[Alpha and beta sympathomimetics. Principles and rules of use].
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In suspected Horner's syndrome, cocaine eye drops are applied to verify the diagnosis. Subsequent application of hydroxyamphetamine or pholedrine eye drops allows localization of the site of the interruption in the oculosympathetic pathway. In the present study the influence of cocaine on subsequent pholedrine testing was examined. Cocaine 5% and pholedrine 5% eye drops were applied to eight (72-h interval only six) normal volunteers with light-colored irides. The ages of the subjects ranged from 23 to 40 years. Eye drops were applied to the same eye at varying intervals of up to 72 h, with the cocaine being given between 8:30 and 9:30 a.m. Pupil diameters were recorded by means of a frame-grabber card in a personal computer and were subsequently measured before and at 50-60 min after each drug application in 1.7 cd/m2 ambient light. In the absence of pretreatment with cocaine, pholedrine changed the mean pupil diameter from 6.89 to 8.57 mm. At 12 h after cocaine pretreatment the pupil remained dilated. Pholedrine dilated the pupil further, from 7.69 to 8.61 mm. When cocaine was given 24 h before pholedrine, the pupil dilated from 6.75 to 8.25 mm; at 48 h after cocaine application, pholedrine dilated the pupil from 6.14 to 8.20 mm; and at 72 h after cocaine pretreatment, pholedrine dilated the pupil from 5.74 to 8.00 mm. As compared with the mean diameter of the untreated contralateral pupil, the pholedrine-induced dilation amounted to 2.32 mm in the absence of cocaine pretreatment, 1.04 mm at 12 h after cocaine application, 1.29 mm at 24 h after cocaine administration, 1.89 mm at 48 h after cocaine pretreatment, and 2.18 mm at 72 h after cocaine application. The residual cocaine effect interfered with the mean pupil dilation produced by pholedrin for at least 48 h. To ensure that the sensitivity of the pholedrine test is maximal, the examiner should delay its use for more than 48 h after the cocaine test.
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A toxicological method of sensitive and specific confirmation of methamphetamine and other primary and secondary amines in biological samples after extractive perfluorobenzoylation is described. The method is based on the principle of gas chromatography with parallel specific nitrogen detection and electron capture detection. The other alternative is the gas chromatography combined with mass spectrometry in chemical ionization mode. The method described allows the detection of methamphetamine and amphetamine in urine in concentrations below 10 ng/ml.
PURPOSE: To assess the influence of inotropic IV therapy--dobutamine and/or dopamine--versus vasodilator therapy--nitroprusside, captopril or hydralazine--in aortic flow ejection phase indexes obtained by pulsed Doppler echocardiography. METHODS: In 17 patients admitted to the ICU (11 males, 62 +/- 14 years, 9 with ischemic cardiomyopathy and 8 with dilated cardiomyopathy, all in sinus rhythm), with congestive heart failure, and submitted to tailored therapy, 53 serial pulsed Doppler and hemodynamic evaluations were made as the therapy changed the hemodynamic and clinical status. Considering serial consecutive evaluations, a hemodynamic improvement was obtained only with inotropics in 13 (group A), and with vasodilators in only 15 (group B). The following ejection phase indexes were calculated from Doppler registers: average acceleration (AvAc) and ejection force (EFor), calculated according to the formula: Efor = 1.06 x Aortic Orifice Area x AvAc x Acceleration Velocity Time Integral. RESULTS: Arterial blood pressure increased in gr A (76.2 +/- 14.1 to 81.4 +/- 14.8 mm Hg, p < 0.05) and decreased in gr B (85.1 +/- 12.6 to 76.2 +/- 9.7 mm Hg (p < 0.05). In both groups there was a significant (p < 0.05) increase in cardiac output (CO)-from 3.9 +/- 1.1 to 4.9 +/- 1.4 L/min in group A, and from 3.9 +/- 1.2 to 4.4 +/- 1.2 L/min in group B. CO increased 18.7% in group A and 13.8% in group B (NS). There was a decrease in pulmonary capillary wedge pressure (PCWP) from 19.5 +/- 6.0 to 15.1 +/- 5.8 mm Hg in group A (p < 0.05), and from (16.9 +/- 5.7 to 12.1 +/- 4.6 mm Hg in group B (p < 0.05). PCWP decreased 19.7% in group A and 27.8% in group B (NS). Systemic vascular resistance (SVR) changed from 18.2 +/- 7.0 to 16.2 +/- 7.1 Wood U in group A (p < 0.05), and from 22.3 +/- 9.3 to 17.7 +/- 5.7 Wood U in group B (p < 0.05). In group A, AvAc increased-from 1347 +/- 611 cm.s-2 (p < 0.05), as did Efor-from 15.4 +/- 10.7 to 20.2 +/- 11.0 g.cm,s-2 (p < 0.05), whereas in group B there was no significant change in either AvAc-from 1337 +/- 284 to 1277 +/- 256 cm.s-2, or Efor-from 22.7 +/- 17.0 to 23.8 +/- 15.0 g.cm.s-2. CONCLUSIONS: Vasodilator therapy, although inducing hemodynamic changes similar to inotropics, does not alter the ejection phase indexes. Therefore, AvAc and Efor, in spite of being calculated from the aortic flow, are independent of the changes in PCWP and SVR and seem to reflect changes in inotropism in the clinical setting.
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Beta blockade constitutes efficient therapy for stable angina pectoris. The effects of lowering blood pressure and heart rate with such treatment are not always desired. Epanolol is a beta 1-selective partial agonist with minor effects on blood pressure and heart rate at rest. Atenolol is a pure beta 1-selective antagonist with more pronounced effects on blood pressure and heart rate at rest. The effects of epanolol, 200 mg o.d., and atenolol, 100 mg o.d., were compared in 173 middle-aged patients with stable angina pectoris in a randomized, double-blind, parallel group-controlled study for one year. No significant differences were shown in angina attack rate, nitrate consumption, or exercise performance. Resting heart rate and blood pressure were significantly lower on atenolol. Epanolol tended to be better tolerated than atenolol, as shown by visual analogue scales of well-being, activity, energy, and warm extremities, further supported by fewer reports on possible adverse reactions. In conclusion, epanolol appears to be as effective as atenolol and better tolerated in patients with stable angina pectoris.