Platelet function and microvesicle generation in patients with hemophilia A

Melero-Amor, Antonia; Romecín, Paola; Iyú, David; García‐Bernal, David; García-Navaro, Esther; Moraleda, José Marı́a; Garcı́a-Estañ, Joaquı́n; García-Candel, Faustino; Atucha, Noemı́ M.

doi:10.1002/ccr3.3788

Cited by 1 publication

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“…Thus, it would be interesting to perform other studies for instance, in whole blood, to study platelet function aggregation by means of light optical aggregometry, platelet-related primary hemostasis function using the PFA-100 System or the Multiplate Analyzer System. Also, the use of intravital microscopy to study platelet aggregation in vivo may be another useful technique to apply in order to circumvent the problems related to in vitro techniques [ 24 ].…”

Section: Discussionmentioning

confidence: 99%

Role of Nitric Oxide in the Altered Calcium Homeostasis of Platelets from Rats with Biliary Cirrhosis

Aghdam

Romecín

Garcı́a-Estañ

et al. 2023

IJMS

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Introduction: Previously, we found that intracellular calcium (Ca2+) homeostasis is altered in platelets from an experimental model of liver cirrhosis, namely the bile-duct-ligated (BDL) rat. These alterations are compatible with the existence of a hypercoagulable state. Objective: In the present study, we analyzed the role of nitric oxide in the abnormal calcium signaling responses of an experimental cirrhosis model, the bile duct-ligated rat. Methods: Chronic treatment with L-NAME was used to inhibit NO production in a group of control and BDL animals, and the responses compared to those obtained in a control and BDL untreated group (n = 6 each). The experiments were conducted on isolated platelets loaded with fura-2, using fluorescence spectrometry. Results: Chronic treatment with L-NAME increased thrombin-induced Ca2+ release from internal stores in both control and BDL rats. However, the effect was significantly greater in the BDL rats (p < 0.05). Thrombin-induced calcium entry from the extracellular space was also elevated but at lower doses and, similarly in both control and BDL platelets, treated with the NO synthesis inhibitor. Capacitative calcium entry was also enhanced in the control platelets but not in platelets from BDL rats treated with L-NAME. Total calcium in intracellular stores was elevated in untreated platelets from BDL rats, and L-NAME pretreatment significantly (p < 0.05) elevated these values both in controls and in BDL but significantly more in the BDL rats (p < 0.05). Conclusions: Our results suggest that nitric oxide plays a role in the abnormal calcium signaling responses observed in platelets from BDL rats by interfering with the mechanism that releases calcium from the internal stores.

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Section: Discussionmentioning

confidence: 99%