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Biomedical subjects

U Riede

Publications and source records attributed to U Riede.

10 recordsLinked to original sources
PubMed1992

Alterations of skeletal muscle in chronic heart failure.

BACKGROUND: The present study was designed to define the prevalence and characteristics of skeletal muscle alterations in patients with chronic heart failure (CHF) and their relation to exercise capacity. METHODS AND RESULTS: The ultrastructure of skeletal muscle was analyzed by ultrastructural morphometry in 57 patients with CHF and 18 healthy controls. The volume density of mitochondria (Vvm) and the surface density (Svmc) of mitochondrial cristae were evaluated as a structural correlate of oxidative capacity of skeletal muscle. Vvm and Svmc were reduced by approximately 20% in patients with severe CHF irrespective of age and etiology. The cytochrome oxidase activity in mitochondria as determined by cytochemistry and subsequent morphometry in a subset of patients (n = 10) was significantly decreased in heart failure (p less than 0.01). The capillary length density of skeletal muscle was reduced in CHF (n = 12, p less than 0.05), and the fiber type distribution was shifted to type II fibers (n = 15, p less than 0.05). Vvm and Svmc were significantly related to peak exercise VO2 (r = 0.56, p less than 0.001, n = 60) and to VO2 at anaerobic threshold (r = 0.535, p less than 0.0001, n = 60). In 16 patients with severe heart failure, Vvm was inversely related to the duration of heart failure (r = 0.545, p less than 0.03). In 11 patients who underwent repeat biopsies after 4 months, a correlation was observed between the change in Vvm and the change in peak exercise VO2 (r = 0.89, p less than 0.001). CONCLUSIONS: These findings indicate that patients with CHF develop significant ultrastructural abnormalities of skeletal muscle reflecting a depressed oxidative capacity of working muscle. It appears that these alterations of skeletal muscle contribute to the decreased exercise capacity of these patients but are, in principle, reversible by an effective treatment regimen.

Aging↗
PubMed1992

Effects of inhibition of nitric oxide formation on regional blood flow in experimental myocardial infarction.

BACKGROUND: Large myocardial infarction is associated with reactive hypertrophy and dilation of the left ventricle, depressed coronary flow reserve, and the development of heart failure including systemic vasoconstriction. We hypothetized that changes in endothelial function, e.g., in the synthesis or action of nitric oxide in the coronary and peripheral vasculatures, might be involved in the depressed coronary flow reserve and increased systemic vascular resistance observed in postinfarction myocardial hypertrophy and failure. METHODS AND RESULTS: The regional blood flow changes that occur as a result of inhibiting the basal release of nitric oxide with NG-monomethyl-L-arginine (L-NMMA) and how this regional pattern may be altered in large MI (infarct size, 30-51% of left ventricle) were examined. Measurements were made 24 hours and 8 weeks after myocardial infarction or sham operation in conscious rats. The left ventricular end-diastolic pressure and effects of L-NMMA on left ventricular end-diastolic pressure was similar 24 hours and 8 weeks after myocardial infarction. The effects of L-NMMA (30 mg/kg i.v.) on heart rate and blood pressure were similar in infarcted and sham animals. L-NMMA exerted a marked vasoconstriction in the renal, splanchnic, cutaneous, and cerebral circulations of similar magnitude in sham-operated rats and animals with myocardial infarction. The coronary vasoconstrictor effect of L-NMMA was attenuated significantly in the hypertrophied right and noninfarcted left ventricle of 8-week-old infarcted rats (p less than 0.01 versus sham-operated animals) but not 24 hours after induction of myocardial infarction when cardiac hypertrophy has not yet developed. The increase in left ventricular coronary resistance in 8-week-old infarcted animals was inversely related to infarct size (r = -0.787, p = 0.012, n = 9). Nitroglycerin exerted similar increases in coronary blood flow in rats with chronic myocardial infarction and sham-operated animals, arguing against a reduced vascular responsiveness to nitric oxide. Transmission electron microscopy of coronary resistance vessels in 8-week-old infarcted animals did not reveal endothelial abnormalities. CONCLUSIONS: These data suggest that the basal release of nitric oxide in the renal, intestinal, and cutaneous circulations is not affected adversely in this model of myocardial infarction and failure. However, the blunted coronary vasoconstrictor effect of L-NMMA late after large myocardial infarction supports the view that the basal release of nitric oxide is impaired in postinfarction reactive cardiac hypertrophy.

Animals↗
PubMed1991

Beta-human chorionic gonadotropin-positive extragonadal germ cell neoplasia of the renal pelvis.

