Effect of Beta Blockers on Human Blood Plaletets in Vivo

1975 ◽  
Author(s):  
K. Zawilska ◽  
M. Komarnicki ◽  
B. Manka
Keyword(s):  
Platelet Aggregation ◽  
Human Blood ◽  
Beta Blockers ◽  
Normal Subjects ◽  
Platelet Factor ◽  
Induced Aggregation

ADP and collagen-induced platelet aggregations are diminished one hour after propanolol administration to normal subjects while adrenalin-induced aggregation and platelet factor 3 availability are not influenced. This effect of propanolol in vivo is very different from its in vitro action and is possibly related to the interaction adrenalin-ADP and collagen-ADP. Intermediary products of propanolol metabolism may also be involved in this effect.The administration of practololol to a second group of normal subjects had no effect on platelet aggregation and on platelet factor 3 availability.

scholarly journals Release of arachidonic acid from human platelets. A key role for the potentiation of platelet aggregability in normal subjects as well as in those with nephrotic syndrome

Blood ◽  
1978 ◽  
Vol 52 (5) ◽  
pp. 969-977 ◽  
Author(s):  
N Yoshida ◽  
N Aoki
Keyword(s):  
Arachidonic Acid ◽  
Nephrotic Syndrome ◽  
Platelet Aggregation ◽  
Normal Subjects ◽  
Human Albumin ◽  
Membrane Phospholipids ◽  
Platelet Aggregability ◽  
Induced Aggregation

Abstract Low (nonaggregating) concentrations of collagen that potentiate platelet aggregation did not induce the formation of measurable amount of malondialdehyde (MDA) but released small but significant amounts of radioactivity from 14C-arachidonic acid-labeled platelets. A major portion of the radioactive compounds released by nonaggregating concentrations of collagen existed as arachidonic acid and a minor part as thromboxane B2. The nephrotic syndrome enhances platelet aggregability, and this effect is abolished by correcting hypoalbuminemia in vitro and in vivo by the addition of albumin, which is the main carrier for free fatty acids, including arachidonic acid. Human albumin (fatty acid free) inhibited collagen-induced aggregation, MDA formation, and release of the radioactivity from 14C-arachidonic acid-labeled platelets in normals as well as in those with nephrotic syndrome. These data support our hypothesis that the main mechanism responsible for the potentiation of platelet aggregation is the release of arachidonic acid from platelet membrane phospholipids via the activation of phospholipase A2. Furthermore, enhanced platelet aggregation in the nephrotic syndrome was at least partly attributable to an increased availability of arachidonic acid released secondary to hypoalbuminemia. Albumin inhibits aggregation probably by binding to released arachidonic acid preventing arachidonic acid from being metabolized to potent aggregating substances, endoperoxides and thromboxane A2. The mechanism of release of arachidonic acid may play a key role in the potentiation of platelet aggregability in normals as well as in pathologic conditions such as the nephrotic syndrome.

scholarly journals Release of arachidonic acid from human platelets. A key role for the potentiation of platelet aggregability in normal subjects as well as in those with nephrotic syndrome

Blood ◽  
1978 ◽  
Vol 52 (5) ◽  
pp. 969-977
Author(s):  
N Yoshida ◽  
N Aoki
Keyword(s):  
Arachidonic Acid ◽  
Nephrotic Syndrome ◽  
Platelet Aggregation ◽  
Normal Subjects ◽  
Human Albumin ◽  
Membrane Phospholipids ◽  
Platelet Aggregability ◽  
Induced Aggregation

