RESUMEN

Aim To study the role of Cx43 hemichannel in rats with acute incision pain. Methods Adult male rats were randomly divided into normal saline group(C group), incision pain group(I group), Gap19 group. Western blot was used to determine the expression of Cx43 and GFAP at 6 h, 3 d and 7 d after paw incision surgery of rats. The rats were intrathecal injected with Gap19 30 min before incision surgery, followed by the measurement of the paw withdrawal threshold to mechanical stimuli at several time points. Immunofluorescence was used to detect the expression of Cx43 and GFAP. ELISA was performed to detect the different inflammatory cytokine levels in rats after surgery. Results Compared with group C, the expression of Cx43 and GFAP of rats increased significantly 6 h after incision surgery in group I, while their expression at postoperative 3 d and 7 d showed no obvious alteration. Compared with the preoperative baseline, the mechanical paw withdrawal threshold in I group and Gap19 group rats was significantly reduced at 2 h, 6 h, 24 h and 3 d post-incision(P<0.01), but it had no obvious change on postoperative 7 d. Compared with group I, the mechanical paw withdrawal threshold in rats of Gap19 group increased 2 h, 6 h, 24 h post-incision, while it showed no statistical difference on 3 d and 7 d post-incision. Compared with group C, immunofluorescence results showed that the expression of GFAP and Cx43 in spinal cord dorsal horn astrocytes also increased significantly in Group I 6 h after incision surgery. Compared with group I, GFAP and the expression of Cx43 were markedly reduced in Gap19 group. There was no statistical difference on 7 d post-incision. Compared with those in group C, the inflammation factors including IL-1β, IL-6 and TNF-αobviously increased in group I. However, in contrary to the rats in group I, the rats pretreated with gap19 showed increased expression of Cx43 and GFAP in spinal cord dorsal horn. Conclusions Specific inhibition of Cx43 hemichannel significantly suppresses astrocyte activation and alters the inflammatory microenvironment in the spinal cord dorsal horn and reduces postoperative hyperalgesia in rats with acute incision pain.

RESUMEN

OBJECTIVE@#To analyze the effect of dexmedetomidine on the inflammatory factors level and cognitive function after femoral head replacement in elderly patients.@*METHODS@#From January 2016 to December 2017, 60 elderly patients(more than 60 years old, and Grade I to II of ASA) treated with femoral head replacement were divided into three groups, and 20 in each group. All patients received midazolam, fentanyl, etomidate, cisatracurium anesthesia induction and sevoflurane inhalation anesthesia maintenance. The patients in group B and group C were first given 1.0 μg·kg⁻¹ of dexmedetomidine 10 minutes during the operation. The maintenance volume was 0.3 μg·kg⁻¹·h⁻¹ of dexmedetomidine(in group B) and 0.6 μg·kg⁻¹·h⁻¹ of dexmedetomidine(in group C) by pumping. The same amount of saline was given to the patients in group A in the same way. The time of extubation, wakefulness and recovery, the simple intelligent mental state score (MMSE), the incidence of postoperative cognitive dysfunction (POCD) and the levels of interleukin-6 (IL-6), interleukin-10 (IL-10) and S100β protein expression in the 3 groups were compared.@*RESULTS@#There were significant differences in the time of spontaneous breathing recovery, eye opening tome and the time of extubation, as well as the dosage of propofol among the three groups(0.05); but one hour after the operation, the levels of IL-6 IL-10 and S100β protein in group B and group C was statistically different from those in group A(<0.05). The IL-6 and S100β protein in group C were significantly lower than those in group B (<0.05), and IL-10 was significantly higher than that in group B (<0.05).@*CONCLUSIONS@#For elderly patients operated for femoral head replacement, dexmedetomidine can reduce the level of inflammatory factors level and propofol consumption, and the incidence of postoperative POCD is low, indicating a dose dependence of dexmedetomidine. But it is necessary to choose the right dose according to the patient's condition.

Asunto(s)

RESUMEN

Objective To investigate the effects of acute normovolemic hemodilution(ANH)on intraoperative intracranial pressure(ICP),jugular venous oxygen saturation(SvO_2),and venous blood lactate(VBL)of patients with intracranial tumor, Methods Forty-two patients,elected to perform supratentorial intracranial tumor resection on some certain days,were randomly divided into ANH(n=21)and control (n=21)groups.Bloodletting was performed in the radial artery after anesthesia induction and the same amount of hydroxyethyl starch was injected into the internal jugular vein at the same time so as to induce the haematocrit reaching to 30% in the ANH group.ANH was not performed in the control group.Acetated Ringer's solution was used during the operation in both groups.The level of arterial partial pressure of oxygen(PaO_2),arterial oxygen saturation(SaO_2),venous oxygen partial pressure (PvO_2),mixed venous O_2 saturation(SvO_2)and VBL was measured before hemodilution(T_0),30 min after the hemodilution(T_1),1 h after the hemodilution(T_2),and at the time the operation was finished(T_3)in both groups.And the changes of ICP before hemodilution(T_0),immediate after hemodilution(T_1),30 min after the hemodilution(T_Ⅱ),and before the endocranium was cut open(T_Ⅲ)in both groups. Results The ICP value in the two groups was not significantly different at different time points;The level of SvO_2 in the control group was significantly lower than that in the ANH group at T_2 and T_3(P<0.05);Significantly decreased level of SvO_2 and increased level of VBL was found in the control group at T2 and T_3 as compared with those in the control group at T_0 and T_Ⅱ(P<0.05). Conclusion Maintaining ICP in patients with intracranial tunlor during the operation through performing ANH with Hct reaching 30%,can significantly improve the oxygen supply and consumption in the brain tissue.

RESUMEN

Objective To investigate the effect of hypertonic saline on cerebral water content, tumor necrosis factor-α (TNF-α) level and neuronal apoptosis following focal cerebral ischemia-reperfusion (IR) injury in rats and explore the mechanisms involved. Methods Ninety-six rats were randomized equally into 4 groups, namely the shame-operated group, untreated IR injury group, and 4.2% and 7.5% hypertonic saline groups (HS-A and HS-B groups, respectively). In the latter 3 groups, cerebral ischcmia was induced by middle cerebral artery occlusion for 2 h followed by administration of the corresponding treatments. Serum sodium concentration was measured at 5 min before and at 30, 60 and 90 min after the reperfilsion. At 22 h of rcperfusion, the rats were sacrificed after neurological deficit evaluation, and brain edema was assessed by measuring the wet-to-dry weight ratio of the brain tissue. TNF-α expression in the ischemic brain tissue was measured by enzyme-linked immunosorbent assay (ELISA), and the neuronal apoptosis was analyzed using TUNEL assay. Results In the saline-treated rats, serum sodium level increased significantly after saline administration, lasting for 60 min before recovering the normal levels in HS-A group and for over 90 min in HS-B group. Compared with that in the sham-operated group, the brain water content in rats of the IR group increased in both of the hemispheres, but more obviously in the ischemic hemisphere. In the two saline-treated groups, the water content decreased significantly in the bilateral hemispheres, which was especially obvious in the ischemic hemisphere;administration of 7.5% saline resulted in greater water content reduction in the ischemic hemisphere than 4.2% saline. Compared with the IR group, the two saline-treated groups showed significant reduction in TNF-α levels and apoptotic cells in the brain along with decreased neurological deficits. Conclusion Hypertonic saline can ameliorate cerebral focal IR injury by decreasing the cerebral water content, TNF-α level and neuronal apoptosis following the injury.