Correspondence  |   October 2016
Relevance of Clinical Relevance
Author Notes
  • Weill Cornell Medicine, New York, New York (P.M.R.). par9082@med.cornell.edu
  • (Accepted for publication June 23, 2016.)
    (Accepted for publication June 23, 2016.)×
Article Information
Correspondence
Correspondence   |   October 2016
Relevance of Clinical Relevance
Anesthesiology 10 2016, Vol.125, 821-822. doi:10.1097/ALN.0000000000001257
Anesthesiology 10 2016, Vol.125, 821-822. doi:10.1097/ALN.0000000000001257
We are concerned by an article published in the April 2016 issue of Anesthesiology by Han et al.1  entitled “Propofol-induced Inhibition of Catecholamine Release Is Reversed by Maintaining Calcium Influx.” The authors addressed the molecular mechanisms underlying propofol-induced hypotension and describe a number of proposed molecular mechanisms thought to underlie this clinical effect. They focus their study on one such mechanism: the effect of propofol on catecholamine release from rat PC12 neuroendocrine cells and isolated cortical nerve terminals. In contrast to a number of previous studies showing that propofol inhibits catecholamine release,2,3  the authors report that when intracellular calcium concentration was maintained constant, catecholamine release was enhanced by propofol. Our principal concern is that enhanced catechoamine release was observed only at propofol concentrations greater than 10 μM, a value that the authors suggest represents a “clinically relevant concentration.
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