scholarly journals The release of 5-hydroxytryptamine from rabbit platelets by antigen-antibody reaction in vitro

1965 ◽  
Vol 61 (4) ◽  
pp. 238-254 ◽  
Author(s):  
Sumiji SASAKI
Keyword(s):  
Rabbit Platelets ◽  
Antibody Reaction ◽  
Antigen Antibody

Independence of activation of the fibrinolytic system from certain immunologic systems

1959 ◽  
Vol 196 (2) ◽  
pp. 431-435 ◽  
Author(s):  
S. N. Kolmen ◽  
D. R. Celander ◽  
M. Mason Guest
Keyword(s):  
Fibrinolytic Activity ◽  
Complement Fixation ◽  
Fibrinolytic System ◽  
Complement Activity ◽  
Antibody Reaction ◽  
Antigen Antibody

Activation of the immunologic system either in vitro or in vivo results in nearly complete consumption of complement without activation of the fibrinolytic system. However complement activity decreased upon the induction of fibrinolytic activity even in the absence of an antigen-antibody reaction. Presumably this is due to proteolysis of some part of the complement complex since complement activity was found to be destroyed in the presence of small quantities of purified fibrinolysin. These observations are consistent with the conclusion that a) the components of complement and those of the fibrinolytic system are separate and discrete entities; b) that reactions involving complement fixation and activation do not directly influence the fibrinolytic system; and c) that activation of the fibrinolytic system results in decreases in complement through proteolysis of one or more of its components by the fibrinolysin which develops.

scholarly journals MECHANISM OF HISTAMINE-RELEASE INHIBITION BY NICOTINAMIDE IN IN VITRO ANTIGEN-ANTIBODY REACTION

1962 ◽  
Vol 11 (1) ◽  
pp. 54-64 ◽  
Author(s):  
HIDEMASA YAMASAKI ◽  
SABURO MURAOKA ◽  
MIE SUGIYAMA ◽  
KOITI ENDO
Keyword(s):  
Histamine Release ◽  
Antibody Reaction ◽  
Antigen Antibody

scholarly journals Leukocyte Antigen-Antibody Reaction and Lysis of Paroxysmal Nocturnal Hemoglobinuria Erythrocytes

Blood ◽  
1970 ◽  
Vol 36 (3) ◽  
pp. 334-336 ◽  
Author(s):  
GIROLAMO SIRCHIA ◽  
SOLDANO FERRONE ◽  
FRANCESCO MERCURIALI
Keyword(s):  
Paroxysmal Nocturnal Hemoglobinuria ◽  
Cell Lysis ◽  
Red Cells ◽  
Clinical Implications ◽  
Specific Antibodies ◽  
Leukocyte Antigen ◽  
Leukocyte Antigens ◽  
Antibody Reaction ◽  
Antigen Antibody

Abstract The interaction between leukocyte antigens and specific antibodies can cause lysis of the red cells of paroxysmal nocturnal hemoglobinuria (PNH) in vitro. It is suggested that the activation of complement ensuing from the antigen-antibody interaction is responsible for PNH cell lysis. The clinical implications of this finding are briefly outlined.

scholarly journals The Antigen-Antibody Reaction in Immunohistochemistry

2003 ◽  
Vol 51 (1) ◽  
pp. 1-4 ◽  
Author(s):  
Claudio Montero
Keyword(s):  
Antigen Retrieval ◽  
Fixed Tissue ◽  
Immunohistochemical Reaction ◽  
Histochemical Methods ◽  
Antibody Reaction ◽  
Antigen Antibody

The problems of major concern in immunohistochemical practice are discussed in the following order: (a) the mechanism of the Ag-Ab reaction in fixed tissue as opposed to the in vitro reaction; (b) the chemistry of fixation and its influence on the final result of the immunohistochemical reaction; (c) the various procedures used for antigen retrieval in formaldehyde-fixed tissue; and (d) the consideration of the possible mechanism underlying heat-induced antigen retrieval. Suggestions for further work to attempt a clarification of the mechanism involved in the Ag-Ab reaction in immunohistochemistry resorting to existing histochemical methods for the demonstration of protein side groups are presented, together with some examples already published.

