Correction to: "in-vitro examination of the positive inotropic effect of caffeine and taurine, the two most frequent active ingredients of energy drinks".

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In-vitro examination of the positive inotropic effect of caffeine and taurine, the two most frequent active ingredients of energy drinks.

BACKGROUND: Our study aimed to evaluate changes in the contractile behavior of human myocardium after exposure to caffeine and taurine, the main active ingredients of energy drinks (EDs), and to evaluate whether taurine exhibits any inotropic effect at all in the dosages commonly used in EDs. METHODS: Myocardial tissue was removed from the right atrial appendages of patients undergoing cardiac surgery and prepared to obtain specimens measuring 4 mm in length. A total of 92 specimens were exposed to electrical impulses at a frequency of 75 bpm for at least 40 min to elicit their maximum contractile force before measuring the isometric contractile force (ICF) and duration of contraction (CD). Following this, each specimen was treated with either taurine (group 1, n = 29), or caffeine (group 2, n = 31) or both (group 3, n = 32). After exposure, ICF and CD measuring were repeated. Post-treatment values were compared with pre-treatments values and indicated as percentages. RESULTS: Exposure to taurine did not alter the contraction behavior of the specimens. Exposure to caffeine, in contrast, led to a significant increase in ICF (118 ± 03%, p < 0.01) und a marginal decrease in CD (95 ± 1.6%, p < 0.01). Exposure to a combination of caffeine and taurine also induced a statistically significant increase in ICF (124 ± 4%, p < 0.01) and a subtle reduction in CD (92 ± 1.4%, p < 0.01). The increase in ICF achieved by administration of caffeine was similar to that achieved by a combination of both caffeine and taurine (p = 0.2). The relative ICF levels achieved by administration of caffeine and a combination of taurine and caffeine, respectively, were both significantly higher (p < 0.01) than the ICF resulting from exposure to taurine only. CONCLUSION: While caffeine altered the contraction behavior of the specimen significantly in our in-vitro model, taurine did not exhibit a significant effect. Adding taurine to caffeine did not significantly enhance or reduce the effect of caffeine.

Snoring and upper airway properties.

Habitual snoring in adults may be related to upper airway dysfunction, although the precise relationship has never been studied. We quantitatively measured snoring and correlated it with upper airway properties in 50 apneic and 59 nonapneic adult male patients. Both groups were similar in terms of nasal airflow resistance and pulmonary function tests. We found a significant correlation between the severity of snoring and nasal airflow resistance in both groups, and between the severity of snoring and pharyngeal and glottic areas in the apneic group. We conclude that snoring may be associated with abnormalities in upper airway properties.

Site of upper airway obstruction in patients with idiopathic obstructive sleep apnea.

We developed a technique to determine the site of upper airway obstruction in patients with idiopathic obstructive sleep apnea (OSA). This technique is based on the analysis of inspiratory airflow pressures at various levels of the pharyngeal airway during sleep. Pharyngeal pressure was measured by a moveable Millar catheter pressure transducer. The catheter's position in the airway was localized radiographically. Ten patients with OSA were tested: five patients were found to have upper airway obstruction at the level of the soft palate, and five had upper airway obstruction at the base of the tongue. We concluded that measuring airway pressures at multiple sites along the airway is useful in localizing the site of obstruction in patients with OSA, and may have important implications in terms of the patient's response to surgical treatment.

Simulated septal deviations.

Effects of simulated septal deviations on nasal airflow resistance were measured in two healthy young adults by computer-assisted rhinomanometry. Within the decongested bony cavum, simulated deviations, 30 x 5 x 5 mm perpendicular to the maxillary crest, elevated resistance only slightly, but severely when the mucosa was not decongested. Caval resistance was unaffected by simulated maxillary crest spurs, 30 x 5 x 5 mm, in either vascular state. Between inferior turbinate and anterior naris, 5-mm septal protrusions from floor to roof increased resistance severely, but when shortened by one third, their resistive effects were markedly decreased, especially when positioned near the roof. The cavum can accommodate large septal spurs, deviations, and congested mucosa with little effect on airflow resistance. By contrast, resistance of the anterior nasal airway beyond the inferior turbinate bone is acutely responsive to changes in mucosal congestion and to septal protrusions, especially when they are situated near the floor of the nose.

