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Correspondence  |   August 2013
Does Helium Act on Vascular Endothelial Function in Humans?
Author Affiliations & Notes
  • The authors declare no competing interests.
    The authors declare no competing interests.×
  • (Accepted for publication April 17, 2013.)
    (Accepted for publication April 17, 2013.)×
Article Information
Correspondence
Correspondence   |   August 2013
Does Helium Act on Vascular Endothelial Function in Humans?
Anesthesiology 08 2013, Vol.119, 488. doi:10.1097/ALN.0b013e3182987cd2
Anesthesiology 08 2013, Vol.119, 488. doi:10.1097/ALN.0b013e3182987cd2
To the Editor:
Smit et al.1  have demonstrated intriguing results that preconditioning with helium can preserve acetylcholine-induced vasodilator responses in the human forearm exposed to ischemia–reperfusion. This study seems to have many questions regarding the mechanisms of helium’s action, whereas we would congratulate their impressive results. First, Smit et al. used a nonselective nitric oxide synthase inhibitor, NG-monomethyl-l-arginine, to document that the acetylcholine-induced enhancement of forearm blood flow is due to the activation of endothelial nitric oxide synthase.1–3  However, they failed to show that the inhibition by NG-monomethyl-l-arginine in the control condition, as well as that with the effect of helium-preconditioning.1  Therefore, it is quite difficult to conclude that nitric oxide, derived from endothelial enzyme, is a source of acetylcholine-induced vasodilator effects in their study. Second, it is unclear that the dosage of NG-monomethyl-l-arginine, used by Smit et al., is comparable with those are sufficiently effective to inhibit acetylcholine-induced vasodilation in humans (32–64 µmol/min or 5 mg/min).1–3  Third, Smit et al. did not evaluate roles of oxygen-derived free radicals including superoxide, which should modify vasodilator function in several pathological conditions including ischemia–reperfusion.4–6  Indeed, it is possible to obtain endothelial cells from patients using J-wires to determine the degree of oxidative stress.4  Fourth, it is possible that deflation of a blood pressure cuff placed on the arm to a pressure of 200 mmHg for 20 min induces flow-mediated dilation, which is mediated by endothelium-derived nitric oxide.7  This possibility has to be ruled out because this dilation may play a role in the protective effects of helium on forearm blood flow after ischemia–reperfusion.7  Therefore, further studies are needed to clarify the mechanistic insight into helium’s protective effects on the vascular function exposed toward ischemia–reperfusion.
References
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