Biomedical subjects
Publications and source records attributed to B A Spencer.
Informed selection of treatment requires knowledge of the size and composition of a calculus. Spiral CT has a growing role in the detection of calculi, with an overall accuracy in excess of 95%. Moreover, the margin of error in determining stone size does not exceed 3.6%, and stone volume is underestimated by <5%. Pixelograms, the compilation of multiple points of attenuation, may provide clues to stone composition and durility.
The advantages of nonenhanced helical CT for the diagnosis of ureteral calculi include rapid scan time and patient throughput, safety (no contrast, less radiation), cost-effectiveness, high accuracy, minimal invasiveness, and ability to suggest of alternative diagnoses for flank pain--urologic and otherwise. Size measurement and location in the ureter, the two most important determinants of therapy, are precise with CT. It is particularly good for imaging small or radiolucent calculi, and calculi located at the ureterovesical. Secondary signs of obstruction and the soft-tissue rim sign are additional aids to the routine diagnosis of ureteral calculi. CT numbers indicate the fragility and therefore the likelihood of successful treatment of a calculus. Postprocessing options may help guide management decisions and may help plan interventions. The authors' experience after 30 months of using helical CT exclusively in the work-up of ureteral colic has been extremely favorable. Without hesitation, the authors believe that nonenhanced helical CT is the study of choice for the work-up of ureteral calculi.
New Zealand albino rabbits received classical conditioning training in which a 35-sec tone conditioned stimulus was paired with a bolus injection of methoxamine hydrochloride (Vasoxyl), an alpha 1-adrenergic agonist. Heart rate (HR) and blood pressure (BP) responses were recorded. Methoxamine produced a precipitous rise in BP and bradycardia as an unconditioned response (UR); pairings of tone and methoxamine over a 5-day period resulted in a gradually appearing tachycardia conditioned response (CR) which occurred shortly following tone onset. On the other hand, the BP CR was a pressor response. Accordingly, the HR CR was opposite in direction and, thus, apparently compensatory to the UR, whereas the BP CR was similar in direction to the UR. Neither of these cardiovascular changes were observed in control animals receiving either unpaired presentations of tone and methoxamine or tones paired with physiological saline. Most animals receiving either paired or unpaired infusions of methoxamine also showed consistent elevations in baseline HR as training progressed, relative to their respective day 1 levels, thus suggesting the development of compensatory HR CRs to the contextual cues associated with training.
Four rats were trained on concurrent schedules of shock avoidance and timeout from avoidance, where responses on one lever postponed shock and responses on another lever occasionally (VI 45 sec schedule) produced a 2-min timeout during which the avoidance schedule was suspended. These procedures maintained stable rates of responding on both levers, providing a baseline for studying the effects of drugs on behavior under different types of aversive control (shock avoidance and timeout from avoidance). In the first experiment the effects of ethanol (0.5, 1.0, 1.5, and 2.0 g/kg) and an opiate antagonist, naltrexone (1 mg/kg) were assessed alone and in combination. Ethanol produced a dose-dependent decrease in avoidance characterized by increased shock rates and decreased response rates. At the same time, however, responding on the timeout lever generally increased relative to avoidance lever rates. All of these effects were largely confined to the early parts of the 2-hr session, when blood-ethanol levels were relatively high. Naltrexone had no effect on performances and did not interact with ethanol. In a second experiment, the effects of the benzodiazepine antagonist CGS 8216 were studied alone, and in combination with ethanol. CGS 8216 (5 mg/kg) generally disrupted both avoidance and timeout responding but did not reverse ethanol actions.
Guide cannulae for unilateral push-pull perfusion were implanted stereotaxically to rest just dorsal to the hippocampus of the rat. On recovery, a tissue site in the hippocampus was double-labelled with a 1.0 microliter volume of [14C]-5-hydroxytryptamine (5-HT) and [3H]-norepinephrine (NE). Then the site was perfused by means of push-pull cannulae at a rate of 25 microliters/min with an osmotically-balanced CSF. When tetrahydro-beta-carboline (THBC) was added to the CSF perfusate in a concentration of 0.5-5.0 micrograms/125 microliters, the pattern of efflux of both of the monoamines exhibited an increase in release which was either immediate or delayed depending on the concentration and site of the hippocampal perfusion. Further, if the interval of a sequence of repeated perfusions was less than one day, the efflux of either [3H]-NE or [14C]-5-HT was attenuated. The addition of chlordiazepoxide to the CSF perfusate in a dose of 1.6 microgram/1.0 microliter did not affect the resting efflux of either of the monoamines, but did tend to reduce the THBC-induced release. A morphological "mapping" showed that the anatomical sites of perfusion in the hippocampus were homologous to those within which THBC injected locally induces anxiety-like behavior in the rat. Thus, it is envisaged that this beta-carboline serves to alter the behavior of the animal by a differential shift in the synaptic activity of monoamines within neurons of this limbic system structure which is implicated in emotional responses.
Several recent studies have suggested that some effects of ethanol may be mediated by the opioid receptor systems. The present study examined the possibility of a common link between ethanol and opiates by determining whether the effects of ethanol on rat's free operant avoidance behavior could be reversed by the opiate antagonist naltrexone. In Experiment 1 ethanol produced a dose-dependent impairment of avoidance performance (characterized by a decrease in response rate and/or an increase in shock rate) in all three subjects. Naltrexone (3 mg/kg) alone suppressed avoidance rates, but failed to reverse or reduce the effects of ethanol. In contrast to the expectations of the "common-link" hypothesis, the greatest impairment of performance was observed after high doses of ethanol in combination with naltrexone. In Experiment 2 the effects of chronic naltrexone administration were examined. Since previous research has suggested that chronic treatment with opiate antagonists produces a heightened sensitivity to opiate agonists and antagonists, Experiment 2 addressed the issue of whether sensitization to naltrexone would transfer to ethanol. Although increased sensitivity to the rate-decreasing effects of naltrexone was observed, there was no evidence of heightened sensitivity to ethanol. Taken together the results provided little support for the hypothesis that the effects of ethanol on avoidance performance are mediated by the opiate receptor system.
The present study assessed the effects of ethanol and naloxone on the extinction of a jump-up avoidance response in Sprague-Dawley rats. Rats were first trained to jump onto a shelf to escape or avoid shock (0.5 mA). Upon reaching an acquisition criterion of 8 consecutive avoidance trials, animals were removed from the apparatus and exposed to 1 of 4 doses of ethanol (0, 1.0, 2.0, or 2.5 g/kg), and either naloxone (3 mg/kg) or saline. Rats were then returned to the conditioning apparatus with the shock turned off, and resistance to extinction was assessed. Ethanol had biphasic effects with low doses (1 g/kg) facilitating, and higher doses (2 and 2.5 g/kg) suppressing number of extinction responses by comparison to controls. Naloxone did not influence the course of extinction, and did not reverse any of the effects of ethanol. These results did not support the hypothesis that the effects of ethanol on aversively-motivated behavior are opioid-mediated.