Expression of functional postjunctional alpha 2-adrenoceptors in rabbit isolated distal saphenous artery--a permissive role for angiotensin II?

In the rabbit isolated distal saphenous artery, the population of postjunctional adrenoceptors is of the alpha 1 variety under normal in vitro experimental conditions, based on the potency order of selective agonists and on the effects of the antagonists prazosin and rauwolscine against responses to UK-14304. Angiotensin II (A II, 0.05 microM) however, without affecting resting baseline tension, markedly enhanced responses to UK-14304, particularly at low concentrations. This previously unseen component of the response to UK-14304 was resistant to prazosin (0.1 microM) but susceptible to rauwolscine (1 microM). A II would therefore appear to have a permissive role for the expression of a quiescent population of postjunctional alpha 2-adrenoceptors in the rabbit distal saphenous artery.     

Chiari II malformation: MR imaging evaluation

The purpose of this study was to explore the value of high-detail MR imaging in the diagnosis of the Chiari II malformation. Twenty-four patients with known Chiari II malformation as diagnosed by CT scanning were evaluated with cranial MR scans. Two patients also had spine scans. The sagittal-plane images were the most informative, and abnormalities of the telencephalon, diencephalon, mesencephalon, rhomboencephalon, upper spinal cord, and mesencephalon were shown extremely well. We found MR to be an easy and accurate method for demonstrating the abnormalities of the Chiari II malformation, and it is our procedure of choice.     

Effects of diet-induced ketosis in rats with hypoglycaemia due to a serially transplantable insulinoma

In view of the ability of ketones to partially replace glucose as an alternative fuel in the brain, the potential protective effects of diet-induced ketosis were examined in male NEDH rats with hypoglycaemia due to a serially transplantable radiation-induced insulinoma. Ketosis was induced by daily oral administration of medium chain triglycerides to normal rats and to insulinoma-bearing rats 1 day after subcutaneous subscapular implantation of tumours fragments. All rats treated with medium chain triglycerides became ketotic within 72 hours, and plasma 3-hydroxybutyrate concentrations remained 5-10 fold elevated at 24 days. Untreated insulinoma-bearing rats became moderately hyperinsuliaemic and hypoglycaemic by 17 days, with the later manifestation of more marked hyperinsulineamia (21.6 +/- 0.8 ng/ml, mean +/- SEM) severe hypoglycaemia (1.5 +/- 0.1 mmol/l) and death by 24-28 (26 +/- 1) days. Induction and maintenance of hyperketonaemia did not affect the development of hyperinsulineamia, hypoglycaemia or the exaggerated fall of plasma glucose produced by an 8 hour fast in these rats. However by day 21, the severity of hypoglycaemia was greater in insulinoma-bearing rats receiving medium chain triglycerides, culminating in accelerated death by 22-25 (23 +/- 1) days and an accompanying 50% decrease in final tumour weight. These results demonstrate that induction of ketosis in the face of marked hyperinsulinaemia did not afford protection against the profound hypoglycaemia produced by a serially transplantable rat insulinoma.     

Correlations between the functional activity and proliferation of the thyroid parenchyma. The proliferative forms of the parenchyma of the thyroid

Multiple thyroid adenomas formed by straight or coiled epithelial cords developed in experiments on adult male rats as a result of prolonged intermittent 6-MTU administration. Such epithelial cords could be sometimes observed in thyroid parenchyma regeneration after partial thyroidectomy. These cords originated from thyrocytes of the follicle epithelium. In the proliferating thyroid parenchyma DNA replication mainly terminated in endomitoses (previously reported data) which in thyrocytes of prismatic form resulted in their separation from proximal and distal daughter cells. Proximal daughter cells kept contact with the follicle lumen but distal ones lost it, hence their iodine uptake and origination weakened. Therefore, the biosynthesis of thyroglobulin decreased in cytoplasm of distal daughter cells but the formation of thyroalbumin increased. In consequence the distal daughter cells with this shift in protein biosynthesis underwent hypertrophy and further originated the proliferation of extra follicular epithelial cords. The formation of new follicles mainly took place with the differentiation of interfollicular islets separated from proliferating extrafollicular epithelial cords. Thyrotropin, the principal stimulator of hormonopoietic thyrocyte activity, did not necessarily influence the activation of thyroid parenchyma proliferative processes.