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Biomedical subjects

H Degenhardt

Publications and source records attributed to H Degenhardt.

8 recordsLinked to original sources
PubMed2001

TGF-beta(1) downregulates PTHrP in coronary endothelial cells.

Parathyroid hormone-related peptide (PTHrP) is expressed throughout the cardiovascular system including coronary endothelial cells. Factors involved in the regulation of cardiac PTHrP expression have not been examined before. This study investigates the influence of transforming growth factor (TGF)-beta(1)on ventricular PTHrP expression. Coronary endothelial cells were isolated from ventricles of adult rats and PTHrP protein expression in these cultures was analysed by immunoblotting. TGF-beta(1)caused a concentration-dependent reduction in PTHrP protein within 24 h. In transgenic mice over-expressing TGF-beta(1)ventricular PTHrP protein expression and release was reduced compared to non-transgenic littermates. Similar concerns hold for PTHrP mRNA content (RT-PCR). Since ventricular TGF-beta(1)expression increases under pathophysiological conditions like arterial hypertension, ventricular PTHrP expression was further determined in aging spontaneously hypertensive (SHR-SP) and normotensive rats. TGF- beta(1)expression was increased in SHR-SP and ventricular PTHrP mRNA expression was downregulated at the age of 10 months. PTHrP expression did not recover in elder SHR-SP in which TGF-beta(1)expression was normalized again. Finally, we investigated ventricular PTHrP expression in rats after banding of the ascending aorta which generates a pressure induced hypertrophy without an induction of TGF-beta(1)expression. In ventricles from these animals, PTHrP expression was transiently increased and normalized at day 3. In conclusion, PTHrP expression was reduced under all conditions in which coronary endothelial cells were exposed to TGF-beta(1). PTHrP expression does not correlate with cardiac hypertrophy. Since coronary endothelial cells represent the majority of PTHrP producing cells in the ventricle its downregulation by TGF- beta(1)seems to be relevant for the paracrine effects of PTHrP.

Aging↗
PubMed1990

[Polymerase chain reaction: an overview].

In an unprecedented short time, the polymerase chain reaction (PCR) has developed into an indispensible analytical tool which facilitates gene analyses and recombinant techniques, enables DNA detection from single cells, and permits sequence determinations even from extinct species. Like the PCR process itself, the number of laboratories making use of this novel technique has been growing exponentially. This report covers critically the PCR from the basic principle to selected examples. It illustrates the strengths of the method: speed, sensitivity, and versatility and discusses aspects which still need improvement and development.

DNA↗
PubMed1989

Rioprostil, a new prostaglandin E1, prevents cyclosporin A-induced damage to endocrine and exocrine pancreas.

The possibility that rioprostil can prevent cyclosporin A-induced damage to the pancreas is investigated. Cyclosporin A is given to rats once daily intragastrically in doses of 5, 10 and 20 mg/kg body weight. These doses cause dose dependent significant reduction of insulin release and enzyme secretion from the arterially perfused isolated pancreas. The subcutaneous injection of rioprostil, 15 micrograms/kg twice daily, could completely prevent the effects of 5 mg/kg cyclosporin A on insulin release and could completely prevent the effects of 5 mg/kg cyclosporin A on insulin release and could completely prevent the effects of 5 mg/kg cyclosporin A on insulin release and could also afford significant protection from the effects of 10 and 20 mg/kg cyclosporin A on both insulin release and enzyme secretion. The cytoprotective action of rioprostil on the pancreas may have therapeutic implications.

Animals↗
PubMed1988

Differential sensitivity of rat exocrine and endocrine pancreas to cyclosporine.

The effect of 5, 10, and 20 mg/kg bw cyclosporine on rat endocrine and exocrine pancreatic function was studied. Glucose-dependent insulin secretion from the endocrine pancreas was shown to be significantly impaired 8 days after cyclosporine was given once daily at a dose as low as 5 mg/kg. CCK-8-stimulated amylase and lipase secretion were less sensitive to the noxious effect of cyclosporine being impaired at a dose of 10 mg/kg. Trypsin secretion was shown to be impaired at 20 mg/kg cyclosporine only. Our results demonstrate that cyclosporine causes dose-dependent impairment of both pancreatic endocrine and exocrine functions: the endocrine pancreas being more sensitive to the noxious action than the exocrine pancreas.

Amylases↗
PubMed1988

Prevention of toxic effects of cyclosporin on pancreatic B-cells of rats by Rioprostil, a new prostaglandin analogue.

Cyclosporin 5, 10, and 20 mg/kg bw was given to rats once daily intragastrically and caused a dose dependent, significant decrease of glucose dependent insulin release from the arterially perfused isolated pancreas, without affecting animal behaviour, weight gain, microscopic appearances of the pancreas, or kidney function. Subcutaneous injection of a new synthetic prostaglandin analogue Rioprostil 7.5 micrograms/kg bw twice daily completely prevented the effect of cyclosporin 5 mg/kg bw and protected significantly against the effects of cyclosporin 10 and 20 mg/kg bw.

Animals↗
PubMed1978

[Arrhythmias in athlets (author's transl)].

380 athletes in optimal performance were examinated within 10 years between 2 and 13 times (average: 4 times): ECG were taken at rest, during breathing tests and under maximal physical load by ergometry. 88 (23.2%) of them showed arrhythmias, 32 in the same examination different forms of premature beats. All kinds of arrhythmias were seen except atrial flatter, total av-block and paroxysmal tachycardias. Breathing tests provoked most of arrhythmias followed by the recovery after maximal physical load. Follow-up studies and clinical examinations proved that in 86 sportsmen these arrhythmias were not a symptom of heart disease. Only in 2 athletes heart injury could not be excluded. But in nearly 50% extracardial inflammations, like tonsillitis, bronchitis etc., were found. It is discussed that bradycardia and vagotonia of the highly trained sportsmen cause the arrhythmias. This vagotonia is intensified by breathing tests. But arrhythmias found in athletes should cause an examination for other chronical sicknesses.

Adolescent↗