A missed diagnosis of sputum crust with fiberoptic bronchoscope causing extubation failure: a case report.

BACKGROUND: Fiberoptic bronchoscopy (FOB) and bronchoscopic biopsy are the established methods for diagnosing and treating sputum crust. However, sputum crust in concealed locations can sometimes be missed or undiagnosed, even with bronchoscopy. CASE PRESENTATION: We present the case of a 44-year-old female patient who experienced initial extubation failure and postoperative pulmonary complications (PPCs) due to the missed diagnosis of sputum crust by FOB and low-resolution bedside chest X-ray. The FOB examination showed no apparent abnormalities prior to the first extubation, and the patient underwent tracheal extubation 2 h after aortic valve replacement (AVR). However, she was reintubated 13 h after the first extubation due to a persistent irritating cough and severe hypoxemia, and a bedside chest radiograph revealed pneumonia and atelectasis. Upon performing a repeat FOB examination prior to the second extubation, we serendipitously discovered the presence of sputum crust at the end of the endotracheal tube. Subsequently, we found that the sputum crust was mainly located on the tracheal wall between the subglottis and the end of the endotracheal tube during the "Tracheobronchial Sputum Crust Removal" procedure, and most of the crust was obscured by the retained endotracheal tube. The patient was discharged on the 20th day following therapeutic FOB. CONCLUSION: FOB examination may miss specific areas in endotracheal intubation (ETI) patients, particularly the tracheal wall between the subglottis and distal end of the tracheal catheter, where sputum crust can be concealed. When diagnostic examinations with FOB are inconclusive, high-resolution chest CT can be helpful in identifying hidden sputum crust.

Appeared inexplicable disorders of consciousness after general anesthesia tracheal tube drawing in endoscopic tympanoplasty.

Background: Disorders of consciousness (DOC) are neurocognitive disorders related to sharp fluctuations of attention and consciousness, while DOC is characterized by significant interindividual differences, rapid development, and a higher lethal rate. Case information: A 53-year-old female patient underwent general anesthesia with tracheal intubation in otoendoscopic tympanoplasty. The patient suddenly appeared moderate DOC after tracheal tube removal with K+ 3.6 (3.5-5.3 mmol/L). Based on the ancillary testing and routine laboratory workup, the possible causes of DOC, such as general anesthesia drugs and cardio cerebral events, were temporarily excluded. DOC was reversed by intravenous administration of KCl 1 g, with K+ 3.78 mmol/L. On one day after surgery, the patient occurred suddenly DOC again after intravenous guttae of 5% glucose 1000 ml, K+ 3.87 mmol/L, possibly because of her recurrent hypokalemic paralysis (HP) of past medical history. The patient's consciousness gradually improved after effective KCl supplementation therapy. Conclusion: DOC caused by periodic paralysis (PP) has not been reported, we speculate that hypoactive DOC is closely correlated with normokalemic periodic paralysis (NormoPP) in this case.

Study on the anti-tumor mechanism related to immune microenvironment of Bombyx Batryticatus on viral and non-viral infections of hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is a malignant primary liver cancer with poor prognosis. Most previous studies on anti-HCC effects of traditional Chinese medicines (TCM) have focused on the mechanism of direct action and few researchers considered that TCM can inhibit tumor progression and improve prognosis of HCC patients through regulating tumor microenvironment (TME). In this study, network pharmacology combined bioinformatics methods were employed to analysis mechanism of Bombyx batryticatus (B. batryticatus, one of the most frequently used traditional Chinese animal medicines, has been used in some Asian countries for centuries as an anticancer agent, anti-inflammatory agent, and antioxidant.) in regulating TME of HCC. The results showed that 24 core targets and 2 compounds were identified from overlapping between differential expression genes related to HCC in the cancer genome atlas (TCGA) database and targets of B. batryticatus in TCMSP database. For further analyzing the role of TME heterogeneity of HCC on anti-HCC mechanism of B. batryticatus, the correlation of core targets related with overall survival of HCC with TME cells in hepatitis C or hepatitis B virus-associated hepatocellular carcinoma (VIR) and non-hepatitis C or hepatitis B virus-associated hepatocellular carcinoma (NVIR) were calculated, respectively. The results showed that AKR1C3, SPP1 were significantly related with macrophages in VIR and other targets including NR1I2, CYP1A2 and CYP3A4 were significantly associated with macrophages in NVIR; the target protein AKR1C3 was significantly negative correlated with macrophages M1 in VIR (cor=-0.35, P-value<0.001) and the correlation between AKR1C3 and macrophages M1 was poor in NVIR group (cor = 0.064, P-value = 0.36). Additionally, survival curve of AKR1C3 showed that poor prognosis in VIR group can be related to high level of AKR1C3 (HR = 2.32, 95 % CI: 1.18-4.56, P-value = 0.012), and no signified gene can be found in NVIR group (P-value>0.05). In conclusion, the molecular mechanism of anti-HCC of B. batryticatus can be related to the tumor microenvironment to some extent. B. batryticatus may exert its anti-cancer effects and improve prognosis of patients by regulating macrophages M1 in VIR and NVIR through acting on different targets.

