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.

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.