Characterization of cigar tobaccos by gas chromatographic/mass spectrometric analysis of nonvolatile organic acids: application to the authentication of Cuban cigars.

A reliable method based on gas chromatographic/mass spectrometric (GC/MS) profiling of nonvolatile organic acids is described for the characterization of cigars. The method involves an aqueous extraction of ground tobacco and selective isolation of the acids by simply stirring strong anion exchange (SAX) disks in the aqueous tobacco extract. The acids are then directly silylated on the disk with N-methyl-N-trimethylsilyl-trifluroacetamide (MSTFA) in acetonitrile in an autosampler vial. Elution of the derivatized acids in situ allows the sample to be directly analyzed by GC/MS without further sample handling. Compared to the conventional disk-extraction technique using a vacuum manifold, this method is much less labor intensive, and is desirable for multiple sample analysis. Nicotinic acid, succinic acid, glyceric acid, malic acid, pyroglutamic acid, threonic acid, citric acid, uracil, and an unidentified acid were reproducibly quantified in tobacco samples. Principal component analysis (PCA) of the acid profiles of the filler tobaccos of 18 Cuban cigars and 31 non-Cuban cigars shows separation of the two groups, indicating that the acid profiles are potentially useful in the authentication of Cuban cigars.

Effects of nicardipine on left ventricular hemodynamic patterns in systemic hypertension.

To assess left ventricular (LV) functional and structural changes associated with the reduction of blood pressure (BP) values during nicardipine administration (60 mg daily, for two months), 17 hypertensive patients were studied by M-mode echocardiography, according to a double-blind design (11 with nicardipine and six with placebo). Decrease in BP induced by nicardipine was associated with decrease in myocardial afterload (end-systolic stress) (P less than .002) and improvement of systolic function (fractional shortening) (P less than .02), without changes in inotropic state (assessed by systolic BP/end-systolic dimension/posterior wall thickness ratio). At the end of trial, a 5% reduction was found in LV mass (P less than .002), whereas relative wall thickness did not change. Diastolic phase (assessed by relaxation time index, and the slope of EF tract of the anterior mitral valve leaflet) was improved (.01 less than P less than .001). Patients with concentric and eccentric hypertrophy were separately considered. Relaxation time index and fractional shortening were significantly improved only in patients with concentric hypertrophy (P less than .01), whereas in the other ones the effect of treatment was variable. These differences were probably due to different effects on preload in the two LV hemodynamic patterns. Thus, nicardipine shows powerful effects on cardiac mechanics in systemic hypertension, but these effects are different according to LV anatomic pattern. Only in the presence of concentric hypertrophy is it possible to foresee the improvement of LV function; LV hypertrophy can be also reduced in concentric hypertrophy, but in the short term the reduction is too small to assume pathophysiologic significance.

[Echocardiographic analysis of anatomical and functional changes in the left heart ventricle during antihypertensive treatment with nicardipine]. / Analisi ecocardiografica delle variazioni anatomiche e funzionali del ventricolo sinistro in corso di trattamento antiipertensivo con nicardipina.

Changes in hemodynamic variables regulating systolic function were assessed by M-mode echocardiography, under 2D control, in 11 patients with primary uncomplicated hypertension treated with nicardipine (60 mg/daily). At the end of treatment (8 weeks) blood pressure and end-systolic stress were greatly reduced (p less than 0.001), and systolic fractional shortening was increase (p less than 0.02). The percentage increase in fractional shortening was correlated with a decreased in end-systolic stress (r = 0.67). The index of left ventricular performance (systolic pressure/end-systolic dimension ratio) was reduced: no variation was found in the hypertrophy-independent index of the inotropic state (systolic pressure/end-systolic dimension ratio normalized for posterior wall thickness). No change in the inotropic state was caused by a negligible sympathetic reflex outflow: heart rate also remained unchanged. The only index of left ventricular hypertrophy which was slightly reduced after two months of treatment was left ventricular mass (p less than 0.001). In conclusion, the short-term treatment with nicardipine, in hypertensive patients, showed powerful effects in the improvement of systolic function; the possible regression of left ventricular hypertrophy must be confirmed in long-term therapy.

Supernormal contractility in primary hypertension without left ventricular hypertrophy.

