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Biomedical subjects

P Ries

Publications and source records attributed to P Ries.

29 records · Page 2Linked to original sources
PubMed1975

[Obliterative intimofibrosis of the renal arteries under the influence of hemodialysis in patients with chronic renal insufficiency (author's transl)].

Histologic and morphologic methods were employed to study the influence of chronic hemodialysis on kidney vessels in chronic renal insufficiency. Arteries of contracted kidneys from patients with and without hemodialysis treatment were investigated. The dialysis group was made up of 33 patients, 28 having undergone bilateral nephrectomy and 5 having died. The control group consisted of 21 patients with chronic renal insufficiency, who died in uremic coma without prior hemodialysis. A statistical evaluation was done by comparing measurements from corresponding arteries in the dialysis- and control groups. The correlation pattern from a BMD 03D-program, in which each group was separately assessed for the possible influence of various clinical findings, was determined. Clinical influences taken into account included the course of the kidney disease, grade of renal insufficiency, duration and degree of hypertension as affecting the renal arteries. The statistical results showed that hemodialysis treatment, even taking clinical data into consideration, influenced the development of intimal fibrosis in the arteries of contracted kidneys in an increasing positive manner. Decreased perfusion of the kidneys during hemodialysis suggested as a possible cause. The examination of early lesions in renal arteries following short-term dialysis treatment lends support to this possibility. Here edema and proliferation of the intimal cells in the arteries, similar to that in vessels having a reduced blood flow, is observed.

Adolescent↗
PubMed1975

[Special and functional pathomorphology of parathyroid glands as revealed in non-selected autopsies (589 cases) (author's transl)].

1637 parathyroid gland dissections were performed on 589 unselected autopsy preparations in order to study both pathomorphology and functional aspects in an unselected group of patients. In no case had primary or tertiary hyperparathyroidism been suspected clinically; but in about 10 patients on chronic hemodialysis, a secondary hyperplasia of the glands was known. In about 33% of the cases pathological changes were observed: 3 chief cell adenomas, 3 adenomas combined with hyperplasia, 12 primary nodular hyperplasias including 6 microadenomas and 145 cases with secondary regulative hyperplasia. Cysts, purulent parathyroiditis, lipomatous pseudohyperplasia, metastases of carcinomas, hemorrhagic infarctions and amyloidosis were also detected in serial sections of the parathyroid glands. The remarkably large group of secondary hyperplasias (about 20%) was divided into 3 categories according to weight and cytology. The first category (118 cases) was characterized by a lack of the normal age-related involution of the parenchyma and prevalence of light (active) chief cells. Statistical evaluation of the other autopsy findings, histomorphology of the bone in particular, led to the conclusion that this group represented a slightly activated gland with possibly reversible hyperplasia, mostly connected with pathological alterations in the kidney and with minimal changes in bone morphology consistent with hyperparathyroidism. The microadenomas displayed different levels of endocrine activity as demonstrated by bone histology in accordance with the cytology of the adenomas (dark or resting chief cells versus active chief cells and waterclear cells). No specific alterations with respect to endocrine function could be attributed to diffuse and nodular hyperplasia of oxyphil (oncocytic) cells except their increase with age and arteriosclerosis, especially in women.

Adenoma↗
PubMedDate not supplied

Differential effects on sympathetic neurotransmission of mast cell degranulation by compound 48/80 or antigen in the rat isolated perfused heart.

The aim of the present study was to investigate whether or not release of endogenous mast cell mediators modulates exocytotic noradrenaline overflow. Therefore, we perfused rat isolated hearts with the right sympathetic innervation intact and investigated the effect of mast cell degranulation on the efflux of noradrenaline. Compound 48/80 (48/80), a mast cell degranulating agent, caused a large release of histamine and serotonin and a facilitation of evoked noradrenaline overflow. When 48/80 was introduced into the perfusion medium 4 min before sympathetic nerve stimulation (SNS), evoked noradrenaline overflow was increased by about 60%. In the presence of the uptake 1-blocker cocaine, facilitation was attenuated (increase by only 30%). This effect was abolished by the histamine H2 receptor antagonist cimetidine or the inhibitor of nitric oxide synthesis NG-nitro-(L)-(-)-arginine. When the preexposure time to 48/80 was reduced to 30 s, the facilitation was less pronounced (15%) and inverted to an inhibition in the presence of cocaine (plus idazoxan) by 17% and/or cimetidine (by about 30%). The resulting inhibition of noradrenaline efflux was attenuated by the serotonin 5-HT1/2 receptor antagonist methiothepin or the 5-HT2 antagonist ketanserin. Infusion of ovalbumin into hearts of not specifically sensitized, but sham treated rats (in vivo injection of a saline-alumina mixture 10-12 days before the in vitro experiment) did not affect histamine, serotonin or (basal and evoked) noradrenaline efflux. In hearts from rats that were previously sensitized by an injection of an ovalbumin-alumina adsorbate, ovalbumin induced a marked increase of histamine and serotonin efflux. When the infusion of the antigen started 30 s before SNS, evoked noradrenaline overflow was inhibited by about 60%. The inhibition was unaffected by histamine receptor antagonists, but attenuated by purinoceptor (suramin plus 1,3-dipropyl-8-cyclopentylxanthine), or serotonin receptor (methiothepin, rauwolscine or ketanserin) antagonists. When the preexposure time to ovalbumin was prolonged to 4 min before SNS, no significant change of stimulation-induced noradrenaline overflow was observed. Basal, immunologically and non-immunologically induced histamine and serotonin efflux were not significantly affected by SNS or any of the drugs tested. The results indicate a complex influence of various mediators released upon mast cell degranulation induced by two different stimuli on exocytotic noradrenaline release from rat heart. Depending on the stimulus and on the time interval between the start of the application of the mast cell degranulating agent and SNS, a histamine- and nitric oxide-mediated facilitation, or a serotonin- and purine-mediated inhibition prevails.

Animals↗