scholarly journals IMMUNOLOGICAL INDUCTION OF INCREASED VASCULAR PERMEABILITY

1969 ◽  
Vol 129 (1) ◽  
pp. 167-184 ◽  
Author(s):  
P. M. Henson ◽  
C. G. Cochrane
Keyword(s):  
Complement System ◽  
Soluble Antigen ◽  
Soluble Factor ◽  
Release Process ◽  
The Third ◽  
Rabbit Platelets ◽  
Antigen Antibody ◽  
Antibody Preparations ◽  
The Complement System

Two mechanisms have been described whereby rabbit platelets in vitro may be induced to release their contained histamine by the reaction of antigen and antibody. Both processes require the participation of the complement system. In the first, the adherence of platelets to particulate antigens such as zymosan or erythrocytes which have fixed complement through the third component was followed by histamine release. Plasma lacking C6 activity was fully active in this system. In the second mechanism, the reaction of soluble antigen with antibody in the presence of plasma also caused release of histamine from platelets and platelet clumping was observed. The release process, which appeared to follow the adherence of platelets to the immune complex, required the action of C6 and perhaps the later-acting components. No evidence could be obtained that a soluble factor was produced which caused the release. Instead, an inhibitor of the release process was detected after incubation of antigen, antibody, and plasma. Antibody preparations capable of giving complement-dependent PCA reactions in rabbits were also shown to induce the release of histamine from platelets in vitro.

LY53857, a 5HT2 Receptor Antagonist, Delays Occlusion and Inhibits Platelet Aggregation in a Rabbit Model of Carotid Artery Occlusion

1991 ◽  
Vol 66 (03) ◽  
pp. 355-360 ◽  
Author(s):  
Harve C Wilson ◽  
William Coffman ◽  
Anne L Killam ◽  
Marlene L Cohen
Keyword(s):  
Electrical Stimulation ◽  
Platelet Aggregation ◽  
Carotid Artery ◽  
Receptor Antagonist ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Rabbit Platelet ◽  
Rabbit Platelets ◽  
5Ht2 Receptor

SummaryThe present study was designed to evaluate the effectiveness of the ergoline 5HT2 receptor antagonist, LY53857 in a rabbit model of vascular arterial occlusion. LY53857 (1 and 10 εM) inhibited serotonin amplified platelet aggregation responses to threshold concentrations of ADP in rabbit platelets in vitro. LY53857 (1 εM) not only inhibited the serotonin component of rabbit platelet aggregation, but also inhibited in vitro aggregation induced by ADP (48.7 ± 16.7% inhibition), collagen (76.1 ± 15.9% inhibition) and U46619 (65.2 ± 12.3% inhibition). The effectiveness of this ergoline 5HT2 receptor antagonist in blocking aggregation to ADP, collagen and U46619 may be related to its ability to inhibit a serotonin component of platelet aggregation since rabbit platelets possess high concentrations of serotonin that may be released during aggregation produced by other agents. Based on the effectiveness of LY53857 to inhibit rabbit platelet aggregation, we explored the ability of LY53857 to extend the time to carotid artery occlusion in rabbits following electrical stimulation of the artery. Reproducible carotid artery occlusion was induced in rabbits by moderate stenosis coupled to arterial cross clamping, followed by electrical stimulation. With this procedure, occlusion occurred at 47.0 ± 7 min (n = 30) after initiation of the electrical stimulation. Animals pretreated with LY53857 (50 to 500 εg/kg i.v.) showed a delay in the time to carotid artery occlusion (at 100 εg/kg i.v. occlusion time extended to 164 ± 16 min). Furthermore, ex vivo platelet aggregation from animals treated with LY53857 (300 εg/kg i.v.) resulted in 40.5% inhibition of platelet aggregation in response to the combination of ADP (1 εM) and serotonin (1 εM). These studies document the ability to obtain reproducible arterial occlusion in the rabbit and showed that intravenously administered LY53857 prolonged the time to carotid artery occlusion. Prolongation of carotid artery occlusion time was accompanied by inhibition of serotonin-amplified ADP-induced aggregation in rabbit platelets, an effect observed both in vitro and ex vivo. Thus, the rabbit is a useful model for studying the effectiveness of 5HT2 receptor antagonists in prolonging vascular occlusion induced by insult of the carotid artery.

