REDUCED DOPAMINERGIC INHIBITION OF THYROTROPHIN RELEASE IN STATES OF PHYSIOLOGICAL HYPERPROLACTINAEMIA

We have tested the hypothesis that physiological puerperal hyperprolactinaemia may be secondary to reduced hypothalamic dopaminergic inhibition of prolactin (PRL) release. Nine post-partum females with physiological hyperprolactinaemia (aged 19–40 years; mean basal PRL±SE, 2099±257 mU/l, range 1002–3762 mU/l) were studied and results compared with fourteen normoprolactinaemic females (basal PRL<400 mU/l; aged 18–36 years). Puerperal hyperprolactinaemic females showed a reduced TSH response to dopamine (DA) receptor blockade with metoclopramide (10 mg i.v.) compared with normal females over a 60-min period following drug administration (total incremental TSH change, mean ±SE, mU/l; 0.5±0.3 v. 3.1±1.0, P<0.005). This finding of reduced dopaminergic inhibition of TSH release in females with physiological puerperal hyperprolactinaemia supports the view that an overall reduction in hypothalamic dopaminergic tone may contribute towards hyperprolactinaemia in post-partum women.     

PATHOLOGY OF DISULFIRAM NEUROPATHY

Bouldin T.W., Hall CD & Krigman M.R.1980 Neuropathology and Applied Neurobiology 6, 155–160
Case report. Pathology of disulfiram neuropathy
The pathological changes in a sural nerve biopsy from a 42-year-old woman with disulfiram-induced peripheral neuropathy were assessed by quantitative light microscopy, electron microscopy, and the study of teased nerve fibres. The nerve had a marked loss of myelinated fibres; of the remaining myelinated fibres some were undergoing Wallerian-type axonal degeneration. Large myelinated fibres were preferentially involved. Primary demyelination, remyelination, and evidence of regeneration were not present. Because of the marked differences between the pathological findings in disulfiram neuropathy and carbon disulfide neuropathy, it is concluded that carbon disulfide is not responsible for the neurotoxic effect of disulfiram.     

THYROID HORMONE KINETICS: IMPROVED METHOD FOR QUANTITATIVE SEPARATION AND MEASUREMENT OF THE VARIOUS RADIOIODINATED SPECIES IN SERUM AFTER RADIOIODOTHYRONINE INJECTION

An accurate and reproducible method for measurement of radioactive species in blood after in vivo injection of labelled iodothyronines is described. By extraction with high-affinity antisera, radioactive reverse T3 and T3 are separated from serum quantitatively. Radioiodide is quantitatively separated from radio-thyronine species and serum proteins by Sephadex G50 filtration. The residual mixture of radio-T4 and iodoprotein is quantitatively resolved by ion-exchange adsorption. Minimal misclassification of radiospecies occurs, and can be corrected for. Mean recoveries of various radiospecies added to serum were: radioiodide 98.9%, radio-rT3 87.6%, radio-L-T3 94.5%, radio-T4 98.0% and radioiodoprotein 94.5%. The performance of the method is superior to that of chemical methods such as trichloracetic acid precipitation, ion-exchange or alkaline Sephadex extraction, and chromatographic separation.     

THE EFFECTS OF MITOMYCIN C ON THE PROCESS OF REMYELINATION IN THE MAMMALIAN PERIPHERAL NERVOUS SYSTEM

Schwann cell proliferation is a prominent feature of the normal response of a peripheral nerve fibre bundle to injurious stimuli. In this report we have attempted to analyse: (1) the pattern of division of cells in the endoneurium following demyelination induced by lysophosphatidyl choline (LPC), and (2) the consequence of inhibiting this response using mitomycin C. The nuclear uptake of ³H-thymidine was examined in post-LPC nerves with or without pretreatment with mitomycin C by means of light microscope autoradiography and by liquid scintillation counting. It was found that mitomycin C pretreatment inhibited the Schwann cell division that follows LPC injection into the nerve and that the fibires demyelinated thereby remained unmyelinated and surrounded by debris-filled axon-associated Schwann cells, for at least 1 month after injection of LPC. Remyelination was well established in control fibres by the second week after LPC injection. The nature of the stimuli which might initiate mitotic activity in mature Schwann cells and the possible function of this are discussed.     

Redistribution of body heat during anaesthesia

Epidural anaesthesia and high dose fentanyl (50 micrograms/kg) when used to supplement nitrous oxide and oxygen anaesthesia for a standard lower abdominal operation were associated with a mean fall in deep body temperature, as measured in the external auditory meatus, of 0.46 degrees C and 0.6 degrees C/hr respectively. This is significantly different from the mean values of 0.14 degrees C and 0.2 degrees C/hr which were recorded when moderate dose fentanyl (10 micrograms/kg) or 0.5% halothane were used to supplement anaesthesia. When mean skin temperature is combined with the core temperature to provide an estimate for total body heat, there is no difference between the groups. Redistribution of body heat occurs and this may be related to reduced adrenergic stimulation and altered regional blood flow. Where the facilities and environments are inadequate for the maintenance of normothermia, care should be taken in the choice of anaesthetic technique. In the recovery period mean body heat gain showed a wide scatter of results but those patients receiving epidural anaesthesia were slow to rewarm despite a high incidence of shivering in this group. The implications of this are discussed.