Benjamin D Kläsner

Technische Universität München, München, Bavaria, Germany

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Publications (5)19.2 Total impact

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    ABSTRACT: Stroke is the third most common cause of death in industrialized countries. The main therapeutic target is the ischemic penumbra, potentially salvageable brain tissue that dies within the first few hours after blood flow cessation. Hence, strategies to keep the penumbra alive until reperfusion occurs are needed. To study the effect of inhaled nitric oxide on cerebral vessels and cerebral perfusion under physiological conditions and in different models of cerebral ischemia. This experimental study demonstrates that inhaled nitric oxide (applied in 30% oxygen/70% air mixture) leads to the formation of nitric oxide carriers in blood that distribute throughout the body. This was ascertained by in vivo microscopy in adult mice. Although under normal conditions inhaled nitric oxide does not affect cerebral blood flow, after experimental cerebral ischemia induced by transient middle cerebral artery occlusion it selectively dilates arterioles in the ischemic penumbra, thereby increasing collateral blood flow and significantly reducing ischemic brain damage. This translates into significantly improved neurological outcome. These findings were validated in independent laboratories using two different mouse models of cerebral ischemia and in a clinically relevant large animal model of stroke. Inhaled nitric oxide thus may provide a completely novel strategy to improve penumbral blood flow and neuronal survival in stroke or other ischemic conditions.
    Circulation Research 12/2011; 110(5):727-38. DOI:10.1161/CIRCRESAHA.111.253419 · 11.02 Impact Factor
  • Der Nuklearmediziner 06/2011; 34(02):99-107. DOI:10.1055/s-0031-1280787
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    Benjamin D Kläsner · Bernd J Krause · Ambros J Beer · Alexander Drzezga
    Expert Review of Anti-infective Therapy 05/2010; 10(5):609-13. DOI:10.1586/era.10.37 · 2.25 Impact Factor
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    ABSTRACT: Following cerebral ischemia bradykinin/kinin B(2) receptors mediate inflammatory responses resulting in edema formation and secondary brain damage. However, the therapeutic window for B(2) receptor inhibition determining its potential clinical use has not been investigated so far. The aim of the current study was therefore to investigate the effect of delayed B(2) receptor inhibition on morphological and functional outcome following experimental stroke. Rats were subjected to 90 min of middle cerebral artery occlusion (MCAo) by an intraluminal filament. Animals received 0.9% NaCl or 1.0mg/kg/day Anatibant (LF 16-0687 Ms), a selective bradykinin B(2) receptor antagonist, for 3 days beginning at different time points after MCAo: 1, 2.5, 4.5, or 6.5h (n=10 per group). Neurological recovery was examined daily, infarct volume on day 7 after MCAo. Animal physiology was not influenced by B(2) receptor inhibition. Significant improvement of functional outcome was observed when treatment was delayed up to 4.5h after ischemia (p<0.05 versus vehicle). Inhibition of B(2) receptors during ischemia, i.e. when the inhibitor was given 1h after MCAo, reduced infarct volume in the basal ganglia and in the cortex by 49% (p<0.05) and 26% (p<0.05), respectively. Inhibition of B(2) receptors at later time points (2.5, 4.5, or 6.5 after MCAo) reduced penumbral damage, i.e. cortical infarction, by 19-26% (p<0.05). In conclusion, the current study shows that the therapeutic window of B(2) receptor inhibition extends for up to 6.5h after MCAo. Our data therefore suggest that inhibition of kinin B(2) receptors represents a treatment strategy for ischemic stroke which may warrant clinical validation.
    Neurochemistry International 11/2006; 49(5):442-7. DOI:10.1016/j.neuint.2006.02.010 · 3.09 Impact Factor
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    ABSTRACT: Bradykinin, an endogenous nonapeptide produced by activation of the kallikrein-kinin system, promotes neuronal tissue damage as well as disturbances in blood-brain barrier function through activation of B2 receptors. In a rat model of focal cerebral ischemia, blockade of B2 receptors before initiation of ischemia with the B2 receptor antagonist, LF 16-0687 Ms, afforded substantial neuroprotection. In order to assess the potential clinical value of this approach, we evaluated the effect of LF 16-0687 Ms given at reperfusion following focal cerebral ischemia on local cerebral blood flow (LCBF), neurological outcome, and infarct size. Sprague-Dawley rats were subjected to MCA occlusion for 90 min by an intraluminal filament. Animals were assigned to one of four treatment arms (n = 7 each): (1) vehicle, (2) LF 16-0687 Ms (1.0 mg/kg/day), (3) LF 16-0687 Ms (3.0 mg/kg/day), or (4) LF 16-0687 Ms (10.0 mg/kg/day) given at reperfusion and repetitively over 2 days. Neurological recovery was examined daily, and infarct volume was assessed histologically on day 7 after ischemia. Physiological parameters and local CBF were not influenced by the treatment. Significant improvement of neurological outcome was observed on postischemic day 3 in animals receiving 1.0 and 3.0 mg/kg/day of LF 16-0687 Ms (P < 0.05). Inhibition of B2 receptors significantly reduced infarct volume in all treated animals predominantly in the cortex. B2 receptor blockade with LF 16-0687 Ms showed neuroprotective effectiveness even when therapy was initiated upon reperfusion, i.e. 90 min after induction of ischemia. Therefore, blockade of B2 receptors seems to be a promising therapeutic approach after focal cerebral ischemia, which deserves further experimental and clinical evaluation.
    Brain Research 01/2006; 1069(1):227-34. DOI:10.1016/j.brainres.2005.11.043 · 2.84 Impact Factor

Publication Stats

77 Citations
19.20 Total Impact Points


  • 2011
    • Technische Universität München
      München, Bavaria, Germany
  • 2010
    • Deutsches Herzzentrum München
      München, Bavaria, Germany
  • 2006
    • Ludwig-Maximilian-University of Munich
      • Department of Neurosurgery
      München, Bavaria, Germany