We conducted the present study to investigate the effects of the different loading doses of dexmedetomidine hydrochloride in the prevention of adverse reactions after combined spinal-epidural anesthesia. A total of 200 patients that were admitted to the Department of Obstetrics at the Second Affiliated Hospital of Xi'an Jiaotong University hospital and treated with cesarean section through the use of combined spinal-epidural anesthesia from December, 2014 to June, 2016, were randomly divided into 4 groups. The therapeutic regimens of patients were shown as follows: group A was administered an intravenous pump of 10 ml/l physiological saline in surgery until the end of the delivery. group B was administered 0.2 µg/kg dexmedetomidine. group C was administered 0.4 µg/kg dexmedetomidine. group D was administered 0.6 µg/kg dexmedetomidine. The anesthesia plane was adjusted to the level below the T10 plane. After the onset of anesthesia, participants of each group were treated with an intravenous pump of dexmedetomidine at loading dose. After intravenous pumping for 10 min in each group during the surgery, patients were administered with an intraoperative maintenance dose of 0.2 µg/kg/h until the end of the delivery. The heart rate (HR), mean arterial pressure (MAP), Narcotrend index (NI), Ramsay sedation score and the incidence of adverse reactions at each time-point of the start of drug administration (T0), 10 min (T2), 30 min (T3), 60 min (T4), 90 min (T5) and the end of surgery (T6) were recorded. Within 24 h post-delivery, the degree of amnesia from using dexmedetomidine until the end of the delivery were followed up. Compared to group A and T0, the HRs of participants at T3-6 in groups B and C were decreased. The MAP at T1 in group D was increased. In groups B and C, the NIs were significantly decreased at T2-6, the Ramsay scores were increased at T3-6, and the differences were statistically significant (P<0.05). The follow-up within 24 h after delivery showed that the degree of anterograde amnesia from groups B to D was significantly higher than group A, with statistically significant difference (P<0.05). A combined spinal-epidural anesthesia with 0.6 µg/kg loading dose of dexmedetomidine, by intravenous pumping within 10 min before cesarean section, can achieve a satisfied sedative effect at 30 min after administration. It maintains the characteristics of intraoperative hemodynamic stability and less adverse reactions. Therefore, it is of great significance to improve the quality of cesarean section delivery.

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Apoptosis and mitochondrial dysfunction are the main cause of neurological injury after cardiopulmonary resuscitation (CPR). However, the effects of distal ischemic treatments on ischemia induced apoptosis are rarely studied, and the mechanism by which mitochondrial dysfunction contributes to CPR still unclear. A rat model of distal ischemia was established by clipping the right femoral artery. Rats were divided into blank, model, pre distal ischemic treatment, per-treatment, and post-treatment groups. Neurological deficit score was scored to evaluate neurologic function after cardiopulmonary resuscitation for 72 hr. We employed TUNEL and flow cytometry to measure the rate of apoptosis of hippocampal neurons, the integrity of mitochondrial membrane and the degree of mitochondrial permeability transition pore (mPTP) opening. The rate of apoptosis rate of hippocampal CA1 neurons in the pre-treatment and post-treatment groups were significantly lower than that of the model group. Moreover, the integrity of the mitochondrial membrane in the pre-treatment and post-treatment groups was higher than that in the model and per- treatment groups. Furthermore, the degree of mPTP opening was lower in the pre-treatment and post-treatment groups than the untreated and per-treatment groups. Taken together, our results show that ischemic preconditioning and post processing can maintain the integrity of mitochondria, perhaps by inhibiting the opening of mPTP, and reducing apoptosis of hippocampal neurons by regulating expression of apoptosis related proteins after CPR, to improve neurological function. This study highlights a novel target pathway for treatment of CPR.

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