Cortex and medulla of rat kidney generate different amounts of PG I2-like activity.
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Biomedical subjects
Publications and source records attributed to K Silberbauer.
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Intravenous glucose tolerance test(taking the age dependent variabilities of the glucose assimilation into consideration) was performed in 68 blood relations (30 siblings, 19 parents, 19 children) of 19 patients with juvenile onset diabetes mellitus (JODM). In 29,4% of the first degree relatives (in 20% of the siblings, in 42% of the parents and in 31,6% of the children) an abnormal glucose tolerance was found. Four of the siblings presented with insulin dependent JODM. Glucose intolerance was detected more often (42%) in siblings and parents of patients with later onset (after age 25) JODM than in siblings and parents of JODM-patients with onset before age 25 (20%).
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Angiotensin II's influence on circulating levels of prostaglandin I2 metabolite 6-keto-PGF1-alpha were determined during a pharmacological stress test of left ventricular function in 10 control subjects and 5 patients with coronary artery disease. Angiotensin II infusion (1.5 +/- 0.34 micrograms/min) led to a significant increase of mean arterial blood pressure in both study groups (p less than 0.001). Heart rate decreased in control subjects (p less than 0.01) whereas in patients with coronary artery disease no significant change occurred. Global left ventricular ejection fraction determined by gated blood pool scanning decreased significantly in both study groups (p less than 0.05). The lack of reflex bradycardia in patients with coronary artery disease may be due to a compensatory increased sympathetic tone, prohibiting a more pronounced decline in ejection fraction. 6-keto-PGF1-alpha levels could be measured only in 6 of 15 persons. In the others they were below the limit of detection of the assay (70 pg/ml). During angiotensin II infusion 6-keto-PGF1-alpha increased significantly and could be determined in all persons. Patients with coronary artery disease reached slightly higher 6-keto-PGF1-alpha levels than controls (119 +/- 19 pg/ml versus 91.5 +/- 7 pg/ml; n.s.). Thus although angiotensin II infusion leads to vasoconstriction and increases peripheral resistance it also stimulates the production of vasodilating prostaglandins which may play a role in preserving microcirculation.
In 70 patients with juvenile-onset, insulin-dependent (type I) diabetes and 75 age- and sex-matched controls the reversible platelet aggregates expressed as platelet count ratio (PCR) and the ADP-induced platelet aggregation were studied. Retinal microangiopathy was staged by retinal fluorescein angiography. The mean PCR of the patients (0.82 +/- 0.02) was statistically significantly lower than that of the controls (0.97 +/- 0.01). However, in different stages of retinopathy no significantly different PCR could be observed. ADP-induced platelet aggregation (0.5 and 1.0 micromol/l) exhibited a higher reactivity of diabetic platelets, but with the exception of tangent alpha (see later), the differences were not statistically significant in comparison to the controls. After collagen-induced platelet aggregation (0.5 and 1 microgram/ml) the lag time in diabetics was significantly (p less than 0.001) lower than in the controls, whereas the other quantitative parameters exhibited higher platelet reactivity in general, though not statistically significant. No relationship between PCR and the in vitro induced aggregation was found. The degree of retinopathy had no significant influence on platelet aggregation. In general, the data demonstrate an increase in sensitivity of platelets in juvenile-onset diabetics, whereas no influence of stage of microangiopathy could be detected.