The exudates obtained from the bullae were examined by superfusion cascade bioassay, by radioimmunoassay for PGF2alpha and by column, thin-layer and gas-liquid chromatography. Ultraviolet B (u.v.-B) irradiation of human skin produced an erythema which appeared after 2 hr, increased in severity up to 24 hr and persisted for more than 48 hr.
Bioassayable and radioimmunoassayable prostaglandin activity was elevated at 6 hr, was maximal at 24 hr and had returned to normal 48 hr. Topical application of indomethacin suppressed both the erythema and the increased concentration of PGF2alpha as measured by radioimmunoassay.
Chromatographic studies confirmed increased prostaglandin activity at 6 and 24 hr and in addition demonstrated an increase in arachidonic acid-like activity. The results suggest that prostaglandins may play an important role between 6 and 24 hr of u.v.-B-induced erythema.
Whether the reduction of erythema by indomethacin can be partially or wholly attributable to inhibition of prostaglandin biosynthesis is uncertain. Some workers have attempted to fit prostaglandins into a simple model, i.e. inflammatory leads to chemical mediator leads to vascular response. An alternative model is proposed, involving the interaction of two chemical agents, i.e. a vascular permeability-increasing mediator (such as histamine or bradykinin) and a vasodilator (prostaglandin) which potentiates the plasma exudation produced by the permeability-increasing mediator. The results obtained in testing this model support the further proposal that non-steroidal anti-inflammatory compounds suppress inflammatory swelling by inhibiting vasodilatation.
The possible role of prostaglandins (PGs) in thrombosis was determined by examining their effects in models of thrombosis which included platelet aggregation (in vitro), blood flow (in vivo) and thrombus formation (in vivo).
It was found that blood flow and thrombosis can be effectively modulated by the various types of prostaglandins produced by the blood and the vascular tissue. Corethium 2 has been known to be a valuable biological dressing which encourages re-epithelization in cases of tissue loss, especially in varicose ulcers. It ensures a superior quality of healed tissue even in difficult chronic cases. It also reduces the overall treatment time and can be used as an out-patient dressing. Blood nicotine levels were measured in eight subjects over a 5-week period, while smoking normally, while smoking and chewing gum containing 2 mg nicotine, and while smoking and chewing placebo gum.
Despite a small but significant rise in blood nicotine levels during the period of the nicotine gum chewing (mean 35.3 ng/ml) compared with placebo (mean 28.9 ng/ml) and control (mean 26.3 ng/ml), cigarette consumption butt lengths, filter nicotine and blood carboxyhaemoglobin levels did not change indicating that there had been no significant changes in smoking patterns. The reasons for this failure to demonstrate an effect are discussed. It is concluded that the dose of nicotine used was probably not adequate to produce an effect. Charcoal haemoperfusion used to treat a 56-year-old woman who had taken a very large overdose of meprobamate was followed by fully recovery. The plasma clearance of meprobamate was 153 ml/min and this compares favourably with values obtained for haemodialysis.
A case of papilloedema secondary to respiratory failure is reported which caused considerable diagnostic difficulty and led to extensive neurological investigation. Neurological complaints of headache and visual impairment overshadowed respiratory symptoms and were associated with gross haemorrhagic papilloedema. The authors recall two cases of round atelectasis without any known pleural past-record. The first showed, on successive X rays, an increase in size of the image. In the second case a pleural effusion occurred after the discovery of a round opacity. They stress the various small radiological signs as a way of including the etiology of a purely mechanical atelectasis among the difficult diagnosis of intraparenchymal round opacities.
Morphine infused into this site also caused significant depression of self-stimulation, but the doses were considerably lower than those of Substance P (5 and 10 microgram/rat). Pretreatment with naloxone, a narcotic antagonist, significantly antagonized the effects of Substance P on self-stimulation.