In Vitro Effects of Ethanol on Rabbit Platelet Aggregation, Secretion of Granule Contents, and Cyclic AMP Levels in the Presence of Prostacyclin

1989 ◽  
Vol 61 (02) ◽  
pp. 254-258 ◽  
Author(s):  
Margaret L Rand ◽  
Peter L Gross ◽  
Donna M Jakowec ◽  
Marian A Packham ◽  
J Fraser Mustard
Keyword(s):  
Cyclic Amp ◽  
Inhibitory Effect ◽  
Rabbit Platelet ◽  
Inhibitory Effects ◽  
Low Concentrations ◽  
Rabbit Platelets ◽  
High Concentrations ◽  
In Vitro Effects ◽  
Aggregation Of Platelets

SummaryEthanol, at physiologically tolerable concentrations, inhibits platelet responses to low concentrations of collagen or thrombin, but does not inhibit responses of washed rabbit platelets stimulated with high concentrations of ADP, collagen, or thrombin. However, when platelet responses to high concentrations of collagen or thrombin had been partially inhibited by prostacyclin (PGI2), ethanol had additional inhibitory effects on aggregation and secretion. These effects were also observed with aspirin- treated platelets stimulated with thrombin. Ethanol had no further inhibitory effect on aggregation of platelets stimulated with ADP, or the combination of ADP and epinephrine. Thus, the inhibitory effects of ethanol on platelet responses in the presence of PGI2 were very similar to its inhibitory effects in the absence of PGI2, when platelets were stimulated with lower concentrations of collagen or thrombin. Ethanol did not appear to exert its inhibitory effects by increasing cyclic AMP above basal levels and the additional inhibitory effects of ethanol in the presence of PGI2 did not appear to be brought about by further increases in platelet cyclic AMP levels.

Effects of Bupranolol, a New β-Blocker, on Platelet Functions of Rabbit and Human in Vitro

1976 ◽  
Vol 36 (02) ◽  
pp. 376-387 ◽  
Author(s):  
Teruhiko Umetsu ◽  
Kazuko Sanai ◽  
Tadakatsu Kato
Keyword(s):  
Platelet Aggregation ◽  
Platelet Adhesion ◽  
Human Platelets ◽  
Rabbit Platelet ◽  
Rabbit Platelets ◽  
Β Blocker ◽  
Platelet Aggregates ◽  
Induced Aggregation ◽  
Platelet Functions

SummaryThe effects of bupranolol, a new β-blocker, on platelet functions were investigated in vitro in rabbits and humans as compared with propranolol, a well-known β-blocker. At first, the effect of adrenaline on ADP-induced rabbit platelet aggregation was studied because adrenaline alone induces little or no aggregation of rabbit platelets. Enhancement of ADP-induced rabbit platelet aggregation by adrenaline was confirmed, as previously reported by Sinakos and Caen (1967). In addition the degree of the enhancement was proved to be markedly affected by the concentration of ADP and to increase with decreasing concentration of ADP, although the maximum aggregation (percent) was decreased.Bupranolol and propranolol inhibited the (adrenaline-ADP-)induced aggregation of rabbit platelets, bupranolol being approximately 2.4–3.2 times as effective as propranolol. Bupranolol stimulated the disaggregation of platelet aggregates induced by a combination of adrenaline and ADP, but propranolol did not. Platelet adhesion in rabbit was also inhibited by the β-blockers and bupranolol was more active than propranolol. With human platelets, aggregation induced by adrenaline was inhibited by bupranolol about 2.8–3.3 times as effectively as propranolol.From these findings. We would suggest that bupranolol might be useful for prevention or treatment of thrombosis.

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