Deep sedation with dexmedetomidine in a porcine model does not compromise the viability of free microvascular flap as depicted by microdialysis and tissue oxygen tension.
BACKGROUND
Deep sedation is often necessary after major reconstructive plastic surgery in the face and neck regions to prevent sudden spontaneous movements capable of inflicting mechanical injury to the transplanted musculocutaneous flap(s). An adequate positioning may help to optimize oxygenation and perfusion of the transplanted tissues. We hypothesized that dexmedetomidine, a central alpha2-agonist and otherwise potentially ideal postoperative sedative drug, may induce vasoconstriction in denervated flaps, and thus increase the risk of tissue deterioration.


METHODS
Two symmetrical myocutaneous flaps were raised on each side of the upper abdomen in 12 anesthetized pigs. The sympathetic nerve fibers were stripped from the arteries in one of the flaps (denervated flap), while nerve fibers were kept untouched in the other (innervated flap). After simulation of ischemia and reperfusion periods, the animals were randomized to deep postoperative sedation with either propofol (n = 6) or dexmedetomidine (n = 6). Flap tissue metabolism was monitored by microdialysis and tissue-oxygen partial pressure. Glucose, lactate, and pyruvate concentrations were analyzed from the dialysate every 30 min for 4 h.


RESULTS
Mean arterial blood pressure was higher in the dexmedetomidine group (P = 0.036). Flap tissue metabolism remained stable throughout the experiment as measured by lactate-pyruvate and lactate-glucose ratios (median ranges 14.3-24.5 for lactate-pyruvate and 0.3-0.6 for lactate-glucose) and by tissue-oxygen partial pressure, and no differences were found between groups.


CONCLUSIONS
Our data suggest that dexmedetomidine, even if used for deep sedation, does not have deleterious effects on local perfusion or tissue metabolism in denervated musculocutaneous flaps.
Nunes
Silvia
S
Critical Care Medicine Research Group, Department of Intensive Care, Tampere University Hospital, Tampere, Finland.
Berg
Leena
L
Raittinen
L-P
LP
Ahonen
Heikki
H
Laranne
Jussi
J
Lindgren
Leena
L
Parviainen
Iikka
I
Ruokonen
Esko
E
Tenhunen
Jyrki
J
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002302:Cardiac Output / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D002496:Central Venous Pressure / Q000187:drug effects; D003243:Consciousness / Q000187:drug effects*; D020927:Dexmedetomidine / Q000494:pharmacology*; D005260:Female; D005947:Glucose / Q000378:metabolism; D006993:Hypnotics and Sedatives / Q000494:pharmacology*; D019344:Lactic Acid / Q000378:metabolism; D008833:Microcirculation / Q000187:drug effects / Q000378:metabolism; D017551:Microdialysis; D023421:Models, Animal; D010100:Oxygen / Q000378:metabolism*; D010313:Partial Pressure; D015742:Propofol / Q000494:pharmacology*; D019289:Pyruvic Acid / Q000378:metabolism; D017568:Rectus Abdominis / Q000098:blood supply / Q000187:drug effects* / Q000294:innervation / Q000378:metabolism / Q000473:pathology; D013524:Surgical Flaps / Q000098:blood supply* / Q000473:pathology; D034421:Sus scrofa; D013562:Sympathectomy; D013997:Time Factors; D014655:Vascular Resistance / Q000187:drug effects
D006993:Hypnotics and Sedatives; D019344:Lactic Acid; D020927:Dexmedetomidine; D019289:Pyruvic Acid; D005947:Glucose; D010100:Oxygen; D015742:Propofol