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Selenase® In Intensive Care

Protection Against Reperfusion Injury

  • Sepsis
  • Myocardial infarction
  • Ischaemic stroke
  • Transplantation
  • Vascular surgery
  • Plastic/reconstructive surgery
  • Hypovolaemic shock, resuscitation

Tissue Damage Due to Ischaemia/Reperfusion

Selenium Status Correlates With The Extent of Damage

Altekin et al. 2005
Study in 70 patients with myocardial infarction

Grade of damage

cTnT [ng/ml] cTnI [ng/ml] CK-MBm [ng/ml]
low (n=29) 0.1-0.3 0.2-0.5 7.0-10.0
medium (n=14) 0.4-0.8 0.6-1.0 10.0-30.0
high (n=27) > 0.9 > 1.0 > 30

High Selenite Doses Protect Against Ischaemia / Reperfusion Damage

Venardos et al. 2004:
Study in the isolated rat heart (pre-treatment for 5 weeks)

Ischaemic contraction at the end of the ischaemic phase is a measure for the severity of ischaemic damage.

Percentage of cardiac function regained after ischaemic and reperfusion phases.

∗RPP (Rate Pressure Product) = Product of heart rate and blood pressure


Selenase® Protects From ROS

  • Initially
  • During ischaemia
  • During reperfusion

Less damage to

  • blood vessels
  • tissues
  • organs

Dosage recommendation∗:
1000 µg selenium/day, until normal levels have been restored (cf. SIC Study (3): 2000 µg day 1; 1000 µg/day day 2 ­ 14)

∗Further information on dosage and application see national SPC.

1 µmol Se = 78.96 µg Se

Action of Selenite Supplementation In Ischaemia/Reperfusion

For example:

Clinical Chemistry

  • Maintenance of antioxidant capacity (GSH/GSSG-ratio)
  • Increase of expression and activity of ROS degrading selenoenzymes (glutathione peroxidases, thioredoxin reductases)
  • Reduction of
    • Inflammatory markers (e.g. CRP)
    • Ischaemic markers in myocardial infarction (e.g. troponins, CK-MB)
    • Oxidative markers (e.g. malondialdehyde)
    • Redox signals (e.g. NF-kB activation)

Animal Experiments

  • Reduction of the extent of tissue damage
  • Improvement of post-ischaemic mean arterial blood pressure (in myocardial I/R)
  • Reduction of oedema (in cerebral I/R)
Selenium effect in general Selenium effect in detail Selenium level/dose
Selenium supplementation reduces mortality in sepsis patients (3, 15) Sepsis patients: increase of glutathione peroxidase activity; reduction of MDA, NF-kB activity, IL-6, acute renal failure Up to 1000 μg/day (2000 μg on day 1 only) up to 14 days i.v. as sodium selenite. Med Klin 1997, Crit Care Med 2007
Selenium supplementation increases ischaemic tolerance in neonatal hearts (7) In hearts of immature rat foetuses: increase of ischaemic tolerance, reduction of lipofuscin pigments and serum NO concentration Oral pre-treatment of pregnant rats: 2000 μg/kg drinking water vs. 237 μg/kg feed Chin Med J 2000
Selenium levels correlate with the extent of myocardial damage (2) In 70 patients with myocardial infarction: low selenium levels correlate with: inflammatory markers: CRP↑, prognosis markers: CK-MB↑, cardiac troponins↑ 107 μg/l vs. 68 μg/l (median) (= 1.36 μmol/l vs. 0.86 μmol/l) J Trace Elem Med Biol 2005
Selenium supplementation increases antioxidant capacity and reduces cardiac damage (12) In isolated rat hearts:dose dependent im­ provement of heart function, less reduc­tion of GSH (vs. GSSG), reduction of increase in MDA as well as reduction of increased NF-kB values, reduced cardiac damage due to xanthine oxidase, •OH or Ca2+. Selenium administration 10 min. before ischaemia and during 30 min. of reperfusion­. Up to 78.7 μg/l selenium in perfu­sion medium. Antioxid Redox Signal 2005
Pre-ischaemic selenium status is the deciding factor for outcome (9) In Wistar rats:high dose selenium diet: reduced extent of infarction, maintains postischaemic GSH/GSSG ratio; increases GPx activity; improves postischaemic average arterial blood pressure 1500 μg vs 50 μg Se/kg feed during 10 weeks Antioxid Redox Signal 2004
Sufficiently high doses of selenium increase tolerance of ischaemia and reperfusion (13) In isolated rat hearts:increase of expression­ of thioredoxin reductases (Txrd-1, Txrd-2) and glutathione peroxidases (GPx-1, GPx-2), increase of I/R tolerance Oral pre-treatment over 5 weeks: 1000 μg/kg vs. 240 μg/kg [sodium selenite/feed] Mol Cell Biochem 2005
Selenium supplementation before I/R increases the antioxidant capacity of the myocardium In 23/23 patients with acleistocardia or a defect of the interventricular septum:no significant increase of Se blood levels but higher myocardial Se concentration and GPx-mRNA expression and activity, as well as lower MDA concentration 400 μg selenium over 7 days pre heart surgery Zhonghua Y; Xul Za Zhi 1999 Chin Med J 2000
Sufficiently high selenium doses protect against cerebral cell death due to Ischaemia/ Reperfusion (14) In Wistar rats:positive effect on: ATP levels, intracellular Ca2+, heat shock protein 70, caspase-3 activity; less oedema and cell separation with minimal microglial cell infiltration. i.p. pre-treatment over 7 days: up to 100 μg/kg body weight as sodium selenite Brain Res 2007
Se-supplementation protects against neurodegeneration in cerebral ischaemia (4) In rats:protection against neuronal lipidperoxidation Pre-treatment over 7 days up to 200 μg/kg body weight as sodium selenite Biol Trace Elem Res 2004
Selenite as a possible therapy to reduce peroxynitrite forma­tion from NO in vascular surgery (1) Theoretical observations on data of 40 patients with aortic aneurysm and peripheral arterial occlusive disease. Med Klin 1997
Selenite supplementation of the perfusion solution protects transplanted kidneys against oxidative damage (11) Animal model: Non-heart-beating donor: malondialdehyde concentration in venous blood of donor kidneys is significantly reduced Selenium supplementation over 120 minutes after organ donation Transplant Proc 2003

