The autoradiographic distribution of [³H]arginine vasopressin, [³H]spiperone, [³H]GABA, [³H]dihydroalprenolol and the peripheral-type benzodiazepine ligand [³H]Ro5-4864 were examined in the rat pituitary before and after pituitary stalk transection. Stalk transection produced dramatic changes in the cellular architecture of the pars nervosa. Glial fibrillary acidic protein, an astrocyte marker reported in pituicytes, increased after stalk transection, whereas neurofilament, a marker for neuronal innervation, was lost. These structural changes demonstrated a successful stalk transection, permitting interpretation of changes in the densities of several [³H]-ligands over the three lobes. [³H]Ro5-4864 binding was markedly increased, suggesting that this site was located on the pituicytes. Conversely [³H]spiperone and [³H]arginine vasopressin binding density over the pars nervosa decreased. In the mutant diabetes insipidus rat (Brattleboro), which lacks pituitary vasopressin, [³H]arginine vasopressin binding was undetectable in the pars nervosa. [³H]dihydroalprenolol and [³H]GABA binding sites were unchanged by the lesion. These results are discussed in terms of the occurrence of functional acceptors on pituicytes and their possible role in neurohydrophyseal secretions.

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This report describes a 55-year-old man admitted for renal colic and found to have an infarcted right kidney, for which he was treated with heparin. Heparinization for this condition was stopped on day 12 when the patient developed pain in his left foot. Heparin-induced thrombocytopaenic thrombotic syndrome was confirmed, and despite treatment with danaparoid and bilateral femoral embolectomy, a left above-knee amputation was required. Echocardiogram showed a sessile mural thrombus in the left ventricle, which was considered a likely embolic source. The preoperative development of acute renal failure delayed recovery and necessitated haemodialysis. Anticoagulation of the patient was complicated; however, warfarin was introduced slowly and with good effect.

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