guinea pig. When given intraperitoneally, the fatal dose for mice was as high as 200 M.F.D. 2. There was no significant difference in the lethal action of diphtheria toxin for normal mice and mice in which an elimination of the reticulo-endothelial system had been attempted by means of blocking injections of India ink, or splenectomy, or a combination of both operations. 3. Attempts to infect normal mice and mice treated as described with large doses of a highly virulent diphtheria strain were unsuccessful with both groups of animals.


2004 ◽  
Vol 5 (1) ◽  
Author(s):  
Shingo Nakamura ◽  
Masuo Terashima ◽  
Natsuko Kikuchi ◽  
Minoru Kimura ◽  
Tadaaki Maehara ◽  
...  

1973 ◽  
Vol 29 (02) ◽  
pp. 353-362
Author(s):  
J Lisiewicz ◽  
A Pituch ◽  
J. A Litwin

SummaryThe local Sanarelli-Shwartzman phenomenon (SSP-L) in the skin of 30 rats was induced by an intr a cutaneous sensitizing injection of leukaemic leucocytes isolated from the peripheral blood of patients with chronic lymphocytic leukaemia (CLL), acute myeloblastic leukaemia (AL) and chronic granulocytic leukaemia (CGL) and challenged by an intravenous injection of 100(μ of E. coli endotoxin. SSP-L was observed in 7 rats after injection of CLL lymphocytes and in 6 and 2 rats after AL myeloblasts and the CGL granulocytes, respectively. The lesions in the skin after AL myeloblasts appeared in a shorter time and were of longer duration compared with those observed after CLL lymphocytes and CGL granulocytes. Histologically, the lesions consisted of areas of destruction in the superficial layers of the skin ; the demarcation line showed the presence of neutrophils, macrophages and erythrocytes. Haemorrhages and fibrin deposits near the demarcation line were larger after injection of CLL lymphocytes and AL myeloblasts than after CGL granulocytes. The possible role of leucocyte procoagulative substances in the differences observed have been discussed.


1978 ◽  
Vol 39 (01) ◽  
pp. 201-209 ◽  
Author(s):  
Hiroshi Hasegawa ◽  
Hiroshi Nagata ◽  
Makoto Murao

SummaryAttempts were made to demonstrate ultrastructural changes of the tissue thromboplastin after intravenous injection, as a model experiment on the pulmonary microthrombi formation induced by the tissue thromboplastin circulating from venous return.Concentrically arranged membrane structures of the injected thromboplastin disappeared in extremely short time after the injection of the thromboplastin in rabbits. The long sheet membrane of the injected thromboplastin was frequently seen as adhered to the vascular endothelium or to the surface of blood corpuscles. Furthermore, fibrin fibres were formed in contact with the long sheet membrane of the thromboplastin. Membrane structures were not found anywhere in the control rabbits.


1981 ◽  
Vol 46 (03) ◽  
pp. 658-661 ◽  
Author(s):  
C Korninger ◽  
J M Stassen ◽  
D Collen

SummaryThe turnover of highly purified human extrinsic plasminogen activator (EPA) (one- and two-chain form) was studied in rabbits. Following intravenous injection, EPA-activity declined rapidly. The disappearance rate of EPA from the plasma could adequately be described by a single exponential term with a t ½ of approximately 2 min for both the one-chain and two-chain forms of EPA.The clearance and organ distribution of EPA was studied by using 125I-labeled preparations. Following intravenous injection of 125I-1abeled EPA the radioactivity disappeared rapidly from the plasma also with a t ½ of approximately 2 min down to a level of 15 to 20 percent, followed by a small rise of blood radioactivity. Gel filtration of serial samples revealed that the secondary increase of the radioactivity was due to the reappearance of radioactive breakdown products in the blood. Measurement of the organ distribution of 125I at different time intervals revealed that EPA was rapidly accumulated in the liver, followed by a release of degradation products in the blood.Experimental hepatectomy markedly prolonged the half-life of EPA in the blood. Blocking the active site histidine of EPA had no effect on the half-life of EPA in blood nor on the gel filtration patterns of 125I in serial plasma samples.It is concluded that human EPA is rapidly removed from the blood of rabbits by clearance and degradation in the liver. Recognition by the liver does not require a functional active site in the enzyme. Neutralization in plasma by protease inhibitors does not represent a significant pathway of EPA inactivation in vivo.


1961 ◽  
Vol 06 (01) ◽  
pp. 157-159 ◽  
Author(s):  
Saul B. Gilson

ConclusionExperimental glomerulitis in rabbits following intravenous injection of gamma globulin was inhibited by heparinization. The physiological and patho-physiological significance of this observation is considered.


1967 ◽  
Vol 18 (01/02) ◽  
pp. 057-065 ◽  
Author(s):  
G Zbinden

SummaryIntravenous injection of 0.5% lauric acid solution into rabbits caused moderate to marked thrombocytopenia. With small doses (2.5 mg/kg) this thrombocyte decrease was reversible and microscopically demonstrable thrombosis in the lungs was only seen or suspected in a small number of rabbits 10 to 30 min after lauric acid injection. High doses were followed by partly reversible thrombocytopenia and by moderate to marked, sometimes lethal, thrombosis in the lungs still demonstrable 24 hrs after injection. Repeated administration of small doses of lauric acid did not lead to a depletion of the circulating thrombocytes. Thrombocytopenic response, however, appeared to be less pronounced after the second and subsequent injections. Studies with Cr51-labeled platelets indicate that during the reversible thrombocytopenia following a small intravenous dose of lauric acid platelets are retained in various organs, particularly the lungs.


1983 ◽  
Vol 50 (02) ◽  
pp. 557-559 ◽  
Author(s):  
J F Fracasso ◽  
A M Rothschild

SummaryIntravenous injection of E. coli endotoxin (ETX), of adrenaline (AD) or of carbamylcholine (CBCH), caused fibrinolytic activity (FA), directly detectable on plasminogen-rich fibrin plates, to appear in the plasma of the rat. Adrenodemedul- lation abolished responses to ETX or CBCH, but enhanced those to AD. Rats given ETX exhibited marked hypotension, followed by a compensatory phase of normotension abolished by adrenodemedullation and significantly attenuated by phenoxy- benzamine, an a-adrenergic blocking agent which however failed to block FA caused by either ETX or AD. Aspirin, but not indomethacin, inhibited FA evoked by ETX, AD or CBCH. These results suggest that FA evoked by ETX in the rat is caused by AD released from the adrenal gland and does involve the fatty acid cyclooxygenase system.


1955 ◽  
Vol 19 (2) ◽  
pp. 181-184 ◽  
Author(s):  
Carl A. Gemzell ◽  
Frank Heijkenskjöld ◽  
Lars Ström

Sign in / Sign up

Export Citation Format

Share Document