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ANESTHETIC PHARMACOLOGY

Helium Breathing Provides Modest Antiinflammatory, but No Endothelial Protection Against Ischemia-Reperfusion Injury in Humans In Vivo

Eliana Lucchinetti, PhD^*, Johannes Wacker, MD, Christian Maurer, MD, Marius Keel, MD, Luc Härter, PhD, Kathrin Zaugg, MD, PhD, and Michael Zaugg, MD^||

From the *Department of Anesthesiology and Pain Medicine, University of Alberta, Edmonton, Canada; Institute of Anesthesiology, Department of Trauma Surgery, Department of Radiation Oncology, University Hospital Zurich, Zurich, Switzerland; and ||Department of Anesthesiology and Pain Medicine, University of Alberta and Perioperative Translational Medicine, Mazankowski Alberta Heart Institute, Edmonton, Canada.

Address correspondence to Michael Zaugg, MD, DEAA, FRCPC, Department of Anesthesiology and Pain Medicine, University of Alberta, CSB Room 8-120, Edmonton AB T6G 2G3. Address e-mail to michael.zaugg{at}ualberta.ca.

BACKGROUND: The noble gas helium is devoid of anesthetic effects, and it elicits cardiac preconditioning. We hypothesized that inhalation of helium provides protection against postocclusive endothelial dysfunction after ischemia-reperfusion of the forearm in humans.

METHODS: Eight healthy male subjects were enrolled in this study with a crossover design. Each volunteer was randomly exposed to 15 min of forearm ischemia in the presence or absence of helium inhalation. Helium was inhaled at an end-tidal concentration of 50 vol% from 15 min before ischemia until 5 min after the onset of reperfusion ("helium conditioning"). Hyperemic reaction, a marker of nitric oxide bioavailability and endothelial function, was determined at 15 and 30 min of reperfusion on the forearm using venous occlusion plethysmography. Expression of the proinflammatory markers CD11b, ICAM-1, PSGL-1, and L-selectin (CD62L) on leukocytes and P-selectin (CD62P), PSGL-1, and CD42b on platelets were measured by flow cytometry during reperfusion.

RESULTS: Ischemia-reperfusion consistently reduced the postocclusive endothelium-dependent hyperemic reaction at 15 and 30 min of reperfusion. Periischemic inhalation of helium at 50 vol% did not improve postocclusive hyperemic reaction. Helium decreased expression of the proinflammatory marker CD11b and ICAM-1 on leukocytes and attenuated the expression of the procoagulant markers CD42b and PSGL-1 on platelets.

CONCLUSIONS: Although inhalation of helium diminished the postischemic inflammatory reaction, our data indicate that human endothelium, which is a component of all vital organs, is not amenable to protection by helium at 50 vol% in vivo. This is in contrast to sevoflurane, which protects human endothelium at low subanesthetic concentrations.