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Hydrogen sulfide (H2S), a gasotransmitter, plays a variety of roles in the mammalian body including the cardiovascular system. Given evidence that H2S donors including NaHS inhibit human platelet aggregation, we examined and characterized the effects of NaHS on rabbit platelet aggregation and cytosolic Ca(2+) mobilization. Rabbit platelet aggregation was determined in platelet-rich plasma (PRP) and washed platelets. Intracellular Ca(2+) levels were monitored in Fura2-loaded washed platelets. NaHS prevented rabbit platelet aggregation induced by collagen or ADP, and the effective concentration range of NaHS was 0.1-0.3 mM in PRP and 1-3 mM in washed platelets. In washed platelets, NaHS attenuated cytosolic Ca(2+) mobilization induced by collagen or ADP and also reduced platelet aggregation induced by ionomycin, a Ca(2+) ionophore. The anti-platelet effect of NaHS was blocked by an adenylyl cyclase inhibitor and enhanced by a phosphodiesterase inhibitor. H2S thus suppresses rabbit platelet aggregation by interfering with both upstream and downstream signals of cytosolic Ca(2+) mobilization in a cAMP-dependent manner.
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http://dx.doi.org/10.1248/bpb.b13-00018 | DOI Listing |
J Pediatr Hematol Oncol
September 2025
Children's Hospital of Michigan, Division of Hematology/Oncology.
Glanzmann thrombasthenia (GT) is a rare autosomal recessive platelet disorder characterized by abnormalities in platelet aggregation, resulting from quantitative or qualitative defects in integrins αIIb and β3. Currently, allogeneic hematopoietic stem cell transplantation (allo-HSCT) is the only potentially curative therapeutic approach for severe GT. In this report, we present 2 children with GT that underwent successful allo-HSCT, along with 2008 to 2022 data from the Center for International Blood and Marrow Transplant Research and a summary of the existing literature providing further evidence that allo-HSCT can be a curative approach that prevents severe and life-threatening bleeding in GT.
View Article and Find Full Text PDFCrit Care Explor
September 2025
Interdepartmental Division of Critical Care Medicine, University of Toronto, Toronto, ON, Canada.
Objective: Vitamin C has been linked to alterations in platelet count and aggregation behavior. Given recent findings suggesting an association between vitamin C and adverse outcomes in patients with septic shock, we aimed to investigate whether vitamin C influences mortality in septic patients through its impact on platelets.
Design: Post hoc analysis of the Lessening Organ Dysfunction With Vitamin C (LOVIT) randomized trial (clinicaltrials.
Vasc Health Risk Manag
September 2025
Department of Functional Diagnostics and Physical Medicine, Pomeranian Medical University in Szczecin, Szczecin, 71-210, Poland.
The vascular endothelium is responsible for regulating vascular tone, maintaining fluid homeo-stasis, and preventing platelet aggregation, exhibits regulatory properties in vasorelaxation and vasoconstriction - it produces, among others, nitric oxide and endothelin. The imbalance of vasoactive molecules leads to the loss of their function, known as endothelial dysfunction. Impaired endothelial function is observed in people with metabolic disorders, often preceding the onset of the disease by several years.
View Article and Find Full Text PDFArterial thrombosis is a multifaceted process characterized by platelet aggregation and fibrin deposition, leading to the occlusion of blood vessels. It plays a central role in cardiovascular conditions such as myocardial infarction and ischemic stroke. Gaining insight into the mechanisms underlying arterial thrombosis is essential for developing effective treatments aimed at preventing thrombotic events and reducing associated health burdens.
View Article and Find Full Text PDFJ Thromb Thrombolysis
September 2025
Central Laboratory of Yongchuan Hospital, Chongqing Medical University, No. 439, Xuanhua Road, Yongchuan District, Chongqing, 402160, China.
In vitro assessment of the inhibitory effect of antiplatelet drugs on platelet aggregation is frequently employed to guide personalized antiplatelet therapy in clinical practice. However, existing methods for detecting platelet aggregation rely heavily on high concentrations of exogenous agonists, which may obscure part of the inhibitory effect of antiplatelet drugs and lead to an underestimation of their effects. This study validates a novel analytical strategy for evaluating the effects of antiplatelet drugs by quantifying the microscopic three-dimensional morphological parameters of platelet aggregates formed through spontaneous aggregation on a glass surface.
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