Efficacy of dexmedetomidine combined with ropivacaine on postoperative analgesia and delirium in elderly patients with total knee arthroplasty.

This study aimed to investigate the impact of dexmedetomidine combined with ropivacaine on continuous femoral nerve block (CFNB) in postoperative analgesia and delirium in elderly patients with total knee arthroplasty (TKA). A total of 120 patients who undergone TKA were randomly assigned into group D + R (dexmedetomidine combined with ropivacaine) and group R (only ropivacaine), with 60 cases in each group. The pain scores at rest and exercise at 6 h, 12 h, 24 h, and 48 h postoperatively. The occurrence of delirium on Day 1, Day 2, and Day 3 postoperatively were measured, and the sleep quality was evaluated before surgery, the night of surgery, and 24 h postoperatively to observe the occurrence of postoperative complications. The Visual analogu scale (VAS) of group D + R at 12 h, 24 h, and 48 h postoperatively were lower than those of group R in both rest and exercise states. The incidence of postoperative delirium in group D + R was lower than that in group R on Day 1 and Day 2. Pittsburgh sleep quality index (PSQI) scores in group D + R were lower than those in group R. There was no significant difference in postoperative adverse reactions between the two groups. Dexmedetomidine combined with ropivacaine improves postoperative analgesia and sleep quality, and alleviates the occurrence of postoperative delirium in elderly patients with TKA.

The ERK/CREB/PTN/syndecan-3 pathway involves in heparin-mediated neuro-protection and neuro-regeneration against cerebral ischemia-reperfusion injury following cardiac arrest.

BACKGROUND: Heparin, a commonly used anticoagulant, has been found to improve cerebral ischemia-reperfusion injury (CIR-CA) following cardiopulmonary resuscitation (CPR). Here, we aimed to explore the role of pleiotrophin (PTN)/syndecan-3 pathway in heparin therapy for CIR-CA. MATERIALS AND METHODS: The CA-CPR model was constructed in Sprague-Dawley (SD) rats, which were treated with low molecular weight heparin, and the neurological changes and brain histopathological changes were evaluated. For in-vitro experiments, the ischemic injury model of primary neurons was established by oxygen and glucose deprivation (OGD), and the neuron regeneration was detected via the Cell counting Kit-8 (CCK8) method, flow cytometry and microscopy. CREB antagonist (KG-501), ERK antagonist (PD98059) and si-PTN were used respectively to inhibit the expression of CREB, ERK and PTN in cells, so as to explore the role of heparin in regulating neuronal regeneration. RESULTS: Compared with the sham rats, the neurological deficits and cerebral edema of CA-CPR rats were significantly improved after heparin treatment. Heparin also attenuated OGD-mediated neuronal apoptosis and promoted neurite outgrowth in vitro. Moreover, heparin attenuated CA-CPR-mediated neuronal apoptosis and microglial neuroinflammation. In terms of the mechanism, heparin upregulated the expression of ERK, CREB, NF200, BDNF, NGF, PTN and syndecan-3 in the rat brains. Inhibition of ERK, CREB and interference with PTN expression notably weakened the heparin-mediated neuroprotective effects and restrained the expression of ERK/CREB and PTN/syndecan-3 pathway. CONCLUSION: Heparin attenuates the secondary brain injury induced by CA-CPR through regulating the ERK/CREB-mediated PTN/syndecan-3 pathway.

Investigation of the protective effect of heparin pre-treatment on cerebral ischaemia in gerbils.