A 56-year-old woman showed renal obstruction on the right side. Further examinations revealed a tumor of the renal pelvis. Nephroureterectomy on the right side was done. This extragonadal germ cell neoplasia had an immunohistochemically detected beta-human chorionic gonadotropin (beta-hCG) expression. There were no other primary tumors or metastases. Although there were normal values after the operation, during the postoperative follow-up, the serum beta-hCG temporarily reached 2400 IU/l and then dropped to normal without detection of metastases. No further therapy was given. The patient was alive and well 1 year and 10 months after surgery. To the authors' knowledge, this is the first extragonadal germ cell neoplasia of the renal pelvis with secretion of beta-hCG to the serum.

Biomarkers, Tumor↗
PubMed1991

Adaptive changes in the periphery and their therapeutic consequences.

Systemic vasoconstriction in chronic heart failure is due to several compensatory mechanisms with different time courses. Peripheral vasoconstriction mediated by increased sympathetic tone and activation of the plasma renin-angiotensin system may act primarily for short-term control. The effects of the vascular renin-angiotensin system, impaired flow-dependent, endothelium-mediated dilation (resulting from chronically reduced flow) and structural alterations of the vessel wall slowly emerge with time. In addition, fluid retention may contribute to increased vascular stiffness in chronic heart failure. Improved cardiac output with acute administration of vasodilators and inotropes is not immediately translated into increased blood flow to skeletal muscle, because (1) the reversal of the peripheral alterations described develops slowly over time (in fact, vasodilators and inotropes given acutely may cause redistribution of blood flow in skeletal muscle without improving oxygen availability); and (2) intrinsic abnormalities of skeletal muscle exist in chronic heart failure (e.g., due to chronic deconditioning, resulting in reduced oxidative capacity of skeletal muscle, as suggested by ultrastructural analysis and nuclear magnetic resonance spectroscopy). Drugs that interfere with the underlying compensatory mechanisms (e.g., renin-angiotensin system) without development of tolerance during long-term therapy exert beneficial effects after long-term treatment (e.g., the beneficial effects of angiotensin-converting enzyme inhibitors are, in part, due to peripheral mechanisms--the inability of the peripheral vessels to dilate--and to improvement of peripheral oxygen extraction).

Adaptation, Physiological↗
PubMed1979

[Reaction of the liver cells to surgical intervention in obstructive jaundice. Electron microscopic-morphometric studies of the rat liver].

In Wistar rats, bile was drained by biliocutaneous fistulas 7 days after ligation of the common bile duct. Morphometric analysis using a computer program registered about 60 parameters of a hepatocyte. Most cell organelles are again normal 7 days after intervention. The ultrastructural changes are not fully compatible with histologic and biochemical findings.

Animals↗
PubMed1978

Further similarities between Sézary syndrome and mycosis fungoides.

Sézary syndrome and mycosis fungoides, both malignant Non-Hodgkin lymphomas, although characterized as specific entities, show a close relationship. This is based on striking similarities not only uith respect to morphological, cytophotometrical, cytogenetical and immunological findings, but also with respect to a typical common reaction pattern to photochemotherapy.

Aged↗
PubMed1978

[Shock lung].

Explore the source record for details and available documents.

Humans↗
PubMed1977

[Thygeson's superficial punctate keratitis (author's transl)].

Ten cases of Thygeson's bilateral punctate epithelial keratitis were observed during a two year period. The diagnosis, therapy and prognosis are discussed. The common erroneous diagnosis of herpetic keratitis may lead to corneal damage as a result of too intensive therapy. Highly hydrophilic contact lenses have proven to be a valuable aternative to steroid therapy. The etiology remains obscure. Viruses were not detected with either tissue culture technique or with electron microscopy.

Adolescent↗
PubMed1975

[Titanium, steel and their combination in bone surgery].

The combined application of Titanium plates with stainless steel screws appeared interesting, making a more elastic plate available without the risk of screw fractures. 3 different combinations of Titanium und stainless steel implants were tested in the animal and on humans. A morphometric evaluation of the soft tissue (animal) gave similar good results for stainless steel implants as for the combination of Titanium and steel, while pure Titanium gave the best result. Atomic absorption tests (human) showed that in case of the Titanium/steel mixture only the stainless steel screws did corrode. Delayed fracture healing or mechanical instability always gave risk to more metal deposits in the soft tissue than primary bone healing. If the advantages of Titanium seem important and if the rigidity of stainless steel screws may not be missed, the combination of the two metals appears possible and without danger.

Alloys↗