Application of light-scattering theory to the optical effects associated with the morphology of blood platelets

Lattmer, Paul; Born, G. V. R.; Michal, F

doi:10.1016/0003-9861(77)90019-4

Cited by 93 publications

(42 citation statements)

References 33 publications

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“…In contrast to the results obtained with general photometers (O'Brien, 1962), an initial decrease in transmission was observed with the devices specifically designed for platelet aggregometry by Born (Born et al, 1978;Latimer et al, 1977). It was suggested that this optical effect was caused by the morphological change of platelets from discs to spherical cells with pseudopodia (Latimer et al, 1977).…”

contrasting

confidence: 48%

“…The initial decrease in light transmission was first observed with devices specifically designed for platelet aggregometry by Born (Born et al, 1978;Latimer et al, 1977), in which the angle of light collection is small. Based on theoretical calculations, Latimer (1983) predicted that in a Born-type aggregometer microaggregation leads to a decrease in light transmission.…”

Section: Discussionmentioning

confidence: 99%

“…It was suggested that this optical effect was caused by the morphological change of platelets from discs to spherical cells with pseudopodia (Latimer et al, 1977). Transmission electron microscopy was used to support the interpretation that the initial decrease in light transmission was caused by platelet shape change (Born et al, 1978).…”

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confidence: 99%

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Platelet Aggregation Is Not Initiated by Platelet Shape Change

Maurer‐Spurej

Devine

2001

Laboratory Investigation

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SUMMARY:Because the initial decrease in light transmission in platelet aggregometry is attributed to platelet shape change, it is widely held that platelet shape change is a prerequisite for platelet aggregation. We conducted this study to determine the basis of this initial optical effect in aggregometry. Platelets were activated with ADP, thrombin, or the thrombin receptor agonist peptide SFLLRN (TRAP 1-6 ). In every case the initial decrease in light transmission occurred with the concomitant formation of microaggregates. This was also seen when preactivated platelets, which cannot undergo further morphological changes, were used, and when platelets were activated in the presence of shape-change inhibitors such as cytochalasin D and vincristine. Microscopy analysis of samples fixed at minimum light transmission in the aggregometer, which is generally assumed to signal shape change, always showed the presence of microaggregates. Microaggregation appeared to be distinct from full aggregation, as it was not inhibited by the addition of CD61, an antibody to the ␤ 3 integrin. To model these findings, fibrinogen-coated latex spheres, which cannot change shape, were aggregated with thrombin; the initial decrease in light transmission was still seen, and microaggregates formed at this time. These results indicate that platelet shape change is not a prerequisite for aggregation and that the signal widely believed to represent shape change reflects platelet microaggregation instead. We conclude that platelet aggregation occurs independently of shape change and that shape change is not necessarily followed by aggregation. These observations suggest an alternative role for platelet shape change of single platelets. (Lab Invest 2001, 81:1517-1525.

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contrasting

confidence: 48%

Section: Discussionmentioning

confidence: 99%

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Platelet Aggregation Is Not Initiated by Platelet Shape Change

Maurer‐Spurej

Devine

2001

Laboratory Investigation

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“…This change in forward scatter is compatible with platelet shape change and granule release rather than microvesiculation. 48,49 As described for human platelets, 14,39 thrombin plus collagen stimulation induced PS exposure and microvesiculation in only a subpopulation of the control dog platelets. Some surface exposure of PS was also apparent in a subpopulation of the thrombin plus collagen-treated GSD platelets, in contrast to their lack of PS exposure in response to ionophore.…”

Section: Discussionmentioning

confidence: 94%

A hereditary bleeding disorder of dogs caused by a lack of platelet procoagulant activity

Brooks

Catalfamo

Brown

et al. 2002

Blood

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We have discovered a novel canine hereditary bleeding disorder with the characteristic features of Scott syndrome, a rare defect of platelet procoagulant activity. Affected dogs were from a single, inbred colony and experienced clinical signs of epistaxis, hyphema, intramuscular hematoma, and prolonged bleeding with cutaneous bruising after surgery. The hemostatic abnormalities identified were restricted to tests of platelet procoagulant activity, whereas platelet count, platelet morphology under light microscopy, bleeding time, clot retraction, and platelet aggregation and secretion in response to thrombin, collagen, and adenosine diphosphate stimulation were all within normal limits. Washed platelets from the affected dogs demonstrated approximately twice normal clotting times in a platelet factor 3 availability assay and, in a prothrombinase assay, generated only background levels of thrombin in response to calcium ionophore, thrombin, or combined thrombin plus collagen stimulation. While platelet phospholipid content was normal, flow cytometric analyses revealed diminished phosphatidylserine exposure and a failure of microvesiculation in response to calcium ionophore, thrombin, and collagen stimulation. Pedigree studies indicate a likely homozygous recessive inheritance pattern of the defect. These findings confirm the importance of platelet procoagulant activity for in vivo hemostasis and provide a large animal model for studying agonist-induced signal transduction, calcium mobilization, and effector pathways involved in the late platelet response of transmembrane phospholipid movement and membrane vesiculation. (Blood. 2002; 99:2434-2441)

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“…The results were recorded on a Rikadenki recorder B-361 with a full scale deflection of 50 mV. The reversible shape change of the platelets due to the starting and stopping of the stirrer (Latimer, Born & Michal, 1977) was used to adjust the sensitivity of the aggregometer. Agonists and antagonists were added in a volume of 5 to 15 pl, the antagonist being added 1 min before the agonist.…”

Section: Measurement Of Shape Changementioning

confidence: 99%

Shape Change of Blood Platelets—a Model for Cerebral 5‐hydroxytryptamine Receptors?

Gräf

Pletscher

1979

British J Pharmacology

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In blood platelets of rabbits isolated by a stractan gradient and incubated in a protein‐poor medium, tryptamine, 5‐hydroxytryptamine (5‐HT) and derivatives, quipazine and mescaline caused a shape change. This shape change was inhibited by low concentrations of methysergide. The most potent antagonists of the 5‐HT‐induced shape change included ergoline derivatives and neuroleptic drugs, which showed high stereoselectivity. (‐f)‐Lysergic acid diethylamide ((+)‐LSD), psilocine and some N',N′‐dimethylated tryptamines acted as mixed agonist‐antagonists. The compounds found to be agonists or mixed agonist‐antagonists on platelets have previously been shown to act also as 5‐HT agonists in the central nervous system (CNS). With regard to 5‐HT antagonists, the 5‐HT receptors of platelets reacted differently from those described earlier in brain areas with dense 5‐hydroxytryptaminergic innervation, but showed similarities to 5‐HT receptors investigated previously in spinal cord, cerebral cortex and possibly reticular formation. It is concluded that platelets may be considered with caution as models for some, but not for all, 5‐HT receptors in the CNS.

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Application of light-scattering theory to the optical effects associated with the morphology of blood platelets

Cited by 93 publications

References 33 publications

Platelet Aggregation Is Not Initiated by Platelet Shape Change

Platelet Aggregation Is Not Initiated by Platelet Shape Change

A hereditary bleeding disorder of dogs caused by a lack of platelet procoagulant activity

Shape Change of Blood Platelets—a Model for Cerebral 5‐hydroxytryptamine Receptors?

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