Context: The interruption of cerebral blood circulation may cause stroke characterized by high neurological deficits (NDs) as a result of neuronal dysfunction or destruction. Heparin may exert a neuroprotective effect against cerebral ischaemia/reperfusion injury. Objective: The objective of this study was to investigate the mechanism underlying the effects of heparin pre-treatment on cerebral injury in the gerbil. Materials and methods: A total of 80 healthy Mongolian gerbils were randomly divided into four groups to establish cerebral ischaemia model by bilateral carotid artery occlusion: control (no anaesthesia and surgery), sham (no occlusion), non-anticoagulation (occlusion), and anti-coagulation treatment groups (50 IU/100 g heparin pre-treated, occlusion). Gerbils were anesthetized with 40 mg/kg pentobarbital sodium through intraperitoneal injection before operation except for the control group. Then, the ND and histopathological damage (HD) scores were determined. The percentage of tumour necrosis factor (TNF)-α- and interleukin (IL)-1ß-positive cells were calculated based on immunohistochemical results. The mRNA and protein levels of caspase-9, caspase-8, FasL, and calpain were evaluated with real-time polymerase chain reaction (RT-PCR) and western blotting, respectively. Results: Compared with non-anticoagulation group, heparin pre-treatment (50 IU/100 g) delayed the onset of dyspnoea (p < 0.05), and showed a significant decrease in ND (p < 0.01), mortality rate (p < 0.05), HD (p < 0.01) and percentage of positive cells for TNF-α, IL-1ß (p < 0.01) in cerebral ischaemia gerbils. Besides, the expression levels of caspase-9, caspase-8, FasL, and calpain were reduced after pre-treatment with 50 IU/100 g heparin. Discussion and conclusions: The damage caused to gerbil brain was reduced upon pre-treatment with heparin, possibly through the amelioration of neuronal cell apoptosis and expression of TNF-α and IL-1ß. These findings are expected to provide a new breakthrough in the study and treatment of cerebral ischaemia.

Antinociceptive effects of dezocine on complete Freund's adjuvant-induced inflammatory pain in rats.

Inflammatory pain is known to severely impact the life quality of patients. Notably, dezocine is widely used for the treatment of pain. Therefore, the current study aimed to examine the effects of dezocine on a complete Freund's adjuvant (CFA)-induced inflammatory pain model in rats and to investigate the possible underlying molecular mechanisms. Rats were randomly divided into three groups, including the control, CFA and dezocine+CFA groups, and then subcutaneously injected with 100 µl saline, subcutaneously injected with 100 µl CFA or pretreated with 1 ml dezocine (0.4 µg/kg) at 30 min before CFA injection in the plantar surface of right hind paw, respectively. The paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) were measured with a dynamic plantar esthesiometer at 1 day before and 6 h after CFA injection. The ipsilateral lumbar spinal cords of all the rats were harvested for detecting the expression profiles of phosphorylated (p)-p65, p-extracellular signal-regulated kinase 1/2 (p-ERK1/2), cyclooxygenase-2 (COX-2), interleukin (IL)-1ß and tumor necrosis factor (TNF)-α by western blot analysis and/or reverse transcription-quantitative polymerase chain reaction. In addition, prostaglandin E2 (PGE2) expression was determined by enzyme-linked immunosorbent assay. Compared with the control group, CFA-induced peripheral inflammation downregulated the PWT and PWL values of rats, which were significantly alleviated by dezocine treatment. Furthermore, the protein levels of p-p65, p-ERK1/2, COX-2, PGE2, IL-1ß and TNF-α were significantly upregulated following CFA injection, while they were suppressed by dezocine pretreatment. In conclusion, the analgesic effect of dezocine on inflammatory pain induced by CFA may be associated with the inhibition of the spinal ERK1/2-COX-2 pathway.

[Bacterium culture and flora analysis of gunshot wound on limbs of dogs in hot and humid environment].

OBJECTIVE: To investigate the time of bacterial invasion into the blood and conduct flora analysis of the blood and secretions in the gunshot wound in the limbs of dogs in hot and humid environment. METHODS: Gun-shot wound was induced in 8 dogs who were subsequently assigned at random into hot and humid environment (HHE) group and normal environment (NE) group for observation. At the time points of 0, 4, 6, 8, 12, 24 h after injury, body temperature was measured and bacterial culture and flora analysis performed. RESULTS: Body temperature elevation occurred earlier and lasted for longer time in HEE group than in NE group. Bacterial invasion into the blood occurred at 12 h after the injury in NE group, but at 8 h in HHE group. In the wound tracts of the dogs, surface bacteria were found in both groups. Surface bacteria were also found in the blood of dogs in both groups, but in HHE group, even intestinal flora were identified. CONCLUSION: Body temperature elevation and bacterial invasion into the blood occurred at an earlier time in hot and humid environment where migration of intestinal bacteria into the blood easily takes place, indicating the early application of broad-spectrum antibiotics under such environmental conditions.