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ADVANCES in the understanding of anesthetic pharmacology and perioperative physiology, coupled with improved patient monitoring, have significantly contributed to improvements in quality of care and perioperative outcome. In this issue of ANESTHESIOLOGY, Samarska et al. describe preclinical research that addresses the anesthetic modulatory effects on the physiologic adaptation to hemorrhagic shock; their data have led them to the conclusion that nitrous oxide promotes hemodynamic stability. In their studies, mice were exposed to anesthesia, either isoflurane (1.4%) in oxygen (33%) or isoflurane (1.4%) plus nitrous oxide (66%) in oxygen (33%), and underwent a sham procedure, hemorrhagic shock, or shock plus fluid resuscitation, during which time hemodynamic measurements were obtained. Thereafter, vascular responsiveness was assessed ex vivo in aortic rings. Isoflurane treatment attenuated the maximal aortic contractile responses to phenylephrine, corroborating earlier reports with volatile anesthetics. Shock, with or without resuscitation, mitigated the isoflurane-induced attenuation of phenylephrine responses, although the biphasic pattern of relaxation and then contraction with acetylcholine was altered. The ex vivo effects induced by in vivo isoflurane exposure were mitigated when supplemented with nitrous oxide. However, in the shock state the addition of nitrous oxide induced acidosis when compared with isoflurane, and further physiologic differences (such as oxygenation) confounds clear interpretation of the experimental findings. Even though animals were at different depths of anesthesia under these conditions, the authors attribute the pharmacologic properties of nitrous oxide for “normalizing” vasoreactivity, and speculate that nitrous oxide may induce increased perioperative hemodynamic stability. Samarska et al. also observed that nitrous oxide exposure was associated with a higher mean arterial blood pressure in the sham-treated animals despite the increased depth of anesthesia; this finding corroborates previous studies demonstrating the vasoconstrictive properties of nitrous oxide. Yet recent clinical studies have reported minor difference in blood pressure when comparing nitrous oxide or air as the carrier gas. Thus it is highly speculative that the modest increments (of the order of 10 mmHg) reported by Samarska et al. and others will exert a positive long-term clinical benefit.

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