The effect of adenine nucleotides on thrombus formation, platelet count, and blood coagulation

Mustard, J. F.; Rowsell, H. C.; Lotz, Fernanda N.; Hegardt, B.; Murphy, Edmond A.

doi:10.1016/0014-4800(66)90004-9

Cited by 28 publications

(12 citation statements)

References 19 publications

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“…2, it can bc seen by comparison of the slopes of the two curves that the survival pattern of platelets in a pig after an injection of thrombin differs little from that in another pig given an injection of saline. In six such experiments the half-life values for the control animals and animals given thrombin were similar (Robinson, Mustard and Rowsell, 1965). This evidence suggests that a single injection of thrombin leading to revcrsible platelet aggregates does not produce any marked shortening of platelet survival.…”

Section: Reversiuility Of Platelet Aggregationmentioning

confidence: 93%

Platelet Economy (Platelet Survival and Turnover)*

1966

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Investigators studying blood platelet survival and turnover have used the term ‘thrombo‐kinetics’ to describe the subject, by analogy with the usages of thermodynamics. Inasmuch as these phenomena reflect the interactions and hazards which the platelets encounter while discharging their function in the circulation, we prefer the term ‘platelet economy’ and we consider that the function and fate of the platelet cannot usefully be separated as objects of study. A number of beliefs about platelet function and economy are widely held. First, the platelets play a leading role in haemostasis, a function which is discharged mainly when injury to the vessel wall occurs; their second main function is considered to be in coagulation, which they support or may even initiate. Beyond these, the platelets are thought to have little useful function. The platelet in vivo is commonly supposed to be a fragile structure, irreversibly damaged by aggregation. Some consider it to have a finite life span, determined by exhaustion of its inner reserves, while others consider its life span to be determined by the demands of the body without regard to the age of the individual platelet. We shall present evidence suggesting that some of these views are gross over‐simplifications and some are erroneous.

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Section: Reversiuility Of Platelet Aggregationmentioning

confidence: 93%

Platelet Economy (Platelet Survival and Turnover)*

1966

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“…One of the characteristics of platelet aggregates induced by ADP is that they break up rather quickly in vivo and the platelets return to the circulation and survive for a normal length of time (Born and Cross, 1963b;Davey and Lander, 1964;Mustard et al, 1966). A thrombus which is largely composed of ADPinduced platelet clumps adherent to the vessel wall can be expected to undergo dissolution, particularly if it is exposed to the shearing effect of flowing blood .…”

Section: Platelets and Blood Coagulationmentioning

confidence: 99%

Platelets, Thrombosis and Drugs

Mustard

Packham

1975

Drugs

113

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The development of thrombosis involves 4 main factors: the vessel wall, the formed elements of the blood, blood coagulation, and blood flow. In venous thrombosis, however, the major part in both the initiation and growth of thrombi is played by the platelets. In selecting drugs which inhibit platelet function it is helful to know which of the platelet reactions that contribute to thrombus formation can be inhibited by various agents. Platelets adhere to the damaged vessel wall, collagen being probably the most important constituent involved. They are then stimulated to release the contents of their storage granules. Release-inducing agents promote the discharge of adenosine diphosphate (ADP) which causes platelets in the vicinity to swell to a more spherical shape, extend pseudopods and adhere to each other. Platelet aggregation is reversible, and a number of drugs have been shown to be capable of inhibiting platelet function at various stages, both in vitro and in vivo. Adrenaline, noradrenaline, oestrogens and nicotine enhance aggregation. Drugs which inhibit platelet function include the non-steroidal anti-inflammatory drugs, the pyrimido-pyrimidines (e.g. dipyridamole), hydroxychloroquine, clofibrate, and dextran. In this review the effects of drugs which inhibit platelet function are outlined and the extent to which they can be used to influence the course of thromboembolic disease in man is discussed. It is suggested that combination of anti-platelet drugs with anticoagulants could prove clinically useful.

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“…Such Ag-Ab complexes and aggregated or altered IgG and IgM immunoglobulins then promote platelet aggregation and platelet release reaction (Miieller-Eckhardt and Liiseher, 1968), which results in liberation of ADP, platelet factor 3 (Castaldi, Larrieu and Caen, 1965) and platelet factor 4 (Niewiarowski and Thomas, 1969), which stimulate intravascular coagulation. ADI ~ is also known to activate factor XII (Mustard et al, 1966) and thus initiates the coagulation process. Ag-Ab complexes cause direct damage to vascular endothelium and liberate permeability factors (Mustard et al, 1965) and expose collagen and subendothelial elements which are responsible for aggregation and adhesion of circulating platelets (Baumgartner and Haudenschild, 1972) as well as for activation of factor XII (Niewiarowski, Bankowski and Fiedoruk, 1964).…”

Section: Discussionmentioning

confidence: 99%

Blood coagulation and immunological changes associated with frostbite at high altitude

Chohan

Singh²,

Balakrishnan³

1975

Int J Biometeorol

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A B S T R A C T . -In 15 c a s e s of f r o s t b i t e among s o l d i e r s stationed between 3690 and 5540 m altitude in the H i m a l a y a s i n v e s t i g a t i o n s of blood coagulation and i m m u n oglobulins w e r e c a r r i e d out within 24 hours, after 4 weeks and one y e a r . In f r o s tbite e v i d e n c e s of i n t r a v a s c u l a r coagulation w e r e the p r e s e n c e of i n c r e a s e d a m o u n t s of F D P s in s e r u m , reduction of p l a s m a fibrinogen, fall in platelet counts and h a e m a t o c r i t , i n c r e a s e d platelet a d h e s i v e n e s s , and prolonged euglobulin lysis time. Marked lowering of a n t i t h r o m b i n III and p r o t e a s e i n h i b i t o r s a -1 a n t i t r y p s i n and a2 m a c r o g l o b u l i n indicate t h e i r i n c r e a s e d c o n s u m p t i o n in the pathological process. I n c r e a s e d i m m u n o l g l o b u l i n s with r e l a t i v e d e c r e a s e of a l b u m i n and the a p p e a r a n c e of cryoglobulins in the f o r m of IgG, IgA and IgM complexes, also s e e m to p r omote platelet a g g r e g a t i o n and r e l e a s e r e a c t i o n . Anticoagulant t h e r a p y combined with a n t i p l a t e l e t adhesive drugs, if instituted in the e a r l y stages of f r o s t b i t e might be s u c c e s s f u l in p r e v e n t i n g d a m a g e r e s u l t i n g f r o m i n t r a v a s c u l a r coagulation.

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The effect of adenine nucleotides on thrombus formation, platelet count, and blood coagulation

Cited by 28 publications

References 19 publications

Platelet Economy (Platelet Survival and Turnover)*

Platelet Economy (Platelet Survival and Turnover)*

Platelets, Thrombosis and Drugs

Blood coagulation and immunological changes associated with frostbite at high altitude

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