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Bupivacaine is a common local anesthetic that causes neurotoxicity when used at clinical concentrations. Melatonin (MT), is a potent neuroprotective molecule. The study aimed to characterize the neuroprotective effects of MT on spinal neurotoxicity induced by bupivacaine in rats. It showed that bupivacaine, by intrathecal injection, induced spinal injury, and that the protein levels of Nod-like receptor protein 3 (NLRP3), cleaved caspase-1, and the N-terminal region of gasdermin D (GSDMD-N) were significantly increased. NLRP3 was expressed mainly in neurons and microglia. MT treatment ameliorated bupivacaine-induced spinal cord injury in rats by suppressing activation of neuronal NLRP3 inflammasomes.

To investigate the changes in heme oxygenase (HO) system expression in pulmonary thromboembolism (PTE), and the influence to the pulmonary artery blood pressure as a result of the changes.In 23 healthy adult male dogs, autologous thrombus was injected through the jugular vein to reproduce the PTE model. They were divided randomly into 4 groups: A (pulmonary embolism 3 hours group), B (pulmonary embolism 8 hours group), C (pulmonary embolism 24 hours group) and D (control group). Swan-Ganz catheter was placed via the femoral vein to observe the changes in hemodynamics. Pulmonary artery was obtained to detect the expression of HO-1 using semi-quantity reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemical method.The pulmonary artery mean pressure (PAMP), pulmonary artery systolic pressure (PASP) and pulmonary artery diastolic pressure (PADP) of the experimental groups were increased obviously after the pulmonary embolism as compared with those of before the embolism (all P0.05), and were decreased obviously 1 hour after the embolism (all P0.05). The decrease was gradual and stopped after 4-5 hours, but the pressure 8 hours after embolism was still higher than that of before embolism. HO-1 was not expressed in pulmonary artery in control group, but expressed after embolism in each experimental group. The expression was increased gradually after pulmonary embolism, and it was remarkable 24 hours after embolism (all P0.05).The expression of HO-1 increased in PTE, and the increased pulmonary artery blood pressure decreased at the same time. The results suggest that HO-1 is related with dilatation of pulmonary artery after PTE.