Sodium Bicarbonate

Lookabill, Sara K.; Dulaney, Anna Rouse; Shepherd, Greene; Kerns, William

doi:10.1007/978-3-319-17900-1_169

Cited by 2 publications

(2 citation statements)

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“…Sodium bicarbonate acts as a buffer to preserve physiologic pH and counteract acidity, ultimately influencing metabolic function [ 11 ]. In an aqueous environment sodium bicarbonate dissociates to form sodium (Na + ) and bicarbonate (HCO 3 − ) ions.…”

Section: Discussionmentioning

confidence: 99%

“…Standard purge fluid contains heparin (25–50 U/mL) to directly inhibit thrombin generation and clot formation locally in the purge gaps. While heparin has demonstrated efficacy in reducing purge gap thrombosis and for maintaining purge gap patency, the overall net delivery of heparin to a given patient resulting from purge fluid infusion and exit into the bloodstream may differ due to device variation in the purge gaps [ 11 ]. Concurrently with device use, systemic heparin administration is also required to achieve systemic anticoagulation, e.g.…”

Section: Introductionmentioning

confidence: 99%

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Sodium bicarbonate as a local adjunctive agent for limiting platelet activation, aggregation, and adhesion within cardiovascular therapeutic devices

Ammann

Outridge

Roka‐Moiia

et al. 2023

J Thromb Thrombolysis

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Cardiovascular therapeutic devices (CTDs) remain limited by thrombotic adverse events. Current antithrombotic agents limit thrombosis partially, often adding to bleeding. The Impella® blood pump utilizes heparin in 5% dextrose (D5W) as an internal purge to limit thrombosis. While effective, exogenous heparin often complicates overall anticoagulation management, increasing bleeding tendency. Recent clinical studies suggest sodium bicarbonate (bicarb) may be an effective alternative to heparin for local anti-thrombosis. We examined the effect of sodium bicarbonate on human platelet morphology and function to better understand its translational utility. Human platelets were incubated (60:40) with D5W + 25 mEq/L, 50 mEq/L, or 100 mEq/L sodium bicarbonate versus D5W or D5W + Heparin 50 U/mL as controls. pH of platelet-bicarbonate solutions mixtures was measured. Platelet morphology was examined via transmission electron microscopy; activation assessed via P-selectin expression, phosphatidylserine exposure and thrombin generation; and aggregation with TRAP-6, calcium ionophore, ADP and collagen quantified; adhesion to glass measured via fluorescence microscopy. Sodium bicarbonate did not alter platelet morphology but did significantly inhibit activation, aggregation, and adhesion. Phosphatidylserine exposure and thrombin generation were both reduced in a concentration-dependent manner—between 26.6 ± 8.2% (p = 0.01) and 70.7 ± 5.6% (p < 0.0001); and 14.0 ± 6.2% (p = 0.15) and 41.7 ± 6.8% (p = 0.03), respectively, compared to D5W control. Platelet aggregation via all agonists was also reduced, particularly at higher concentrations of bicarb. Platelet adhesion to glass was similarly reduced, between 0.04 ± 0.03% (p = 0.61) and 0.11 ± 0.04% (p = 0.05). Sodium bicarbonate has direct, local, dose-dependent effects limiting platelet activation and adhesion. Our results highlight the potential utility of sodium bicarbonate as a locally acting agent to limit device thrombosis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%