Ischemic postconditioning influences electron transport chain protein turnover in Langendorff-perfused rat hearts.

Ischemia postconditioning (IPo) is a promising strategy in reducing myocardial ischemia reperfusion (I/R) injury (MIRI), but its specific molecular mechanism is incompletely understood. Langendorff-perfused isolated rat hearts were subjected to global I/R and received IPo in the absence or presence of the mitochondrial ATP-sensitive potassium channel (mitoKATP) blocker 5-hydroxydecanoate (5-HD). Myocardial mitochondria were extracted and mitochondrial comparative proteomics was analyzed. IPo significantly reduces post-ischemic myocardial infarction and improved cardiac function in I/R rat hearts, while 5-HD basically cancelled IPo's myocardial protective effect. Joint application of two-dimensional polyacrylamide gel electrophoresis (2DE) and MALDI-TOF MS identified eight differentially expressed proteins between groups. Expression of cardiac succinate dehydrogenase (ubiquinone) flavoprotein subunit (SDHA) increased more than two-fold after I/R, while IPo led to overexpression of dihydrolipoyl dehydrogenase (DLD), NADH dehydrogenase (ubiquinone) flavoprotein 1 and isoform CRA_b (NDUFV1). When the mitoKATP was blocked, MICOS complex subunit Mic60 (IMMT) and Stress-70 protein (Grp75) were over expressed, while DLDH, ATPase subunit A (ATPA) and rCG44606 were decreased. Seven of the differential proteins belong to electron transport chain (ETC) or metabolism regulating proteins, and five of them were induced by closing mitoKATP in I/R hearts. We thus conclude that IPo's myocardial protective effect relies on energy homeostasis regulation. DLD, SDHA, NDUFV1, Grp75, ATPA and rCG44606 may contribute to IPo's cardial protective effect.

Connection changes in somatosensory cortex induced by different doses of propofol.

BACKGROUND: The mechanism by which general anesthetics, widely used in clinical practice for over 160 years, effects on sensory responsiveness has been unclear until now. In the present study, the authors sought to explore the effect of different doses of propofol on somatosensory cortex by whisker stimulation in rats. METHODS: In a fixed cage, rats were anesthetized with propofol 80 mg/kg intraperitoneally and then cathetered tail vein with 23-gauge metal needle connected with a pump. Two holes (2 mm diameter) were drilled and recording electrodes implantated in the primary somatosensory cortex barrel field (S1BF) and secondary somatosensory cortex (S2). The extracellular (20 rats) and intracellular (8 rats) recordings were used to test the neuron activity in both cortices at different doses of propofol (20, 40 and 80 mg/kg/h) through tail vein by pump. Meantime, vibrissal, olfactory, corneal responses (VOCR, sedation), and tail-pinch response (TRP, analgesia) were tested every 10 min during the doses of propofol 20, 40 and 80 mg/kg/h. RESULTS: VOCR and TRP were depressed by propofol in a dose-dependent manner. The amplitude by whisker stimulation in S1BF was stronger and the peak latency was shorter compared with that of in S2. The response latency of S1BF and S2 was increased by raising infusion rate of propofol with the response latency in S2 being longer than that in S1BF at the same doses of propofol. The cross-correlation between S1BF and S2 decreased as the propofol infusion rate increased. The input resistance was higher by increasing infusion rate of propofol. CONCLUSION: The sedation and analgesia effects of propofol were dose-dependent. Both the connectivity and instinctive oscillation between S1BF and S2 were proportionally modulated by the different doses of propofol.

