Preventing Age and Pathological Thrombosis Using Hydrogen Rich Water

Conjecture:. H2S inhibits pathologic platelet activation, adhesion and clots.

Molecular hydrogen has a similar effect as an antioxidant modifier.

H2S is the endogenous gasotransmitter or hydrogen donor.

H2 is the active moiety.

This is analogous to beta hydroxybutyrate the endogenous HDAC inhibitor and starvation gene set gene promoter and Na Butyrate the active moiety that shares the same function in the cell nucleus.

Would molecular hydrogen like H2S prevent clots without increasing bleeding?  Molecular hydrogen reduces oxidative stress without abrogating redox signaling.  It might be a perfect agent for preoperative and postoperative prophylaxis of DVT or adjunctive therapy in DVT.

http://www.sciencedirect.com/science/article/pii/S0014482717303439

Calcium sensing receptor initiating cystathionine-gamma-lyase/hydrogen sulfide pathway to inhibit platelet activation in hyperhomocysteinemia rat

H₂S is involved in protection of ECs and the mediation of anti-thrombotic in HHcy.

Hyperhomocysteinemia (HHcy, high homocysteine) induces the injury of endothelial cells (ECs). Hydrogen sulfide (H₂S) protects ECs and inhibits the activation of platelets. Calcium-sensing receptor (CaSR) regulates the production of endogenous H₂S. However, whether CaSR inhibits the injury of ECs and the activation of platelets by regulating the endogenous cystathionine-gamma-lyase (CSE, a major enzyme that produces H₂S)/H₂S pathway in hyperhomocysteinemia has not been previously investigated. Here, we tested the ultrastructure alterations of ECs and platelets, the changes in the concentration of serum homocysteine and the parameters of blood of hyperhomocysteinemia rats were measured. The aggregation rate and expression of P-selectin of platelets were assessed. Additionally, the expression levels of CaSR and CSE in the aorta of rats were examined by western blotting. The mitochondrial membrane potential and the production of reactive oxygen species (ROS) were measured; the expression of phospho-calmodulin kinases II (p-CaMK II) and Von Willebrand Factor (vWF) of cultured ECs from rat thoracic aortas were measured. We found that the aggregation rate and the expression of P-selectin of platelets increased, and the expression of CaSR and CSE decreased in HHcy rats. In the ECs of HHcy group, the ROS production increased and the mitochondrial membrane potential decreased markedly, the expression of CSE and the p-CaMK II increased after treatment with CaSR agonist while decreased upon administration of U73122 (PLC-specific inhibitor) and 2-APB (IP₃ Receptor inhibitor). CaSR agonist or NaHS significantly reversed the ECs injured and platelet aggregation caused by hyperhomocysteinemia. Our results demonstrate that CaSR regulates the endogenous CSE/H₂S pathway to inhibit the activation of platelets which concerts the protection of ECs in hyperhomocysteinemia.