Low (nonaggregating) concentrations of collagen that potentiate platelet aggregation did not induce the formation of measurable amount of malondialdehyde (MDA) but released small but significant amounts of radioactivity from 14C-arachidonic acid-labeled platelets. A major portion of the radioactive compounds released by nonaggregating concentrations of collagen existed as arachidonic acid and a minor part as thromboxane B2. The nephrotic syndrome enhances platelet aggregability, and this effect is abolished by correcting hypoalbuminemia in vitro and in vivo by the addition of albumin, which is the main carrier for free fatty acids, including arachidonic acid. Human albumin (fatty acid free) inhibited collagen-induced aggregation, MDA formation, and release of the radioactivity from 14C-arachidonic acid-labeled platelets in normals as well as in those with nephrotic syndrome. These data support our hypothesis that the main mechanism responsible for the potentiation of platelet aggregation is the release of arachidonic acid from platelet membrane phospholipids via the activation of phospholipase A2. Furthermore, enhanced platelet aggregation in the nephrotic syndrome was at least partly attributable to an increased availability of arachidonic acid released secondary to hypoalbuminemia. Albumin inhibits aggregation probably by binding to released arachidonic acid preventing arachidonic acid from being metabolized to potent aggregating substances, endoperoxides and thromboxane A2. The mechanism of release of arachidonic acid may play a key role in the potentiation of platelet aggregability in normals as well as in pathologic conditions such as the nephrotic syndrome.

scholarly journals Effect of Diazepam on Platelet Function

1977 ◽  
Author(s):  
A. C. Carvalho ◽  
R. W. Colman ◽  
R. Vaillancourt ◽  
R. Cabrai ◽  
R. Anaya
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Platelet Rich Plasma ◽  
Normal Subjects ◽  
Serotonin Release ◽  
Significant Inhibition ◽  
Function Evaluation ◽  
Induced Aggregation

Diazepam (Valium) is one of the most prescribed medications in the world. Patients on Diazepam may need platelet function evaluation. Therefore, a study of its effect on both in vivo and in vitro platelet function was undertaken in 8 normal volunteers. Diazepam (10–40μg/ml) was incubated in vitro with platelet rich plasma (250,000/μl) at intervals of 15, 30, 60, 120, and 240 minutes followed by determination of platelet aggregation and 14C-serotonin release. Fifty percent inhibition of platelet aggregation and release by Diazepam was obtained at 1 hr with epinephrine (p<0.01) and at 2 hrs with ADP (p<0.01), but no significant effect was noted with collagen. The Diazepam inhibitory effect on platelet aggregation and release was overcome by high concentrations of aggregating agents, suggesting that its primary effect is not mediated by inhibition of prostaglandin synthesis.Following oral ingestion of 5mg of Diazepam, platelet aggregation and 14C-serotonin release were determined serially (2, 4, 8, 12, 24, and 48 hours) in the 8 normal subjects. After 8 hours, Diazepam inhibited ADP-induced aggregation and release by 39% (p<0.01) and epinephrine by 50% (p<0.01). No significant inhibition of collagen was observed. Forty-eight hours after Diazepam intake, platelet function returned to normal in all subjects.Our data show that Diazepam impairs both platelet aggregation and release in vitro and in vivo. Although the effect of Diazepam on in vivo hemostasis is still uncertain, our results suggest caution in the interpretation of platelet function testing in patients on this drug.

EFFECTS OF BLOOD CELLS ON PLATELET AGGREGATION BY IMPEDANCE METHOD

1987 ◽  
Author(s):  
L Mannucci ◽  
R Redaelli ◽  
E Tremoll
Keyword(s):  
Platelet Aggregation ◽  
Whole Blood ◽  
Blood Cells ◽  
White Blood Cells ◽  
Normal Subjects ◽  
Impedance Method ◽  
Induced Aggregation ◽  
Vitro Data ◽  
In Vitro Data

To evaluate the effects of blood cells on the response of platelets to aggregating agents using whole blood impedance aggregometer, studies were carried out on whole blood (WB) of normal subjects and of patients with: polycythemia vera (PV), iatrogenic anemia (IA), primary thrombocytosis (PT), idiopathic thrombotic purpura (ITP), myeloid chronic leukemia (MCL), iatrogenic leukopenia (IL). The in vitro effects of red blood cells (RBC) and of white blood cells (WBC) on platelet rich plasma (PRP) aggregation were also evaluated. WB, PRP, WBC and RBC were prepared by conventional methods. Aggregation was performed using the impedance aggregometer (mod. 540, Chrono Log Corp). In normal subjects the concentration of collagen giving 50 % aggregation (AC50 ) found in PRP did not differ from that of WB, indicating that hematocrit values within the normal range did not appreciably affect platelet aggregation. The results obtained in WB of patients are summarized in the table: In vitro data showed that aggregation in prp in wb of normal subjects was related to the number of platelets present in the sample. RBC added to PRP significant reduced aggregation only when the RBC number was greater than 4.101 cells. No effect of WBC on collagen induced aggregation of PRP was observed, whereas significant inhibition was detected after ADP. It is concluded that the aggregation evaluated in WB with impedance method is dependent on the platelet number. Also, in vitro data and studies in WB of patients indicate that aggregation is significantly affected by the presence of cells other than platelets only in conditions of changes of the ratio between platelets and leukocytes and/or red cells.