The obstructive nasal septum. Effect of simulated deviations on nasal airflow resistance.

Effects of simulated septal deviations on nasal airflow resistances were assessed by rhinomanometry in healthy human adults. Obstructions 5 x 15 mm protruding 1 to 5 mm into the nasal lumen were applied to the septum in untreated and decongested nasal cavities. The most resistive septal site was located opposite the caudal edge of the upper lateral cartilage where a 3-mm deviation increased resistance substantially in untreated noses, but produced no resistive effect when the mucosa was decongested, whereas a 4-mm deviation increased resistance severely at this site in untreated and decongested noses. Deviations at the caudal end of the septum that overlapped the upper lateral cartilage were markedly resistive also, while near the cavum they were less resistive. Decongestion reduced resistance and length of this anterior-resistive nasal segment. By contrast, within the cavum neither deviations of 5 mm nor mucosal status affected resistance. It is concluded that airflow resistance of the nasal cavum is unresponsive to septal deviations and mucosal status, but the anterior part of the nose is most susceptible and differences of 1 mm in lumen can be critical.

The shape of a normal smile: implications for facial paralysis reconstruction.

Sophisticated smile reconstruction for facial paralysis requires an understanding of the facial movements during a normal smile. This study analyzes the direction and extent of movement of the upper and lower lips, nasal labial folds, and nasal base during smiling. Twenty normal subjects were analyzed using cine studies. A stop frame vector analysis was done on reference points on the lips and lower face. The greatest movement occurred at the commissure and upper lip. Intersubject variation in direction and extent of movement is great. Intrasubject variation in movement in comparing left and right sides was also quite large. Techniques of facial paralysis reconstruction that apply forces to the mouth, which mimic the vectors of movement on the patients' normal side, are most likely to provide a symmetrical smile reconstruction.

Unilateral and bilateral nasal resistances.

Plethysmographic rhinomanometric resistance measurements of combined and separate nasal cavities were made at a transnasal differential pressure of 100 Pa. The coefficients of variation over time of 40 consecutive total resistance values obtained at 1 min intervals from untreated noses of five healthy subjects averaged 11.0% measured directly and 11.8% calculated by application of Ohm's Law for parallel resistors. Measurements at 5 min intervals between sides increased variation of calculated total resistances markedly. The coefficients decreased to 4.7% and 5.1% respectively when the noses were decongested and by contrast with untreated noses these resistances varied independently from each other. Facial masking increased the coefficient of variation of resistance in the decongested nose (p less than 0.001) to as much as 11.0% and the magnitude of averaged resistances was moderately increased also (p less than 0.035). Measured values plotted against calculated values for total nasal resistance of 45 consecutive patients produced a regression differing insignificantly (p = 0.94) from the line of identity in the decongested nose but diverging from it (intercept 0.03 Pa/cm3/sec and slope 0.83, p less than 0.03) when the nose was untreated. Resistive variations associated with mucovascular instability and with use of a face-mask contribute substantially to differences between the results of anterior and posterior rhinomanometric assessments of total nasal resistance.

Computer averaged nasal resistance.

Nasal resistances were measured before and after decongestion of the nasal mucosa by posterior rhinomanometry with a head-out body plethysmograph in 95 adults referred to our nasal airflow laboratory. These resistances were calculated by a time averaging method (1), the equation R = delta P/V at delta P 1.0 cm H2O (2) and R = delta P/V at the point of peak flow (3), and the results were compared. Correspondence between resistances from the time averaging method and those from the equation R = delta P/V at delta 1.0 cm H2O, the equation R = delta P/0.83V1.33 was obtained with statistical significance (P less than 0.001) and it is suggested that the value of resistance from the time averaging method represents transitional airflow. At resistances less than 3.5 cm H2O/L/sec, the time averaging method and the equation R = delta P/V at delta 1.0 cm H2O and at peak flow produced almost identical values. At resistances greater than 3.5 cm H2O/L/sec, the time averaging method produced values equivalent to those from the equation R = delta P/V at peak flow but values from the equation R = delta P/V at delta P 1.0 cm H2O different from the former two methods. The results suggest that nasal resistances from the time averaging method and the equation R = delta P/V at the point of peak flow are appropriate expression of nasal patency.