The Role of Needle Fenestration with Platelet-Rich Plasma in Chronic Tennis Elbow with Indication of Partial Extensor Tendon Tear

SummaryIn a model using an isolated rabbit mesenteric preparation microvessels were transected and the time until haemostatic plugs formed was registered. Perfusion of platelet rich plasma gave no haemostasis whereas whole blood did. Addition of chlorpromazine or adenosine to the whole blood significantly prolonged the time for haemostasis, and addition of ADP to the platelet rich plasma significantly shortened it. It is concluded that red cells are necessary for a normal haemostasis in this model, probably by a combination of a haemodynamic and ADP releasing effect.The fundamental role of platelets in haemostatic plug formation is unquestionable but there are still problems concerning the stimulus for this process to start. Three platelet aggregating substances have been discussed – thrombin, adenosine diphosphate (ADP) and collagen. Evidence speaking in favour of thrombin is, however, very minimal, and the discussion has to be focused on collagen and ADP. In an in vitro system using polyethylene tubings we have shown that "haemostasis" can be obtained without the presence of collagen but against these results can be argued that it is only another in vitro test for platelet aggregation (1).To be able to induce haemostasis in this model, however, the presence of red blood cells is necessary. To further study this problem we have developed a model where haemostatic plug formation can be studied in the isolated rabbit mesentery and we have briefly reported on this (2).Thus, it is possible to perfuse the vessels with whole blood as well as with platelet rich plasma (PRP) and different pharmacological agents of importance.

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Testosterone Potentiation of Ionophore and ADP Induced Platelet Aggregation : Relationship to Arachidonic Acid Metabolism

Thrombosis and Haemostasis ◽

10.1055/s-0038-1653405 ◽

1981 ◽

Vol 46 (02) ◽

pp. 538-542 ◽

Cited By ~ 42

Author(s):

R Pilo ◽

D Aharony ◽

A Raz

Keyword(s):

Arachidonic Acid ◽

Platelet Aggregation ◽

Unsaturated Fatty Acids ◽

Human Platelet ◽

Platelet Rich Plasma ◽

Arachidonic Acid Metabolism ◽

Ionophore A23187 ◽

Low Concentrations ◽

Induced Aggregation

SummaryThe role of arachidonic acid oxygenated products in human platelet aggregation induced by the ionophore A23187 was investigated. The ionophore produced an increased release of both saturated and unsaturated fatty acids and a concomitant increased formation of TxA2 and other arachidonate products. TxA2 (and possibly other cyclo oxygenase products) appears to have a significant role in ionophore-induced aggregation only when low concentrations (<1 μM) of the ionophore are employed.Testosterone added to rat or human platelet-rich plasma (PRP) was shown previously to potentiate platelet aggregation induced by ADP, adrenaline, collagen and arachidonic acid (1, 2). We show that testosterone also potentiates ionophore induced aggregation in washed platelets and in PRP. This potentiation was dose and time dependent and resulted from increased lipolysis and concomitant generation of TxA2 and other prostaglandin products. The testosterone potentiating effect was abolished by preincubation of the platelets with indomethacin.

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Tridegin, a Novel Peptidic Inhibitor of Factor XIIIa from the Leech, Haementeria ghilianii, Enhances Fibrinolysis In Vitro

Thrombosis and Haemostasis ◽

10.1055/s-0038-1656085 ◽

1997 ◽

Vol 77 (05) ◽

pp. 0959-0963 ◽

Cited By ~ 18

Author(s):

Lisa Seale ◽

Sarah Finney ◽

Roy T Sawyer ◽

Robert B Wallis

Keyword(s):

Potent Inhibitor ◽

Platelet Rich Plasma ◽

Factor Xiiia ◽

Cross Linking ◽

Fibrinolytic Enzymes ◽

Small Polypeptide ◽

Tissue Plasminogen ◽

Protein Cross Linking

SummaryTridegin is a potent inhibitor of factor Xllla from the leech, Haementeria ghilianii, which inhibits protein cross-linking. It modifies plasmin-mediated fibrin degradation as shown by the absence of D-dimer and approximately halves the time for fibrinolysis. Plasma clots formed in the presence of Tridegin lyse more rapidly when either streptokinase, tissue plasminogen activator or hementin is added 2 h after clot formation. The effect of Tridegin is markedly increased if clots are formed from platelet-rich plasma. Platelet-rich plasma clots are lysed much more slowly by the fibrinolytic enzymes used and if Tridegin is present, the rate of lysis returns almost to that of platelet- free clots. These studies indicate the important role of platelets in conferring resistance to commonly used fibrinolytic enzymes and suggest that protein cross-linking is an important step in this effect. Moreover they indicate that Tridegin, a small polypeptide, may have potential as an adjunct to thrombolytic therapy.