scholarly journals Studies investigating platelet aggregation and release initiated by sera from patients with thrombotic thrombocytopenic purpura

Blood ◽  
1987 ◽  
Vol 69 (3) ◽  
pp. 924-928 ◽  
Author(s):  
JG Kelton ◽  
JC Moore ◽  
WG Murphy
Keyword(s):  
Platelet Aggregation ◽  
Thrombotic Thrombocytopenic Purpura ◽  
Disease Process ◽  
The Other ◽  
Platelet Glycoprotein ◽  
Glycoprotein Ib ◽  
Thrombocytopenic Purpura ◽  
Induced Aggregation

Many patients with thrombotic thrombocytopenic purpura (TTP) have a platelet aggregating factor in their serum that may be pathologically linked with the disease process. To help characterize the type of platelet aggregation and platelet release induced by the sera from seven TTP patients, we measured the ability of a variety of inhibitors of platelet function as well as the ability of monoclonal antibodies (MoAbs) against platelet glycoproteins to inhibit TTP sera-induced platelet aggregation and release. These results were compared with the ability of the same inhibitors to block platelet aggregation induced by ristocetin, collagen, ADP, thrombin, and IgG-immune complexes. Monoclonal antibody directed against platelet glycoprotein Ib totally inhibited ristocetin-induced aggregation and release but had no effect on aggregation and release induced by the TTP sera or by any of the other platelet agonists. However, the MoAb against glycoproteins IIb/IIIa inhibited aggregation and release caused by TTP sera as well as by collagen, thrombin, and ADP but had no effect on aggregation and release induced by ristocetin. The aggregating activity could be abolished by heparin but not by the serine protease inhibitor PMSF (1 mmol/L). And although monomeric human IgG and purified Fc fragments of IgG inhibited IgG-immune complex-induced aggregation and release, they had no effect on TTP sera-induced aggregation and release nor on aggregation and release induced by any of the other agonists. Consistent with these in vitro studies showing no effect of IgG were the in vivo observations that intravenous (IV) IgG was without effect when administered to three patients with TTP. This study indicates that although a von Willebrand factor (vWF)-rich preparation of cryoprecipitate enhances the in vitro platelet aggregation and release caused by sera from the seven TTP patients we studied, the pathway of aggregation and release is not via platelet glycoprotein Ib. Also the aggregating factor of TTP sera is not neutralized in vitro or in vivo by IgG.

scholarly journals Granulocyte aggregometry: a sensitive technique for the detection of C5a and complement activation

Blood ◽  
1980 ◽  
Vol 55 (6) ◽  
pp. 898-902 ◽  
Author(s):  
DE Hammerschmidt ◽  
TK Bowers ◽  
CJ Lammi-Keefe ◽  
HS Jacob ◽  
PR Craddock
Keyword(s):  
Lupus Erythematosus ◽  
Cytochalasin B ◽  
Normal Subjects ◽  
Standard Methods ◽  
Sensitive Technique ◽  
Fresh Serum ◽  
Induced Aggregation ◽  
Transfusion Reactions

