ABSTRACT
Objective: This study aimed to analyze the outcomes and risk factors of early postoperative death (within 30 days after surgery) in a single-center after repair of total anomalous pulmonary venous connection (TAPVC). Methods: The clinical data of 88 children who had been diagnosed with TAPVC and underwent radical operation in the Shandong Provincial Hospital Affiliated with Shandong First Medical University (China) from January 2015 to July 2021 were retrospectively analyzed. All the patients were divided into the survival group (n = 81) and the death group (n = 7) for the analysis of preoperative and postoperative clinical data. The variables associated with early postoperative death were statistically analyzed to obtain the risk factors for early postoperative death of TAPVC. Results: Of the 88 patients included in this study, 7 (7.95%) patients died early, including 4 supracardiac and 3 infracardiac cases. Recurrent pulmonary vein obstruction occurred in 2 patients after discharged from hospital, and both were intracardiac TAPVC. Delayed death occurred in 2 children, both of which were intracardiac TAPVC cases. According to univariate analysis, the risk factors statistically significantly associated with the early postoperative death included infracardiac type (P = 0.08), preoperative maximum pulmonary vein flow velocity (P = 0.031), preoperative mechanical ventilation (P = 0.043), preoperative maximum pulmonary artery pressure (P = 0.000), intraoperative cardiopulmonary bypass time (P = 0.003) and intraoperative aortic cross-clamp time (P = 0.000). Conclusion: Infracardiac type of TAPVC, preoperative maximum pulmonary vein flow velocity, preoperative mechanical ventilation, preoperative maximum pulmonary artery pressure, intraoperative cardiopulmonary bypass time and aortic cross-clamp time are the risk factors for early postoperative death.
ABSTRACT
PURPOSE: Chemotherapy-induced painful neuropathy (CIPN) is a severe adverse effect of many anti-neoplastic drugs that is difficult to manage. Serotonin (5-hydroxytryptamine, 5-HT) is an important neurotransmitter in the rostral ventromedial medulla (RVM), which modulates descending spinal nociceptive transmission. However, the influence of the descending 5-HT from the RVM on CIPN is poorly understood. We investigated the role of 5-HT released from descending RVM neurons in a paclitaxel-induced CIPN rat model. METHODS: CIPN rat model was produced by intraperitoneally injecting of paclitaxel. Pain behavioral assessments included mechanical allodynia and heat hyperalgesia. 5-HT content was analyzed by high-performance liquid chromatography (HPLC). Western blot and immunohistochemistry were used to determine tryptophan hydroxylase (Tph) and c-Fos expression. The inhibitors p-chlorophenylalanine (PCPA) and SB203580 were administrated by stereotaxical RVM microinjection. Ondansetron was injected through intrathecal catheterization. RESULTS: The results demonstrated that Tph, the rate-limiting enzyme in 5-HT synthesis, was significantly upregulated in the RVM, and that spinal 5-HT release was increased in CIPN rats. Intra-RVM microinjection of Tph inhibitor PCPA significantly attenuated mechanical and thermal pain behavior through Tph downregulation and decreased spinal 5-HT. Intra-RVM administration of p38 mitogen-activated protein kinase (p38 MAPK) inhibitor SB203580 alleviated paclitaxel-induced pain in a similar manner to PCPA. Intrathecal injection of ondansetron, a 5-HT3 receptor antagonist, partially reversed paclitaxel-induced pain, indicating that 5-HT3 receptors were involved in descending serotoninergic modulation of spinal pain processing. CONCLUSION: The results suggest that activation of the p38 MAPK pathway in the RVM leads to increased RVM Tph expression and descending serotoninergic projection to the spinal dorsal horn and contributes to the persistence of CIPN via spinal 5-HT3 receptors.