Assessment of the effect of etomidate on voltage-gated sodium channels and action potentials in rat primary sensory cortex pyramidal neurons.

Although it is known that general anesthetics can suppress cortical neurons׳ activity, the underlying mechanisms are still poorly understood, especially the kinetic changes of voltage-gated Na(+) channels, which are mostly related to neuronal excitability. Some general anesthetics have been reported to affect the voltage-gated Na(+) channels in cell culture derived from humans and animals. However no one has ever investigated the effects of etomidate on voltage-gated Na(+) channels in pyramidal neurons using a brain slice. The present study uses a whole cell patch-clamp technique to investigate the changes of voltage-gated Na(+) channels on primary somatosensory cortex pyramidal neurons under the influence of etomidate. We found that etomidate dose-dependently inhibited Na(+) currents of primary somatosensory cortex pyramidal neurons, while shifted the steady-state inactivation curve towards the left and prolonged the recovery time from inactivation. Conversely, etomidate has no effects on the steady-state activation curve. We demonstrated the detailed suppression process of neural voltage-gated Na(+) channels by etomidate on slice condition. This may offer new insights into the mechanical explanation for the etomidate anesthesia. Finding the effects of anesthetics on primary somatosensory cortex also provides evidence to help elucidate the potential mechanism by which tactile information integrates during general anesthesia.

Protective effects of pinacidil hyperpolarizing cardioplegia on myocardial ischemia reperfusion injury by mitochondrial KATP channels.

BACKGROUND: Many studies have indicated that hyperpolarizing cardioplegia is responsible for myocardial preservation and researchers have suggested that the adenosine triphosphate-sensitive potassium channels (K(ATP)) were the end effectors of cardio-protection. But whether mitochondrial K(ATP) plays an important role in hyperpolarizing cardioplegia is not apparent. The present study investigated the effect of hyperpolarizing cardioplegia containing pinacidil (a nonselective K(ATP) opener) on ischemia/reperfusion injury in rat hearts, especially the role of mitochondrial K(ATP) in pinacidil hyperpolarizing cardioplegia. METHODS: Sprague-Dawley rat hearts were Langendorff-perfused for 20 minutes with Krebs-Henseleit buffer at 37°C before equilibration. Cardiac arrest was then induced in different treatments: there was no arrest and ischemia in the normal group, the control group were arrested by clamping the aorta, depolarizing caidioplegia (St. Thomas solution containing 16 mmol/L KCl) and hyperpolarizing cardioplegia groups used St. Thomas solution containing 0.05 mmol/L pinacidil and 5 mmol/L KCl to induce cardiac arrest in group hyperkalemic and group pinacidil, in group hyperkalemic + 5-hydroxydecanote (5HD) and Pinacidil + 5HD, 5HD (0.1 mmol/L) was added to the above two solutions to block mitochondria K(ATP) channels. Global ischemia was then administrated for 40 minutes at 37°C, followed by 30 minutes of reperfusion. At the end of equilibration and reperfusion, hemodynamics, ultrastructure, and mitochondrial function were measured. RESULTS: In the control group, ischemia/reperfusion decreased the left ventricular developed pressure, heart rate, coronary flow, mitochondrial membrane potential, impaired mitochondrial respiratory function, increased reactive oxygen species and left ventricular end diastolic pressure. Damage to myocardial ultrastructure was also evident. Both depolarized arrest and especially hyperpolarized cardioplegia significantly reduced these lesions. 5HD partially blocked the beneficial effects of pinacidil cardioplegia but showing no effects on hyperkalemic arrest. CONCLUSIONS: Pinacidil cardioplegia provides better cardioprotection with preservation of hemodynamics, ultrastructure, and mitochondrial function than traditional cardioplegia. The mitochondria K(ATP) channels may play an important role in the protection mechanism.