Psychomotor stimulant drugs such as caffeine, nicotine, amphetamine and cocaine, have been shown to improve vigilance in man under conditions of fatigue. Nicotine has also been shown to improve performance in some cognitive tests in patients with Alzheimer's disease. In rodents these drugs increase activity which may confound "performance enhancing effects" in rodent models. However, improvements have been found in a number of tests that do not seem to be directly dependent upon an enhancement of locomotor activation. In one example, Evenden and Robbins (1985) reported consistent improvements in a visual tracking test following amphetamine. The present study was undertaken to determine whether these performance enhancing effects of amphetamine could also be obtained with cocaine and apomorphine, which both have psychomotor stimulant effects through their actions as, respectively, indirect and direct dopamine agonists, and by caffeine and nicotine, which do not have a direct dopaminergic mechanism of action. The results of the study indicate that all five drugs improved tracking performance at one or more doses. The most consistent effects were obtained with amphetamine which, like cocaine and nicotine, improved tracking at a dose which did not produce other changes in behaviour. Taking into account previous studies (Evenden and Robbins 1983, 1985), these results were interpreted as indicating that psychomotor stimulant drugs produce a general activation of behaviour. At all but the highest doses of such drugs, the form of behaviour that is observed depends upon the environment.(ABSTRACT TRUNCATED AT 250 WORDS)
We assessed the feasibility of low energy endocardial defibrillation in patients with atrial fibrillation or atrial flutter who had failed a trial of pharmacological reversion with amiodarone. Low energy endocardial defibrillation under general anesthesia was attempted in 9 patients, 5 with atrial flutter and 4 with atrial fibrillation (median duration of arrhythmia 3.75 months). Two large surface area endocardial leads were introduced percutaneously and sited in the right atrial appendage and at the right ventricular apex. A cutaneous patch electrode was placed on the left thorax. Biphasic shocks synchronized to the ventricular electrogram were used to terminate atrial arrhythmias. Three electrode configurations were evaluated in the following sequence at each energy level: atrial cathode to ventricular anode; ventricular cathode to atrial anode; atrial cathode to a combined ventricular and cutaneous anode. If endocardial defibrillation failed (0.5-10 J), transthoracic defibrillation using 200 joules followed by 360 joules, if required, was performed. Endocardial defibrillation was successful in all five patients with atrial flutter (0.5 J, 1.0 J, 1.0 J, 4.0 J, and 10.0 J) but in only one patient with atrial fibrillation (10 J). On no occasion did successful defibrillation occur with one configuration when it had failed with an alternate configuration at that particular energy level. Ventricular fibrillation did not occur, and there were no other significant complications. Low energy endocardial defibrillation is feasible in patients with atrial flutter using large surface area electrodes. Although the success rate of atrial defibrillation was low, further work is required, particularly in patients with more recent onset of the arrhythmia and using a right to left electrode configuration.
The haemodynamic effects and pharmacokinetics of a single orally administered dose of 0.5 mg of prazosin have been compared in six patients with stable severe congestive cardiac failure. Administration of prazosin induced significant decreases in mean pulmonary capillary wedge pressure (from 27.5, s.e.m. = 4.5 to 19.4, s.e.m. = 5.1 mmHg; P less than 0.001), mean arterial blood pressure (from 94.5, s.e.m. = 6.0 to 85.4, s.e.m. = 5.0 mmHg; P less than 0.01), and systemic vascular resistance (from 1690, s.e.m. = 360 to 1420, s.e.m. = 200 dyn. s/cm5; P less than 0.05) and a rise in cardiac index from 1.98 (s.e.m. = 0.07) to 2.28 (s.e.m. = 0.16) litres/min per m2 (P less than 0.05). There was a non-significant fall in heart rate. Pharmacokinetic analysis revealed maximum plasma prazosin concentrations of 4.1 (s.e.m. = 1.4) ng/ml, occurring 2.1 (s.e.m. = 0.4) h after drug ingestion. The mean elimination half-life was 5.1 (s.e.m. = 0.8) h, which is longer than that found in our previous studies in normal subjects. There was considerable interindividual variation in peak plasma prazosin concentrations, elimination half-life and area under the concentration-time curve. While mean maximal haemodynamic effects of prazosin occurred at similar times to the peak plasma concentration of the drug, there was no significant correlation between the extent of haemodynamic response and individual pharmacokinetic parameters. It is concluded that significant and potentially beneficial haemodynamic effects occur with the initial administration of 0.5 mg oral dose of prazosin in patients with stable congestive cardiac failure and it is suggested that in many patients little advantage will be achieved with higher initial doses.
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