Brain cortex slices from rabbits were preincubated with [3H]noradrenaline and then superfused and stimulated electrically at 3Hz. In the presence of cocaine 30 microM, unlabelled noradrenaline, alpha-methylnoradrenaline, clonidine, oxymetazoline, xylazine and guanabenz decreased, whereas yohimbine, corynanthine, phentolamine, tolazoline and azapetine increased the stimulation-evoked overflow of tritium. Phenylephrine and prazosin had no effect on the evoked overflow except at concentrations that greatly accelerated the basal outflow of tritium. The results indicate that the noradrenergic axons of rabbit brain cortex are endowed with presynaptic alpha-adrenoceptors which are exclusively of the alpha 2-type. Addition of various concentrations of cocaine, addition of pargyline, or stimulation at different current strengths was used to obtain either a high or low stimulation-evoked overflow of tritium. Independently of the method used, a low evoked overflow coincided with a large percentage inhibition produced by 0.1 micro M clonidine, whereas a high evoked overflow coincided with a smaller percentage inhibition produced by clonidine. The results indicate that drugs which block the re-uptake of noradrenaline diminish the presynaptic inhibitory effect of alpha-adrenergic agonists by increasing the biophase concentration of released noradrenaline.

No abstract

No abstract

Neurological complications in clavicle fractures are rare. As a primary lesion, it is caused by the trauma itself, more often the neurological symptoms develop later by large callus formation to encroach the costoclavicular space. Neurological complications early after trauma are mostly caused by the figure-of-eight bandage generally used for conservative treatment. Vascular lacerations as well as fractures of the first two ribs have to be excluded. We report about a case of complete brachial nerve paralysis two days after conservative treatment of an uncomplicated clavicle fracture.

The myoelectric activity of the small bowel was evaluated in 6 rabbits following 24 h of complete small-bowel obstruction and in 6 rabbits during an intra-abdominal perfusion with a bacterial suspension containing Bacteroides fragilis and Escherichia coli. Myoelectric recordings were performed before and during pharmacological small-bowel stimulation with ceruletide. Following small-bowel obstruction both slow-wave frequency and spike activity were reduced. Ceruletide stimulation demonstrated a significantly decreased spike activity after 24 h of obstruction. Intra-abdominal bacterial contamination did not affect spontaneous slow-wave frequency and spike activity but induced complete resistance to ceruletide stimulation. Pharmacological stimulation is recommended as an additional method to evaluate the impairment of myoelectric activity in motility disorders.