Point-of-care determination of neonatal bilirubin with the blood gas analyzer RapidLab 1265.

BACKGROUND: The aim of the study was to evaluate the comparability of the new neonatal bilirubin method on the RapidLab 1265 blood gas analyzer. This point-of-care testing (POCT) device has the option for the determination of neonatal bilirubin, making it potentially valuable for use in neonate intensive care units or in outpatient ambulances. METHODS: We paired 240 patient samples for intermethod comparisons between the new POCT method and the routine laboratory method (Vitros 350 chemistry system with BuBc slide). In parallel, a transcutaneous jaundice meter (JM-103) was applied to the newborns. Low birthweight and premature neonates were excluded from the trial. The turn-around-time (TAT) for the POCT method was also compared with the routine method, and the practicality of the new analyzer was evaluated for clinical purposes. RESULTS: Bilirubin measurements using the RapidLab 1265 are suitable for the application in newborns. For imprecision, coefficients of variation between 5.6% and 23% were found. The correlation between the Vitros 350 (x) and RapidLab 1265 (y) was y=1.0x-0.1 (r=0.91), with a mean bias of +0.1 mg/dL and a 95% limit of agreement of ±2.5 mg/dL. As in all POCT methods, the TAT was significantly lower than that of the core laboratory. CONCLUSIONS: In contrast to the JM-103, the results of the RapidLab 1265 correlated closely with the Vitros 350, although occasional results of both methods were more different than expected. In general, the RapidLab 1265 blood gas analyzer provides clinically useful bilirubin results using neonatal whole blood samples, although imprecision data are higher than for the laboratory method. The POCT device is suitable for neonatal intensive care units after thoroughly training the employees that will use the device.

Nitrated fatty acids suppress angiotensin II-mediated fibrotic remodelling and atrial fibrillation.

AIM: Atrial fibrosis, one of the most striking features in the pathology of atrial fibrillation (AF), is promoted by local and systemic inflammation. Electrophilic fatty acid nitroalkenes, endogenously generated by both metabolic and inflammatory reactions, are anti-inflammatory mediators that in synthetic form may be useful as drug candidates. Herein we investigate whether an exemplary nitro-fatty acid can limit atrial fibrosis and AF. METHODS AND RESULTS: Wild-type C57BL6/J mice were treated for 2 weeks with angiotensin II (AngII) and vehicle or nitro-oleic acid (10-nitro-octadec-9-enoic acid, OA-NO2, 6 mg/kg body weight) via subcutaneous osmotic minipumps. OA-NO2 significantly inhibited atrial fibrosis and depressed vulnerability for AF during right atrial electrophysiological stimulation to levels observed for AngII-naive animals. Left atrial epicardial mapping studies demonstrated preservation of conduction homogeneity by OA-NO2. The protection from fibrotic remodelling was mediated by suppression of Smad2-dependent myofibroblast transdifferentiation and inhibition of Nox2-dependent atrial superoxide formation. CONCLUSION: OA-NO2 potently inhibits atrial fibrosis and subsequent AF. Nitro-fatty acids and possibly other lipid electrophiles thus emerge as potential therapeutic agents for AF, either by increasing endogenous levels through dietary modulation or by administration as synthetic drugs.

The effect of sevoflurane and propofol on cerebral neurotransmitter concentrations during cerebral ischemia in rats.

UNLABELLED: Sevoflurane and propofol are neuroprotective possibly by attenuating central or peripheral catecholamines. We evaluated the effect of these anesthetics on circulating catecholamines and brain neurotransmitters during ischemia in rats. Forty male Sprague-Dawley rats were randomly assigned to one of the following treatment groups: fentanyl and N(2)O/O(2) (control), 2.0% sevoflurane, 0.8-1.2 mg x kg(-1) x min(-1) of propofol, and sham-operated rats with fentanyl and N(2)O/O(2). Ischemia (30 min) was produced by unilateral common carotid artery occlusion plus hemorrhagic hypotension to a mean arterial blood pressure of 32 +/- 2 mm Hg. Pericranial temperature, arterial blood gases, and pH value were maintained constant. Cerebral catecholamine and glutamate concentrations, sampled by microdialysis, and plasma catecholamine concentrations were analyzed using high-pressure liquid chromatography. During ischemia, circulating catecholamines were almost completely suppressed by propofol but only modestly decreased with sevoflurane. Sevoflurane and propofol suppressed brain norepinephrine concentration increases by 75% and 58%, respectively, compared with controls. Intra-ischemia cerebral glutamate concentration was decreased by 60% with both sevoflurane and propofol. These results question a role of circulating catecholamines as a common mechanism for cerebral protection during sevoflurane and propofol. A role of brain tissue catecholamines in mediating ischemic injury is consistent with our results. IMPLICATIONS: During incomplete cerebral ischemia, the neuroprotective anesthetics sevoflurane and propofol suppressed cerebral increases in norepinephrine and glutamate concentrations. In contrast, propofol, but not sevoflurane, suppressed the ischemia-induced increase in circulating catecholamines to baseline levels. The results question a role for plasma catecholamines in cerebral ischemic injury.