Adjunct nitrous oxide normalizes vascular reactivity changes after hemorrhagic shock in mice under isoflurane anesthesia.
BACKGROUND
Hemorrhagic shock is associated with changes in vascular responsiveness that may lead to organ dysfunction and, ultimately, multiple organ dysfunction syndrome. Volatile anesthetics interfere with vasoresponsiveness, which may contribute to organ hypoperfusion. In this study, the authors examined the influence of adjunct nitrous oxide on the vascular responsiveness after short-term hemorrhagic shock under isoflurane anesthesia.


METHODS
Spontaneously breathing mice (n = 31, 27.6 +/- 0.31 g) were anesthetized with isoflurane (1.4%) or with isoflurane (1.4%) and adjunct nitrous oxide (66%). Both groups were divided into Sham, Shock, and Resuscitated groups. Vascular reactivity to phenylephrine and acetylcholine and expression of cyclooxygenases were studied in the aorta.


RESULTS
In the isoflurane-anesthetized groups, the contractile response to phenylephrine was increased in the Shock as compared with the Sham and Resuscitated groups (Emax = 3.2 +/- 0.4, 1.2 +/- 0.4, and 2.5 +/- 0.5 mN, respectively). Adjunct nitrous oxide increased phenylephrine contraction to a similar level in all three groups. In the Sham isoflurane group, acetylcholine caused a biphasic response: An initial relaxation followed by a contractile response sensitive to cyclooxygenases inhibition by indomethacine. The contractile response was abrogated in the isoflurane-anesthetized groups that underwent shock. In all groups, adjunct nitrous oxide preserved the contractile phase. Shock induced a down-regulation of cyclooxygenases-1, which was normalized by adjunct nitrous oxide.


CONCLUSIONS
Adjunct nitrous oxide attenuates shock-induced changes in vascular reactivity and cyclooxygenases expression of mice under isoflurane anesthesia. This implies that vascular reactive properties during anesthesia in hemorrhagic shock conditions may be influenced by the choice of anesthetics.
Samarska
Iryna V
IV
Department of Clinical Pharmacology, University Medical Center Groningen, University of Groningen, The Netherlands. i.v.samarska@med.umcg.nl
van Meurs
Matijs
M
Buikema
Hendrik
H
Houwertjes
Martin C
MC
Wulfert
Francis M
FM
Molema
Grietje
G
Epema
Anne H
AH
Henning
Robert H
RH
D000109:Acetylcholine / Q000494:pharmacology; D000769:Anesthesia, Inhalation; D018685:Anesthetics, Inhalation / Q000627:therapeutic use*; D000818:Animals; D001784:Blood Gas Analysis; D001794:Blood Pressure / Q000502:physiology; D001808:Blood Vessels / Q000187:drug effects* / Q000503:physiopathology*; D015153:Blotting, Western; D051545:Cyclooxygenase 1 / Q000096:biosynthesis; D051546:Cyclooxygenase 2 / Q000096:biosynthesis; D007530:Isoflurane; D051379:Mice; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology; D020030:Nitric Oxide Donors / Q000494:pharmacology; D009599:Nitroprusside / Q000494:pharmacology; D009609:Nitrous Oxide / Q000627:therapeutic use*; D012771:Shock, Hemorrhagic / Q000188:drug therapy* / Q000503:physiopathology*; D014661:Vasoconstriction / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology
D018685:Anesthetics, Inhalation; D020030:Nitric Oxide Donors; D014665:Vasodilator Agents; D009599:Nitroprusside; D007530:Isoflurane; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; D009609:Nitrous Oxide; D000109:Acetylcholine