Ten patients with chronic Yersinia enterocolitica infections are described. The initial diagnosis was made by culture, significant agglutinin titres and indirect immunofluorescence (IF) on biopsies. During the chronic phase, culture and agglutinin titres were negative, but specific serum IgA and IgG antibodies reactive with at least two, i.e. the 36 kDa and the 46 kDa, virulence-associated released proteins were demonstrated in nine patients by immunoblot techniques. One patient had only IgG antibodies. The chronically elevated IgA production was the result of chronic stimulation of the gut-associated lymphoid tissue by virulent persistent Yersinia antigen, which was identified by IF with O-specific antiserum and monospecific antiserum to the 46 kDa released protein in biopsies. Virulent Yersinia bacilli were demonstrated in the intestinal mucosa and in the lymphoid tissue of the submucosa associated with macrophages in patients with chronic ileitis and arthritis, in granulomatous centres of lymph nodes in patients with chronic lymphadenopathy and in portal infiltrates in a patient with chronic hepatitis. Recognition of persistent Yersinia infections may have therapeutic implications.

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The present study was concerned with the effects of a transplantable prolactin-secreting pituitary tumor (7315b) on the hypothalamic release of dopamine, luteinizing hormone-releasing hormone (LHRH) and thyrotropin-releasing hormone (TRH) in gonadectomized, adrenalectomized male rats bearing subcutaneously a testosterone capsule and a corticosterone pellet. Similar male rats not inoculated with tumor served as controls. The rats were studied 3–4 weeks after tumor inoculation, while they were anesthetized with urethane. Compared to the controls, prolactin levels in the tumor-bearing rats had increased 70-fold, whereas the levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) decreased to 20 and 27%, respectively. In tumor-bearing rats, the secretion of dopamine into hypophysial stalk plasma increased from 2.3 to 4.9 ng/h (p < 0.025), whereas that of LHRH decreased from 127 to 52 ph/h (p < 0.005). Since the use of urethane anesthesia may change quantitatively and qualitatively the effects of hyperprolactinemia, it was decided to study these effects on the in vivo release of LHRH, dopamine and TRH in conscious rats by a push-pull perfusion of the median eminence-arcuate nucleus area. Using this technique, it was found that in tumor-bearing rats the secretion of LHRH decreased from 20.0 to 9.8 pg/15 min·(p < 0.005), whereas that of dopamine increased from 118 to 246 pg/15 min (p < 0.025). The secretion of TRH was not altered by hyperprolactinemia (4.1 vs. 4.4pg/15 min). Thus, push-pull perfusion experiments in conscious, freely moving rats confirm what was found in hypophysial stalk blood obtained from rats under anesthesia, namely, that hyperprolactinemia stimulates dopamine release and inhibits LHRH release. This study also indicates the value of using conscious rats to determine simultaneously the in vivo output of several substances from the hypothalamus.

The present study was concerned with the effects of a transplantable pituitary tumor secreting prolactin (PRL) and adrenocorticotrophin (ACTH) on the levels of LH and FSH in peripheral plasma and on the hypothalamic release of LH-RH and dopamine in the male rat. Male rats of the same age not inoculated with the tumor served as controls. Hypophysial stalk blood was collected from urethane-anesthetized rats 4-5 weeks after tumor inoculation to measure their LH-RH and dopamine content. A peripheral blood sample was withdrawn from the animals just before sectioning the hypophysial stalk to measure their content of LH, FSH and PRL. It was found that in the tumor-bearing rats the levels of PRL increased 17-fold, whereas plasma levels of LH and FSH decreased by 45 and 70% respectively, when compared with the control rats. In the tumor-bearing rats, the secretion rate of dopamine in hypophysial stalk plasma increased from 1.4 to 4.1 ng/h, whereas the secretion rate of LH-RH decreased from 122 to 61 pg/h. However, when at the time of tumor inoculation adrenalectomy was performed, the tumor did not decrease plasma levels of LH and FSH and the secretion of LH-RH into hypophysial stalk blood any longer. The effect of the tumor on hypothalamic dopamine secretion was, however, still present in the adrenalectomized rats. It is concluded that the effect of the PRL- and ACTH-secreting pituitary tumor on plasma levels of LH and FSH requires the presence of the adrenal gland and that this effect is mediated through an inhibition of the hypothalamic release of LH-RH. Furthermore, this tumor increases the hypothalamic release of dopamine independent of the presence of the adrenal gland.

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