Literature on Reactive Oxygen Species in Intensive Care Medicine

A redox imbalance occurs during sepsis. Supplementation of antioxidant vitamins and enzymes can maintain the redox balance.
Bayir H: Reactive oxygen species. Crit Care Med 2005 Vol 33, No.12 (Suppl.)


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  2. Altekin E, Coker C, Sisman AR, Onvural B, Kuralay F, Kirimli O: The relationship between trace elements and cardiac markers in acute coronary syndromes. J Trace Elem Med Biol. 2005;18(3):235-42.
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  9. Tanguy S, Morel S, Berthonneche C, Toufektsian MC, de Lorgeril M, Ducros V, Tosaki A, de Leiris J, Boucher F: Preischemic selenium status as a major determinant of myocardial infarct size in vivo in rats. Antioxid Redox Signal. 2004 Aug;6(4):792-6.
  10. Treska V, Kuntscher V, Molácek J, Kobr J, Racek J, Trefil L: Can ischemia-reperfusion syndrome in transplanted kidneys procured from non-heart-beating donors be influenced by adding selenium into the reperfusion solution? An experimental study. Transplant Proc. 2003 Dec;35(8):3125-7.
  11. Treska V, Kuntscher V, Molácek J, Kobr J, Racek J, Trefil L: Can ischemiareperfusion syndrome in transplanted kidneys procured from non-heart-beating donors be influenced by adding selenium into the reperfusion solution? An experimental study. Transplant Proc. 2003 Jun;35(4):1584-6.
  12. Turan B, Saini HK, Zhang M, Prajapati D, Elimban V, Dhalla NS: Selenium improves cardiac function by attenuating the activation of NF-kappaB due to ischemia-reperfusion injury. Antioxid Redox Signal. 2005 Sep-Oct;7(9-10):1388-97.
  13. Venardos K, Harrison G, Headrick J, Perkins A: Effects of dietary selenim on glutathione peroxidase and thioredoxin reductase activity and recovery from cardiac ischemia-reperfusion. J of Trace Elem in Med and Bio 18 (2004) 81-88.
  14. Yousuf S, Atif F, Ahmad M, Hoda MN, Khan MB, Ishrat T, Islam F: Selenium plays a modulatory role against cerebral ischemia-induced neuronal damage in rat hippocampus. Brain Res. 2007 May 25;1147:218-25. Epub 2007 Feb 17.
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