Abstract We have previously shown that complement (C) activated plasma causes granulocyte (PMN) aggregation in vitro and that C5a is responsible. The C-induced aggregation of PMNs treated with cytochalasin-B (CB) is markedly enhanced and irreversible, and the magnitude of the response is proportional to the log (concentration of activated plasma), allowing use of this technique to detect C5a and hence C-activation. To compare the sensitivity of granulocyte aggregometry to that of more standard methods of detecting C-activation, we produced graded C- activation in vitro by treating fresh serum with varying amounts of zymosan. Aggregometry was the most sensitive index of C-activation, detecting C-activation, produced by 0.02 mg zymosan/ml of serum--1/10 that required to produce C-activation detectable by C3 immunoelectrophoresis (the next most sensitive technique). Granulocyte aggregometry may also be used to detect in vivo C-activation. We have found aggregating activity in plasmas from patients with systemic lupus erythematosus, immune vasculitis, transfusion reactions, and other conditions associated with in vivo C-activation, but not in the plasmas of normal subjects.

Inhibition of Human Platelet Aggregation by the Proteolytic Effect of Streptokinase (SK). Role of the Factor VIII Related Antigen

1975 ◽  
Author(s):  
R. Castillo ◽  
S. Maragall ◽  
J. A. Guisasola ◽  
F. Casals ◽  
C. Ruiz ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Factor Viii ◽  
Platelet Rich Plasma ◽  
Gel Filtration ◽  
Inhibitory Effect ◽  
Factor Viii Related Antigen ◽  
Human Factor Viii ◽  
Induced Aggregation

Defective ADP-induced platelet aggregation has been observed in patients treated with streptokinase. This same effect appears “in vitro” when adding SK to platelet rich plasma (PRP). Classic hemophilia and normal platelet poor plasmas (PPP) treated with SK inhibit the aggregation of washed platelets; plasmin-treated normal human serum also shows an inhibitory effect on platelet aggregation. However, von Willebrand SK-treated plasmas do not inhibit the aggregation of washed platelets. The same results appear when plasmas are previously treated with a rabbit antibody to human factor VIII.This confirms that the antiaggregating effect is mainly linked to the digested factor VIII related antigen.The inhibition of ADP-induced platelet aggregation has been proved in gel filtration-isolated and washed platelets from SK-treated PRP.Defective ristocetin-induced platelet aggregation has also been observed- This action does not appear in washed platelets from SK-treated PRP in presence of normal PPP, but it does in presence of SK-treated PPP, which suggests that the inhibition of the ristocetin-induced aggregation is due to the lack of factor VIII and not to the factor VIII-related products.Heparin, either “in vivo” or “in vitro”, has corrected the antiaggregating effect of SK.

scholarly journals Survival and recovery of human platelets stored for five days in a non- plasma medium

Blood ◽  
1986 ◽  
Vol 67 (3) ◽  
pp. 672-675 ◽  
Author(s):  
GA Adams ◽  
SD Swenson ◽  
G Rock
Keyword(s):  
Platelet Aggregation ◽  
Human Blood ◽  
Blood Platelets ◽  
Human Platelets ◽  
Plasma Medium ◽  
Release Reaction ◽  
In Vivo Recovery ◽  
Human Blood Platelets

Abstract Human blood platelets were stored for five days as concentrates in 60 mL of: (a) plasma; (b) non-plasma medium with anticoagulant; and (c) non-plasma medium without anticoagulant. All preparations were equally functional when tested for platelet aggregation and release reaction in response to single agonist or synergistic pairs of agonists in vitro. Platelets stored in non-plasma medium with anti-coagulant had lower kallikrein, fibrino(gen)peptide A, lactate, and beta-thromboglobulin than did plasma controls after five days. In vivo recovery and survival of platelets stored in non-plasma medium with anticoagulant were 51.2% +/- 4.3% and 8.7 +/- 0.3 days, respectively, which were not statistically different from plasma controls of 39.2% +/- 4.9% and 7.2 +/- 0.8 days, respectively. It is concluded that platelets can be stored for five days in a non-plasma medium and still have good in vivo recoveries and survivals.

