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Magnesium sulfate neither potentiates nor inhibits tissue plasminogen activator‐induced thrombolysis
Author(s) -
STEWART D.,
MARDER V. J.,
STARKMAN S.,
SAVER J. L.
Publication year - 2006
Publication title -
journal of thrombosis and haemostasis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.947
H-Index - 178
eISSN - 1538-7836
pISSN - 1538-7933
DOI - 10.1111/j.1538-7836.2006.01999.x
Subject(s) - medicine , tissue plasminogen activator , neuroprotection , thrombolysis , pharmacology , stroke (engine) , clinical trial , plasminogen activator , t plasminogen activator , ischemia , myocardial infarction , mechanical engineering , engineering
Summary. Background: Increasing circulating magnesium concentrations to 2‐fold over normal baseline may afford a neuroprotective effect in patients with acute cerebral ischemia. Objectives: As patients receiving magnesium sulfate (MgSO 4 ) in human clinical trials may also be candidates for subsequent thrombolytic therapy with tissue plasminogen activator (t‐PA), preclinical assessment of possible inhibition or potentiation of fibrinolytic activity by MgSO 4 has important clinical relevance. Methods: We utilized an in vitro system, in which D‐dimer release served as a reflection of t‐PA‐induced clot lysis, to measure the effect of magnesium at the target concentration being tested in human stroke clinical trials, and at 2‐ and 3‐fold higher levels. Clots from normal volunteers were exposed to t‐PA at concentrations that correspond to therapeutic or endogenous plasma t‐PA levels. Results: MgSO 4 had no effect on t‐PA‐induced clot lysis at up to 3‐fold target magnesium concentration (6× normal serum concentration). Conclusions: MgSO 4 concentrations well above the targeted level in therapeutic stroke trials does not affect t‐PA‐induced fibrinolytic activity, and therefore is a suitable agent for trials of combined neuroprotective and thrombolytic therapy in patients with acute ischemic stroke.