Abstract
Objective To study the application of dexmedetomidine in patients undergoing temporal muscle sticking for moyamoya disease (MMD), and to discuss the possible mechanism of brain protection. Methods Sixty patients undergoing temporal muscle sticking operation were randomly divided into 2 groups: dexmedetomidine group (Group D, N = 30) and control group (Group S, N = 30), respectively receiving dexmedetomidine intravenous infusion (0.60 μ g/kg) and the same dose of normal saline before anesthesia induction. In Group D, dexemdetomidine was administered continuously (intravenous pumping) with the dose of 0.40 μg/(kg·h) perioperatively, while the same dose of normal saline was administered in Group S. Heart rate (HR) and mean arterial pressure (MAP) were recorded at T 0 (before administration), T 1 (before tracheal intubation), T 2 (1 min after intubation), T 3 (at the moment of skin incision), T 4 (before extubation) and T 5 (1 min after extubation) respectively. Total amount of propofol, remifentanil and patients' recovery conditions after anesthesia were also recorded. Glutamine and malondialdehyde (MDA) were measured and compared before and after operation. Results In group D, HR and MAP decreased significantly at T 2-4 compared with T 0 ( P < 0.05, for all). Total amount of propofol, remifentanil in Group D was lower than that in Group S ( P < 0.05, for all) and the patients' recovery conditions in Group D after anesthesia was better than Group S ( P = 0.000, for all), without occurence of shivering, cough and dysphoria ( P < 0.05, for all). Glutamine and MDA increased after anesthesia compared with that before anesthesia in both 2 groups ( P < 0.05, for all), however, it was higher in Group S than that in Group D ( P < 0.05, for all). Conclusions Dexmedetomidine can provide stable hemodynamic condition during the anesthesia with patients undergoing temporal muscle sticking for moyamoya disease, and has a positive effect on improving both the outcome of the operation and recovery conditions. Also it can provide brain protection effect by decreasing the level of excitatory amino acids. doi: 10.3969/j.issn.1672-6731.2014.06.009
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