Forty-three subjects with uncomplicated primary hypertension and without echocardiographic left ventricular hypertrophy and 54 normotensive volunteers were studied by two-dimensional targeted M-mode echocardiography to evaluate systolic function and contractility before the development of compensatory hypertrophy. The ratio of peak systolic pressure to end-systolic dimension was used to assess left ventricular performance and was divided for either posterior wall thickness or cross-sectional area to generate hypertrophy-independent indices of inotropic state. Fractional shortening was normal in the hypertensive group, despite the increase in end-systolic stress. Systolic pressure/dimension ratio was higher in hypertensive subjects (p less than 0.001), as were hypertrophy-independent indices of inotropic state (p less than 0.005), which were inversely correlated to left ventricular mass (p less than 0.001). Values in 11 hypertensive subjects were above the upper confidence limit of the normal shortening/stress relation, which provides a load-independent measure of inotropic state. They showed high hypertrophy-independent indices of inotropic state (p less than 0.01), while the other hypertensive subjects did not. High fractional shortening, wall stress, and systolic pressure (p less than 0.01) were found in the subgroup with supernormal performance, while left ventricular mass was not different from that of other subgroups, depicting inadequate left ventricular hypertrophy. The duration of hypertension was the same in the subgroups. Supernormal inotropic state could be considered one form of primary adaptation to high wall stress that serves to maintain systolic ventricular performance.

Echocardiographic indexes of left ventricular contractility. Effect of load manipulation in arterial hypertension.

Load changes were obtained in 7 females with untreated primary hypertension by means of controlled intravenous infusion of sodium nitroprusside (0.2 mg/ml), in order to assess variations in the more usual indexes of left ventricular (LV) contractility to different loads and to verify that those indexes were independent of load. 2D-controlled M-mode echocardiograms were performed at baseline and when systolic blood pressure (SBP) had been reduced by 7, 16 and 23% for at least 5 min. Heart rate did not change during the test; decrease in SBP was associated with either decreases in both end-systolic dimension (LVIDs) and end-systolic stress (ESS), or an increase in systolic function. SBP/LVIDs, SBP/end-systolic volume (ESV) and ESS/LVIDs ratios were examined and compared as indexes of contractile state. SBP/ESV and ESS/LVIDs ratios showed great variation at all stages as compared to baseline values, while the SBP/LVIDs ratio did not change. The percent variation between the baseline values and the last stage of the test was 51% for the ESS/LVIDs ratio, 37% for the SBP/ESV and 5% for the SBP/LVIDs ratio. Best-fitting regression showed that a linear relationship existed only between SBP and LVIDs. Echocardiographic two-dimensional (as ESS) or three-dimensional derivations (as ESV) should be carefully employed when the contractile state is studied, while the SBP/LVIDs ratio can be easily used as a baseline value, as it is insensitive to changes in load.

Hemodynamic hypertrophied left ventricular patterns in systemic hypertension.

The hemodynamic pattern of hypertrophied left ventricle in systemic hypertension was studied by M-mode echocardiography in 42 untreated hypertensive patients with left ventricular (LV) mass index greater than 2 standard deviations from the sex-specific mean of 114 normal subjects (normal values of our laboratory), and in 45 normotensive volunteers. Hypertensive patients showed cardiac dimensions, relative diastolic wall thickness, ratio of systolic pressure to end-systolic dimension, cardiac index and stroke index greater than normotensive control subjects (0.01 less than p less than 0.0001). Pressure/dimension ratio was correlated to relative wall thickness (p less than 0.005). End-systolic stress/volume ratio was normal as was systolic pressure to dimension ratio normalized for end-diastolic wall thickness. LV hypertrophy was concentric in 26% and eccentric in 74% of patients and suggested 2 different heart adaptations to overload: eccentric hypertrophy was associated with increased cardiac dimensions, high peak stress, normal systolic function and moderately increased LV contractility; concentric hypertrophy was associated with the highest blood pressure values, normal cardiac dimension, normal peak stress, normal systolic function and much increased LV contractility. Because stress/volume ratio and wall thickness-corrected systolic pressure/dimension ratio were normal in hypertensive patients, LV contractile capacity might be supported by the increase in myocardium available for contraction, rather than by increase in inotropic state.