Superoxide anions enhance platelet adhesion and aggregation

Salvemini, Daniela; Nucci, Gilberto De; Sneddon, J. M.; Vane, John R.

doi:10.1111/j.1476-5381.1989.tb12572.x

Cited by 129 publications

(76 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…19,21,25,26 In the present investigation in stirred whole blood, fMLP-activated leukocytes increased platelet P-selectin expression, and this was inhibited by blockade of PAF receptors by SR27417 and O 2 Ϫ scavenging by SOD, suggesting the involvement of PAF and O 2 Ϫ . Blockade of 5-lipoxygenase by either the 5-lipoxygenase inhibitor Zileuton or the FLAP inhibitor MK-886 inhibited fMLP-induced platelet activation.…”

Section: Discussionmentioning

confidence: 83%

Platelet-Leukocyte Cross Talk in Whole Blood

Lindqvist

et al. 2000

ATVB

191

145

View full text Add to dashboard Cite

Abstract-Thrombosis and inflammation involve complex platelet-leukocyte interaction, the details of which are not fully elucidated. Therefore, we investigated cross talk between platelets and leukocytes in whole blood, under the following physiological conditions: at 37°C, with normal calcium concentrations, and with shear force. Platelet P-selectin and leukocyte CD11b expression were used to monitor platelet and leukocyte activation, respectively, and platelet-leukocyte aggregation (PLA) was analyzed. The leukocyte-specific agonist N-formyl-methionyl-leucyl-phenylalanine (10 Ϫ6 mol/L) increased P-selectin-positive platelets from 2.5Ϯ0.1% to 5.1Ϯ0.6% (PϽ0.05). The increase was inhibited by either the platelet-activating factor (PAF) antagonist SR27417, the superoxide anion scavenger superoxide dismutase, the 5-lipoxygenase inhibitor Zileuton, or the 5-lipoxygenase-activating protein inhibitor MK-886, suggesting the involvement of PAF, superoxide anion, and 5-lipoxygenase products in leukocyte-induced platelet activation. The platelet-specific agonist collagen (1 g/mL) increased leukocyte CD11b expression from 2.

show abstract

Section: Discussionmentioning

confidence: 83%

Platelet-Leukocyte Cross Talk in Whole Blood

Lindqvist

et al. 2000

ATVB

191

145

View full text Add to dashboard Cite

show abstract

“…It was reported that H 2 O 2 and a superoxide radical increased the rate of ADP and collageninduced platelet aggregation. 16,17 Free radicals modify membrane organization and Ca 2+ homeostasis of platelets. Lipid peroxidation results in formation of TxA 2 , hydrolysis of diacylglycerol and inhibition of membrane-bounded enzymes.…”

Section: Discussionmentioning

confidence: 99%

“…Lipid peroxidation results in formation of TxA 2 , hydrolysis of diacylglycerol and inhibition of membrane-bounded enzymes. 16,18 On the other hand, free radicals inhibit PGI 2 synthetase and TxA 2 /PGI 2 imbalance occurs. 16 In our previous study, we found lower superoxide dismutase (SOD) and catalase (CAT) enzyme activities in the patients with spinal injury within the ®rst year.…”

Section: Discussionmentioning

confidence: 99%

“…16,18 On the other hand, free radicals inhibit PGI 2 synthetase and TxA 2 /PGI 2 imbalance occurs. 16 In our previous study, we found lower superoxide dismutase (SOD) and catalase (CAT) enzyme activities in the patients with spinal injury within the ®rst year. 19 It is known that antioxidants play an essential role in the regulation of platelet functions.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Platelet aggregation in traumatic spinal cord injury

