A Study of Variables Affecting the Quality of Platelets Stored at “Room Temperature”

Kunicki, Thomas J.; Tuccelli, M.; Becker, G. A.; Aster, Richard H.

doi:10.1046/j.1537-2995.1975.15576082215.x

Cited by 339 publications

(151 citation statements)

References 11 publications

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“…Cell counts for leukocytes and platelets were performed with an Advia 2120 hematology counter, with special software for counting animal blood samples (Siemens Medical Solutions Diagnostics). The Kunicki morphology score, 23 as well as the aggregation response to adenosine diphosphate (ADP) and to the combination of ADP and collagen, was measured as described. 24 The percentage of platelets positive for annexin V was determined as described earlier.…”

Section: Storage-related Biochemical Changes In Rat Plateletsmentioning

confidence: 99%

Supernatant of stored platelets causes lung inflammation and coagulopathy in a novel in vivo transfusion model

Vlaar

Hofstra

Kulik³

et al. 2010

Blood

100

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Transfusion-related acute lung injury is suggested to be a "2-hit" event resulting from priming and activation of pulmonary neutrophils. Activation may result from infusion of lysophosphatidylcholines (LysoPCs), which accumulate during storage of blood products. In the present study, we developed a syngeneic in vivo transfusion model to test whether storage of platelet concentrates (PLTs) results in lung injury in healthy rats as well as in a "2-hit" model using lipopolysaccharide-pretreated rats. In addition, the effect of washing of platelets was studied. In healthy rats, transfusion of aged PLTs caused mild lung inflammation. In LPS-pretreated rats, transfusion of aged PLTs, but not fresh PLTs, augmented pulmonary and systemic coagulopathy. When PLTs components were transfused separately, supernatant of aged PLTs, but not washed aged platelets, induced pulmonary injury in the "2-hit" model.

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Section: Storage-related Biochemical Changes In Rat Plateletsmentioning

confidence: 99%

Supernatant of stored platelets causes lung inflammation and coagulopathy in a novel in vivo transfusion model

Vlaar

Hofstra

Kulik³

et al. 2010

Blood

100

View full text Add to dashboard Cite

show abstract

“…Morphology score was performed by the method of Kunicki. 15 Hypertonic shock response (HSR) and extent of shape change (ESC) were performed as previously described 16 ; CD62P expression was measured by FITC-labeled CD62P-specific monoclonal antibody S-12 using FACS analysis. Annexin V binding was determined by FACS analysis using fluorescently labeled annexin-V (Vybrant Assay Kit [V-13240]; Molecular Probes, Eugene, OR).…”

Section: Human Platelet Studiesmentioning

confidence: 99%

Galactosylation does not prevent the rapid clearance of long-term, 4°C-stored platelets

Wandall

Hoffmeister

Sørensen

et al. 2008

Blood

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Cold storage of platelets for transfusion is desirable to extend platelet storage times and to prevent bacterial growth. However, the rapid clearance of coldstored platelets prevents their use. A novel method for preventing the rapid clearance of cold-stored platelets has previously been developed in a murine model. Cold storage induces the clustering and recognition of exposed ␤-Nacetylglucosamine (␤GlcNAc) on platelet surfaces. Glycosylation of ␤GlcNAc residues with uridine 5-diphosphogalactose (UDP-galactose) results in the normal survival of short-term (2 h) 0°C-stored murine platelets. Based on this finding, we developed a similar glycosylation process by adding UDP-galactose to human apheresis platelets. A phase 1 clinical trial was conducted transfusing radiolabeled autologous apheresis platelets stored for 48 hours at 4°C with or without pretreatment with UDP-galactose. In contrast to the murine study, galactosylation of human platelets did not prevent the accelerated platelet clearance routinely observed after 4°C storage. We next developed a murine model of platelet storage for 48 hours at 4°C and showed that UDP-galactose treatment of murine platelets also did not prevent their rapid clearance, in agreement with the human platelet study. We conclude that different mechanisms of clearance may exist for short-and long-term cold-stored platelets. (Blood. 2008;111:3249-3256)

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“…A platelet biochemical defect (Caen and Michel, 1972), poor platelet quality (Kunicki et al, 1975), or the presence of inhibitors (Derrick et al, 1998) can reduce or abolish platelet function. Agonist-induced platelet activation is associated with optical effects that can be monitored in a platelet aggregometer (Born, 1962); this method is widely used to assess the functional status of platelets.…”

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confidence: 99%

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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A Study of Variables Affecting the Quality of Platelets Stored at “Room Temperature”

Cited by 339 publications

References 11 publications

Supernatant of stored platelets causes lung inflammation and coagulopathy in a novel in vivo transfusion model

Supernatant of stored platelets causes lung inflammation and coagulopathy in a novel in vivo transfusion model

Galactosylation does not prevent the rapid clearance of long-term, 4°C-stored platelets

Platelet Aggregation Is Not Initiated by Platelet Shape Change

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