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Platelet rich plasma versus extracorporeal shock wave therapy in patients with non-calcific supraspinatous tears

Egyptian Rheumatology and Rehabilitation ◽

10.1186/s43166-020-00020-7 ◽

2020 ◽

Vol 47 (1) ◽

Author(s):

Samah M. Alian ◽

Rabab S. Zaghlol ◽

Sahar S. Khalil

Keyword(s):

Shock Wave ◽

Outcome Measures ◽

Platelet Rich Plasma ◽

Extracorporeal Shock Wave Therapy ◽

Shock Wave Therapy ◽

Tendon Tear ◽

Extracorporeal Shock Wave ◽

Group I ◽

Group Ii

Abstract Background To compare the clinical efficacy of platelet rich plasma (PRP) subacromial injection and extracorporeal shock wave therapy (ESWT) on refractory non-calcific partial thickness supraspinatous tendon tear. Results Significant improvement in all outcome measures achieved in both groups at 4 weeks follow-up period (the end of treatment course) (P< 0.05). At 12 weeks follow-up period, group I, showed significant improvement in all outcome measures compared to baseline and group II; however, in group II, there was no significant difference compared to baseline; moreover, deterioration in the previous improvement was noticed. Conclusion Both PRP (group I) and ESWT (group II) are effective therapeutic methods in the management of refractory non-calcific partial thickness supraspinatous tendon tear; however, PRP (group I) has better long-term effects on both pain and function.

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Effects of intralesional platelet-rich plasma in the patients with lateral epicondylitis of elbow

Bangabandhu Sheikh Mujib Medical University Journal ◽

10.3329/bsmmuj.v12i3.43326 ◽

2019 ◽

Vol 12 (3) ◽

pp. 138-141

Author(s):

Mohammad Tariqul Islam ◽

M. A. Shakoor ◽

Afsana Mahjabin ◽

Md. Ali Emran

Keyword(s):

Visual Analogue Scale ◽

Daily Living ◽

Analogue Scale ◽

Tennis Elbow ◽

Platelet Rich Plasma ◽

Lateral Epicondylitis ◽

Activity Of Daily Living ◽

Evaluation Tool ◽

Plasma Injection ◽

The Difference

Lateral epicondylitis (tennis elbow) is a major cause of musculoskeletal pain involving common extensor origin of the forearm. This study was done to determine the effects of platelet-rich plasma on 15 patients with lateral epicondylitis. Selected patients were given intralesional platelet-rich plasma injection, activity of daily living instructions and paracetamol. Patients were assessed every 14 days interval by visual analogue scale, and the patient rated tennis elbow evaluation. Treatment response according to visual analogue scale and patient rated tennis elbow evaluation tool, the difference of improvement was found in respect to time, from pretreatment W1 (just before 1st Intervention) score to W11 score in every alternate week (p<0.005). This indicates that intralesional platelet-rich plasma is effective in the patients with lateral epicondylitis of elbow.

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First clinical experience with a new injectable recombinant human collagen scaffold combined with autologous platelet-rich plasma for the treatment of lateral epicondylar tendinopathy (tennis elbow)

Journal of Shoulder and Elbow Surgery ◽

10.1016/j.jse.2018.09.007 ◽

2019 ◽

Vol 28 (3) ◽

pp. 503-509 ◽

Cited By ~ 9

Author(s):

Uri Farkash ◽

Erez Avisar ◽

Ido Volk ◽

Omer Slevin ◽

Noam Shohat ◽

...

Keyword(s):

Clinical Experience ◽

Tennis Elbow ◽

Platelet Rich Plasma ◽

Collagen Scaffold ◽

Human Collagen ◽

Autologous Platelet Rich Plasma ◽

Autologous Platelet

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The Role of Factor XI in a Dilute Thromboplastin Assay of Extrinsic Coagulation Pathway

Thrombosis and Haemostasis ◽

10.1055/s-0037-1615963 ◽

2001 ◽

Vol 85 (06) ◽

pp. 1055-1059 ◽

Cited By ~ 17

Author(s):

Shilong Xiong ◽

Xiaofan He ◽

Fayi Liu ◽

Jianzhong Han ◽

Juncheng Li ◽

...

Keyword(s):

Blood Coagulation ◽

Platelet Rich Plasma ◽

Critical Role ◽

Extrinsic Pathway ◽

Thrombin Inhibition ◽

Normal Plasma ◽

Low Concentrations ◽

Plasma Depletion ◽

Coagulation Pathway

SummaryBlood coagulation has been thought to be composed of both intrinsic and extrinsic pathways. Recent evidence strongly supports the critical role of the extrinsic pathway in the initiation of blood coagulation. This investigation established an assay that examines the role of FXI in the thromboplastin-initiated (extrinsic) coagulation based on this new concept. Plasma clotting times were measured at different concentrations of thromboplastin with activated FXII inhibited (FXIIa-inhibited Diluted Thromboplastin Time, FXIIaiDTT). Only at low concentrations of thromboplastin was FXIIaiDTT of FXI-deficient plasma significantly prolonged than that of normal plasma. Depletion of FXI from normal plasma prolonged its FXIIaiDTT and replenishment of FXI shortened it. FXIIaiDTTs of both FVIII-deficient and FIX-deficient plasma were remarkably prolonged, and addition of normal plasma dose-dependently shortened it. Furthermore, earlier α-thrombin inhibition was directly correlated with decreasing FXa generation. The amount of FXa production was: platelet-rich plasma > platelet-poor plasma > FXI-deficient plasma. Therefore, our findings from the FXIIaiDTT assays not only support the critical role of extrinsic pathway in blood coagulation initiation, but also demonstrate the importance of FXI as an amplifier of thrombin generation in thromboplastin-initiated coagulation.

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