The glomerular hemodynamics were studied in streptozotocin diabetic rats 3 months after the induction and in age-matched normal animals. Indomethacin infusion failed to cause changes in glomerular hemodynamics in normal rats but produced striking effects in the diabetic rats: The afferent arteriolar hydraulic resistance increased substantially while the efferent resistance rose moderately causing large reductions in single nephron blood flow and in the hydraulic pressure in the glomerular capillaries. Consequently, single nephron glomerular filtration rate (SNGFR) was reduced significantly below normal. The ultrafiltration coefficient of the glomerular membrane was significantly lower in the diabetic than in the normal animals (2.8 versus 5.0 nl min-1 mm Hg-1) and remained unchanged during indomethacin infusion. Our results suggest that the prostaglandin system compensates for the changes in the glomerular hemodynamics induced by diabetes by reducing the arteriolar resistances to increase the glomerular capillary pressure making it possible to maintain normal values of SNGFR and nephron blood flow.
The in vivo distribution of the intercellular adhesion molecule ICAM-1 was investigated in renal tissue specimens obtained from 17 renal allotransplanted patients, nine normal kidneys (controls), seven native kidneys, nine patients with mesangioproliferative glomerulonephritis, and nine patients with active extracapillary glomerulonephritis. Biopsies from patients with signs of acute rejection showed a significant increase in ICAM-1 expression in the tubular epithelium (P less than 0.05). In normal kidneys (controls) ICAM-1 expression was found in endothelial cells; additional expression in the tubular epithelial cells was induced in patients with extracapillary glomerulonephritis. The in vitro expression of ICAM-1 was examined in cultured human tubular cells after stimulation with gamma-interferon and interleukin-1, treatment with cyclosporin and/or verapamil and coculture with allogenic mononuclear cells. An increased ICAM-1 expression was demonstrated by coculture with allogenic mononuclear cells and after stimulation with gamma-interferon and/or interleukin-1. Cyclosporin or verapamil induced no changes. Our results give support to the hypothesis that ICAM-1 upregulation is important in immune interactions such as allograft rejection. Furthermore, the in vitro model indicates that ICAM-1 expression is regulated by gamma-interferon and interleukin-1 produced by activated T lymphocytes and macrophages.
Prolactin (PRL), thyroid stimulating hormone (TSH) and growth hormone (GH) response to metoclo-pramide and TRH was investigated in seven women with fibrocystic disease and cyclical niastalgia, in eight similar patients without mastalgia, and in six normal controls. The basal PRL level was significantly elevated in patients with cyclical mastalgia (P < 0.025). PRL and TSH response to metoclopramide did not differ significantly between the three groups, indicating that decreased dopaminergic tone is not the cause of elevated basal PRL level in cyclical mastalgia. PRL and TSH response to TRH and the abscent GH response to both metoclopramide and TRH further indicate that the hypothalamicpituitary axis is not primarily disturbed in cyclical mastalgia. The basal GH level was elevated in patients with fibrocystic disease with or without mastalgia. The increased basal GH secretion is not believed to be directly involved in cyclical mastalgia, but may be of importance in fibrocystic disease. Cancer 56500-502, 1985. ASAL SERUM prolactin (PRL) levels have been re-B ported marginally, but significantly elevated in patients with cyclical mastalgia.' The cause of increased PRL secretion in this condition is unknown. Recent data indicate that altered central regulation of PRL secretion may be The primary aim of the present study was to examine the dopaminergic tone in patients with cyclical mastalgia, measuring the response of serum PRL and thyroid stimulating hormone (TSH) to submaximal doses of metoclopramide, a Dopamine (Abbott)-receptor blocking agent.4 For additional evaluation of the hypothalamicpituitary axis, synchronous measurements of growth hormone (GH) were under-taken. Furthermore, the PRL, TSH and G H responses to TRH were studied in the same patients. Patients and Methods The investigation comprised three groups: (A) seven patients with cyclical mastalgia and histologically verified fibrocystic disease of the b r e a ~ t ; ~ (B) eight similar patients without mastalgia; and (C) six normal controls. The
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