The Interaction Of Platelet Active Drugs With Prostacyclin In Vitro And Against Biolaser Induced Intravascular Thrombosis

1981 ◽  
Author(s):  
J S Fleming ◽  
B T Cornish ◽  
J O Buchanan ◽  
J P Buyniski
Keyword(s):  
Platelet Aggregation ◽  
Arachidonic Acid Metabolism ◽  
In Vivo Model ◽  
Additive Interaction ◽  
Antithrombotic Activity ◽  
Intravascular Thrombosis ◽  
Low Levels ◽  
Induced Aggregation

Prostacyclin and thromboxane A2, two of the physiologically most important end products of arachidonic acid metabolism, represent a basic control system which modulates platelet function. Decreased vascular prostacyclin is believed to play a role in the increased thrombotic tendency associated with various clinical diseases including diabetes and atherosclerosis. Compounds which either enhance the formation or release of prostacyclin or potentiate the activity of low levels of prostacyclin may be therapeutically useful in ameliorating this associated pathology. We have studied various inhibitors of platelet aggregation for their ability to potentiate the activity of low levels of prostacyclin both in vitro and in an in vivo model of experimental thrombosis. Anagrelide, aspirin, dipyridamole, sulfinpyrazone and ticlopidine all demonstrated interaction with prostacyclin in vitro against collagen-induced platelet aggregation. More limited interactions were observed against ADP-induced aggregation. Using isobolographic analysis most combinations demonstrated additive interaction. However, pronounced supra-additive interaction was observed vs. both aggregating agents in the case of prostacyclin (0.1-1 ng/ml) - anagrelide (8-90 ng/ml) combinations. Dramatic enhancement of the effects of prostacyclin on biolaser-induced thrombosis was also seen in anagrelide (0.5 mg/kg po) pretreated animals. Other inhibitors of platelet aggregation used in combination with prostacyclin produced less spectacular results. These findings suggest that aside from inherent antiaggregatory and antithrombotic activity, certain platelet active drugs may produce equally important effects by virtue of their ability to interact with prostacyclin in a clinically beneficial manner.

scholarly journals Studies investigating platelet aggregation and release initiated by sera from patients with thrombotic thrombocytopenic purpura

Blood ◽  
1987 ◽  
Vol 69 (3) ◽  
pp. 924-928 ◽  
Author(s):  
JG Kelton ◽  
JC Moore ◽  
WG Murphy
Keyword(s):  
Platelet Aggregation ◽  
Thrombotic Thrombocytopenic Purpura ◽  
Disease Process ◽  
The Other ◽  
Platelet Glycoprotein ◽  
Glycoprotein Ib ◽  
Thrombocytopenic Purpura ◽  
Induced Aggregation

Abstract Many patients with thrombotic thrombocytopenic purpura (TTP) have a platelet aggregating factor in their serum that may be pathologically linked with the disease process. To help characterize the type of platelet aggregation and platelet release induced by the sera from seven TTP patients, we measured the ability of a variety of inhibitors of platelet function as well as the ability of monoclonal antibodies (MoAbs) against platelet glycoproteins to inhibit TTP sera-induced platelet aggregation and release. These results were compared with the ability of the same inhibitors to block platelet aggregation induced by ristocetin, collagen, ADP, thrombin, and IgG-immune complexes. Monoclonal antibody directed against platelet glycoprotein Ib totally inhibited ristocetin-induced aggregation and release but had no effect on aggregation and release induced by the TTP sera or by any of the other platelet agonists. However, the MoAb against glycoproteins IIb/IIIa inhibited aggregation and release caused by TTP sera as well as by collagen, thrombin, and ADP but had no effect on aggregation and release induced by ristocetin. The aggregating activity could be abolished by heparin but not by the serine protease inhibitor PMSF (1 mmol/L). And although monomeric human IgG and purified Fc fragments of IgG inhibited IgG-immune complex-induced aggregation and release, they had no effect on TTP sera-induced aggregation and release nor on aggregation and release induced by any of the other agonists. Consistent with these in vitro studies showing no effect of IgG were the in vivo observations that intravenous (IV) IgG was without effect when administered to three patients with TTP. This study indicates that although a von Willebrand factor (vWF)-rich preparation of cryoprecipitate enhances the in vitro platelet aggregation and release caused by sera from the seven TTP patients we studied, the pathway of aggregation and release is not via platelet glycoprotein Ib. Also the aggregating factor of TTP sera is not neutralized in vitro or in vivo by IgG.

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