et al. 1999

View full text Add to dashboard Cite

Study design: Collagen-induced platelet aggregation and platelet count of ten paraplegic patients (four females, six males, aged 16 ± 42 years) with traumatic spinal cord injury (SCI) (posttraumatic 12 ± 48 weeks) and of ten age-matched healthy volunteers (control group; ®ve females, ®ve males, aged 18 ± 37 years) were investigated. Objectives: Investigation of platelet aggregation in the whole blood of the patients with SCI. Setting: Ankara/Turkey. Methods: Platelet aggregation was evaluated by impedance technique using Chrono Log Model 560 WB aggregometer in whole blood. Platelet count was determined by Medonic Cell Analyser 610. Results: Maximal intensity of collagen-induced platelet aggregation of the patients was 18.50+8.28 ohm (mean+SD) and of the controls was 7.60+4.25 ohm. Maximal rate of collagen-induced aggregation of platelets from the patients was 3.98+1.59 ohm/min, maximal rate of aggregation of platelets from the controls was 1.57+1.01 ohm/min. Platelet counts of the patients and controls were 290 500+50 357/mm 3 and 273 000+48 343/mm 3 respectively. It was determined that both maximal rate (P50.001) and maximal intensity (P50.01) of collagen-induced platelet aggregation of the patients were signi®cantly higher than those of the controls. There was no signi®cant di erence between the two groups in respect to platelet counts. Conclusion: Collagen-induced platelet aggregation of patients with traumatic SCI 12 ± 48 weeks after the trauma was signi®cantly higher than that of the controls. Our results indicate that increased tendency of platelet aggregation, which is probably induced by free radicals, may have a great impact on the late thromboembolic complications reported in patients with traumatic SCI.

show abstract

“…Most of these factors are also modulators of endothelial cell function (Harlan, 1987). One of the most likely factors would be superoxide anions derived from PMNs, since Salvemini et al (1989) have shown that oxygen radicals enhance platelet adhesion to gelatin-coated plastic and aggregation induced by thrombin, in a process that is inhibited by superoxide dismutase (SOD). However, preliminary experiments have shown that SOD at a high concentration only slightly inhibited the platelet adhesion to endothelial cells (Hirafuji & Shinoda, 1990), suggesting the involvement of other mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Platelet‐leukocyte interaction in adhesion to endothelial cells induced by platelet‐activating factor in vitro

Hirafuji

Satoh

1991

British J Pharmacology

View full text Add to dashboard Cite

1 Platelet-activating factor (PAF, 10 nM) did not induce platelet adhesion to endothelial cells cultured in monolayer but it induced their adhesion to protein-coated plastic. However, PAF induced a marked platelet adhesion to endothelial cells when polymorphonuclear leukocytes (PMNs) were present. Lyso-PAF had no effect. 2 Phase-contrast microscopic examination showed that single platelets rather than their aggregates adhered to the endothelial cell surface around aggregating and adhering PMNs. 3 Significant platelet adhesion was induced by PAF at concentrations higher than 0.01 nm with the maximal response at 10nm. Platelet adhesion occurred within minutes after PAF addition, reaching a maximum approximately after 30 min. Platelet adhesion also occurred significantly at a PMN : platelet ratio of 1: 800, and linearly up to 1: 50. 4 The PAF-induced platelet adhesion was suppressed by three structurally unrelated PAF antagonists, WEB 2086, ONO 6240 and BN 52021, in a concentration-dependent manner. 5 PAF also increased PMN adhesion to endothelial cell monolayers, which was further augmented by the presence of platelets. 6 The present study demonstrates that PAF induces platelet adhesion to endothelial cells in vitro when PMNs are present and that there is a close interaction between platelets and PMNs in their adhesion to endothelial cells. The present study further suggests that PMNs could play a central role in platelet adhesion to vascular endothlium in certain pathological conditions.

show abstract

Superoxide anions enhance platelet adhesion and aggregation

Cited by 129 publications

References 28 publications

Platelet-Leukocyte Cross Talk in Whole Blood

Platelet-Leukocyte Cross Talk in Whole Blood

Platelet aggregation in traumatic spinal cord injury

Platelet‐leukocyte interaction in adhesion to endothelial cells induced by platelet‐activating factor in vitro

Contact Info

Product

Resources

About