Interaction between endogenous opioids, cholinergic and adrenergic mechanisms during vagally-induced gastrin release in rats

Endogenous opioids are present in neurons of the vagus and the intrinsic nervous system and they are colocalized with gastrin in antral G-cells. This raises the possibility that endogenous opioids modulate gastrin release. Stimulation of both cervical vagi (10V, 5Hz, 5ms) elicited an increase of arterial plasma gastrin levels at intragastric pH7 or pH2. The response at pH2 was 30% of that at luminal pH7. Atropine reduced vagally stimulated gastrin levels substantially. At luminal pH2 the small residual noncholinergic response was mediated neither by adrenergic mechanisms nor by endogenous opioids. At luminal pH 7 adrenergic blockade with phentolamine and propranolol reduced vagally stimulated gastrin by 60%. In the presence of atropine adrenergic blockade elicited only a small inhibitory effect suggesting that vagal activation of adrenergic mechanisms depends on atropine-sensitive cholinergic pathways. Blockade of opiate receptors by naloxone had no effect on vagal gastrin release, however, the noncholinergic gastrin response was reduced significantly by naloxone, suggesting that cholinergic mechanisms normally restrain activation of endogenous opioids during vagal stimulation. Naloxone had no effect on the noncholinergic, nonadrenergic stimulation of gastrin levels. These data suggest that endogenous opioids can contribute to vagal gastrin release provided the cholinergic restraint is blocked and adrenergic mechanisms stimulate endogenous opioids. In conclusion a major role of endogenous opioids in the regulation of vagal gastrin release can not be detected.     

A HIGH FREQUENCY OF INHERITED DEFICIENCY OF COMPLEMENT COMPONENT C4 IN DARWIN ABORIGINES

Abstract A high frequency of serum complement component C4A deficiency may explain the higher prevalence and greater severity of systemic lupus erythematosus reported in Australian Aborigines. Inherited deficiencies of serum complement components C4A, C4B, and C2 were examined in two Australian Aboriginal populations from Darwin and Alice Springs and compared with the prevalence of complement deficiencies in white Australian blood donors. The frequency of C4A deficiency alleles was 29% in Darwin Aborigines compared with 12% in Alice Springs and 17% in Canberra blood donors. Partial C4B deficiency was also higher in Darwin Aborigines than in the other populations. Inherited deficiency of serum complement component C2 was not observed.     

Inborn errors of the urea cycle

Inborn errors of the urea cycle are an important cause of hyperammonaemia throughout childhood, and are associated with high morbidity and mortality rates. If they are diagnosed early and treated appropriately, the outcome for affected children is significantly improved.     

Fibroepithelial polyps of the ureter. Etiology, diagnosis, treatment and pathology

In order to draw attention to this rather rare condition affecting all age groups, 4 cases of fibroepithelial polyps of the ureter are reported. Conservative surgery is mandatory after adequate preoperative work-up. The pathological findings, incidence and diagnostic and therapeutic modalities are discussed and some etiological factors proposed.     

Analysis of the activities of a geriatric assessment and rehabilitation unit

In a four month period 228 patients were admitted to the Wakari assessment and rehabilitation unit in Dunedin, New Zealand. One hundred and seventy subjects came from the community, 35 were transferred from the local public hospital, and 23 were readmitted. Median lengths of stay were 13, 26 and 10 days respectively. Assessment of activities of daily living (ADL) dependency on admission and discharge showed a significant improvement in ability by discharge, which correlated closely with place to which subjects were discharged, and with survival. There was 5% inpatients death rate which cumulated to 18%, 23%, 34%, 39% and 46% by six weeks, three months, six months, nine months and one year respectively. High discharge dependency was closely related to poor survival after discharge. Use of domiciliary services did not change because the savings from those who moved into institutions were cancelled out by those who were discharged back to the community being in need of increased social support.