We test the hypothesis that quantitative electroencephalogram (qEEG) can be used to objectively assess functional electrophysiological recovery of brain after hypothermia in an asphyxial cardiac arrest rodent model. Twenty-eight rats were randomly subjected to 7-min (n = 14) and 9-min (n = 14) asphyxia times. One half of each group (n = 7) was randomly subjected to hypothermia (T = 33 degrees C for 12 h) and the other half (n = 7) to normothermia (T = 37 degrees C). Continuous physiologic monitoring of blood pressure, EEG, and core body temperature monitoring and intermittent arterial blood gas (ABG) analysis was undertaken. Neurological recovery after resuscitation was monitored using serial Neurological Deficit Score (NDS) calculation and qEEG analysis. Information Quantity (IQ), a previously validated measure of relative EEG entropy, was employed to monitor electrical recovery. The experiment demonstrated greater recovery of IQ in rats treated with hypothermia compared to normothermic controls in both injury groups (P < 0.05). The 72-h NDS of the hypothermia group was also significantly improved compared to the normothermia group (P < 0.05). IQ values measured at 4 h had a strong correlation with the primary neurological outcome measure, 72-h NDS score (Pearson correlation 0.746, 2-tailed significance <0.001). IQ is sensitive to the acceleration of neurological recovery as measured NDS after asphyxial cardiac arrest known to occur with induced hypothermia. These results demonstrate the potential utility of qEEG-IQ to track the response to neuroprotective hypothermia during the early phase of recovery from cardiac arrest.

BackgroundRecent experimental studies have revealed that n-3 fatty acids, such as eicosapentaenoic acid (EPA) regulate postprandial insulin secretion, and correct postprandial glucose and lipid abnormalities. However, the effects of 6-month EPA treatment on postprandial hyperglycemia and hyperlipidemia, insulin secretion, and concomitant endothelial dysfunction remain unknown in patients with impaired glucose metabolism (IGM) and coronary artery disease (CAD).Methods and resultsWe randomized 107 newly diagnosed IGM patients with CAD to receive either 1800 mg/day of EPA (EPA group, n = 53) or no EPA (n = 54). Cookie meal testing (carbohydrates: 75 g, fat: 28.5 g) and endothelial function testing using fasting-state flow-mediated dilatation (FMD) were performed before and after 6 months of treatment. The primary outcome of this study was changes in postprandial glycemic and triglyceridemic control and secondary outcomes were improvement of insulin secretion and endothelial dysfunction. After 6 months, the EPA group exhibited significant improvements in EPA/arachidonic acid, fasting triglyceride (TG), and high-density lipoprotein cholesterol (HDL-C). The EPA group also exhibited significant decreases in the incremental TG peak, area under the curve (AUC) for postprandial TG, incremental glucose peak, AUC for postprandial glucose, and improvements in glycometabolism categorization. No significant changes were observed for hemoglobin A1c and fasting plasma glucose levels. The EPA group exhibited a significant increase in AUC-immune reactive insulin/AUC-plasma glucose ratio (which indicates postprandial insulin secretory ability) and significant improvements in FMD. Multiple regression analysis revealed that decreases in the TG/HDL-C ratio and incremental TG peak were independent predictors of FMD improvement in the EPA group.ConclusionsEPA corrected postprandial hypertriglyceridemia, hyperglycemia and insulin secretion ability. This amelioration of several metabolic abnormalities was accompanied by recovery of concomitant endothelial dysfunction in newly diagnosed IGM patients with CAD.Clinical Trial Registration UMIN Registry number: UMIN000011265 (https://www.upload.umin.ac.jp/cgi-open-bin/ctr/ctr.cgi?function=brows&action=brows&type=summary&recptno=R000013200&language=E)Electronic supplementary materialThe online version of this article (doi:10.1186/s12933-016-0437-y) contains supplementary material, which is available to authorized users.

In this paper, we provide a quantitative electroencephalogram (EEG) analysis to study the effect of hypothermia on the neurological recovery of brain after cardiac arrest. We hypothesize that the brain injury results in a reduction in information of the brain rhythm. To measure the information content of the EEG a new measure called information quantity (IQ), which is the Shannon entropy of decorrelated EEG signals, is developed. For decorrelating EEG signals, we use the discrete wavelet transform (DWT) which is known to have good decorrelating properties and to show a good match to the standard clinical bands in EEG. In measuring the amount of information, IQ shows better tracking capability for dynamic amplitude change and frequency component change than conventional entropy-based measures. Experiments are carried out in rodents (n = 30) to monitor the neurological recovery after cardiac arrest. In addition, EEG signal recovery under normothermic (37 °C) and hypothermic (33 °C) resuscitation following 5, 7, and 9 min of cardiac arrest is recorded and analyzed. Experimental results show that the IQ is greater for hypothermic than normothermic rats, with an IQ difference of more than 0.20 (0.20 ± 0.11 is 95% condidence interval). The results quantitatively support the hypothesis that hypothermia accelerates the electrical recovery from brain injury after cardiac arrest.

The effect of smoking for postoperative pulmonary complications (PPCs) in minor surgical patients who have an early recovery has not been evaluated. Smoking may also affect intraoperative sputum volume. We thus evaluated whether smoking had a relation to intraoperative sputum volume or PPCs in minor surgical patients. Smoking status was determined through the interviewer-assisted questionnaires. Intraoperative sputum volume was judged using the number of trials to suck up sputum from the trachea. Current and Ex-smokers were significantly more likely to have an increased intraoperative sputum volume when compared with Non-smokers (18.3% and 17.9% vs. 9.4%) although the relationship between smoking and PPCs was not demonstrated. In the multivariate models, Current and Ex-Smokers was identified as an independent risk factor of an increased intraoperative sputum volume (odds ratio, 2.7; 95% confidence interval, 1.6-4.6). The patients with < 2 months smoking cessation were more likely to have an increased intraoperative sputum volume. In conclusion, smoking is the risk factor of an increased intraoperative sputum volume, and preoperative smoking cessation > or = 2 months is recommended to reduce the risk of an increased intraoperative sputum volume, although the relationship between smoking and PPCs was not elucidated in minor surgical patients.

Preoperative small-dose ketamine, IV, significantly prevented a systemic arterial pressure increase during prolonged tourniquet inflation in patients under general anesthesia.

Intermediate CD14++CD16+monocytes might be closely related to the pathogenesis of AF and reflect functional remodelling of the left atrium.

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Transmural dispersion of repolarization and the number of patients with VT/VF decreased over time after CRT. Patients with reverse remodelling demonstrated a lower rate of VT/VF and a greater time-dependent reduction of TDR.