OBJECTIVE To determine the 50% effective dose (ED50) of intravenous propofol required for successfully preventing tracheal intubation response in Beagles co-induced with dexmedetomidine. ANIMALS 36 adult male Beagles PROCEDURES The dogs were randomly assigned to either group D1, group D2, or group C (received 1 µg/kg, 2 µg/kg dexmedetomidine intravenously, or the same amount of normal saline as dexmedetomidine, 10 mL). The first dog in each group received 6 mg/kg of propofol for induction. The pump speed of propofol was 600 mL/h. The dosage varied with increments or decrements of 0.5 mg/kg based on the Dixon up-and-down method. The duration of eye-opening after propofol administration was recorded. Changes in heart rate (HR) and respiratory rate (RR) were recorded at 5 timepoints: after entering the operation room and prior to propofol administration (T1), 1 and 3 min after propofol administration (T2 and T3), 3 and 5 min after intubation (T4 and T5). RESULTS The required ED50 of propofol that prevented tracheal intubation response in D1, D2, and C groups were 6.4 mg/kg (95% CI, 6.1 to 6.7 mg/kg), 5.8 mg/kg (95% CI, 5.67 to 6 mg/kg), and 8.3 mg/kg (95% CI, 8 to 8.5 mg/kg), respectively. The recovery time of group D2 was significantly longer than that of groups D1 and C (P < .05). The differences in HR among the 3 groups were significant from T2 up to T5 timepoint (P < .05). The differences in RR among the 3 groups were significant at T2 and T3 timepoints (P < .05). CLINICAL RELEVANCE Dexmedetomidine pre-injection reduces the amount of propofol required for endotracheal intubation response in Beagles, thereby reducing the respiratory inhibition induced by propofol.
Background Tourniquets provide better tissue visibility during arthroscopic surgery. However, multiple postoperative adverse events associated with ischemia may be caused by excessive inflation pressure and duration. We aimed to evaluate the degree of tourniquet-induced ischemia using a noninvasive continuous real-time monitoring method and the relationship between changes in tissue oxygen saturation (StO2) and blood biochemical markers of ischemic injuries in patients undergoing arthroscopic knee surgery. Methods This was a prospective observational study using near-infrared spectroscopy (NIRS). Data were collected from 29 consecutive patients who underwent arthroscopic procedures. Twenty-five patients underwent anterior cruciate ligament reconstruction, and four underwent meniscal repair. We investigated tourniquet‐induced changes in StO2, monitored using NIRS, and blood biochemical markers of ischemic injuries. Results A significant decrease in the mean StO2 from the baseline was observed during tourniquet inflation in the operative legs. The average decrease in the mean StO2 was 58%. A comparison of mean StO2 between the nonoperative and operative legs before tourniquet deflation showed that mean values of StO2 in the operative legs were significantly lower than those in the nonoperative legs. No significant clinical relationships were observed between changes in StO2 and blood biochemical markers of ischemic injuries (creatine kinase) (p = 0.04, r = 0.38) or tourniquet duration (p = 0.05, r = 0.366). Conclusions Our results demonstrated that StO2 could be used to evaluate tissue perfusion in real time but did not support the hypothesis that StO2 is a useful method for predicting the degree of tourniquet-induced injury during arthroscopic knee surgery.
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