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Biomedical subjects

H Kühne

Publications and source records attributed to H Kühne.

At least 37 records · Page 2Linked to original sources
PubMed1988

Determination of kallikreinogen (KKN) in human plasma by activation with Hageman factor fragment (F XIIf).

On the basis of activation of KKN by F XIIf an assay for determination of KKN levels was developed. The esterolytic activity of the activation product PK was measured with BAEE as substrate. After maximal activation of normal human plasma the esterolytic activity amounts to 16.82 +/- 2.03 mukat/l plasma (n = 25). The within run precision and day to day precision characterized by the variation coefficient were 2.5 and 4.9, respectively.

Arginine↗
PubMed1988

[Chromatographic separation of activated proteases from human plasma].

After separation of aceton and dextran sulfate activated human plasma by column chromatography on DEAE-cellulose three esterolytically and amidolytically active fractions, respectively, were obtained, which were assigned to the following species: plasma kallikrein (PK), PK.alpha-macroglobulin.HMW-Kininogen. Their percentage in the whole activity is variable. The proportion of free PK is low (0.11). For characterization of the products we studied inhibition by different polyvalent inhibitors. The Michaelis constant (Km) with p-toluene-sulfonyl-L-arginine methyl ester (TAME) were determined. For simulation of in vivo conditions dextran sulfate activated plasma was inactivated at 37 degrees C. The residual activity and the spontaneous activity in plasma from patients with shock are produced by different active protease inhibitor complexes.

Chromatography, DEAE-Cellulose↗
PubMed1988

Effect of intravenous enkephalin administration on kallikrein-kinin system in experimental hemorrhagic shock. Evidence for activation of kallikrein-kinin system by naloxone.

The effects of enkephalin derivates with different opioid receptor subtype specificity and naloxone on cardiovascular responses and kallikrein-kinin system (KKS) were studied in anesthetized rats exposed to 30% hemorrhage. Administration of a mu-receptor agonist (DAGO) in early hemorrhage improved mean arterial blood pressure (MAP) responses to hemorrhage. This effect could be abolished by naloxone pretreatment. Moreover, a delayed MAP recovery after hemorrhage could be observed. Treatment with a delta-agonist (DADL) resulted in transient depression of MAP and heart rate (HR). Hemorrhage by itself caused only a slight activation of KKS as indicated by decreased plasma kallikreinogen concentration and reduced kallikrein inhibitor capacity after 20% blood loss. Enkephalin administration did not exert significant effects on KKS. Naloxone pretreatment, in contrast, induced prehemorrhagic activation of KKS, which was potentiated by subsequent hemorrhage. Naloxone-induced activation of KKS could be confirmed by an in vitro study. Taken together these results suggest that the KKS is not involved in MAP and HR responses to enkephalin administration during hemorrhage, whereas it might be implicated in naloxone-induced delayed posthemorrhagic MAP recovery.

Animals↗
PubMed1986

[Blood glucose and serum insulin levels in newborn infants of diabetic mothers during feeding with an oligosaccharide mixture].

Macrosome newborns from mothers with an insulin-bound diabetes mellitus and also from mothers with a gestational diabetes show in the cord blood nearly always insulin levels additional to increased glucose values, which, compared with the normal controls are ten-fold higher in some cases. During the first three hours of life the blood glucose values decrease extremely. To prevent central injuries, caused by stronger hypoglycaemia, the early supply of oligosaccharides by continuous gastric infusion has proved as the most careful procedure. Stronger increases of blood glucose do not occur by this method and the insulin levels show a continuous tendency to normalisation.

Adult↗
PubMed1984

[Activation of the kallikrein-kinin system by clonidine].

Our results show that after the application of clonidine an activation of the kallikrein kinin system develops. The activation is characterized by the proof of active kallikrein and the decrease of kallikreinogen and the inhibitor capacity against kallikrein and trypsin. The extent of the activation seems to depend on the dosage of clonidine. The more pronounced reaction of the kallikrein kinin system might be connected with the side effects observed in the clonidine test.

Child↗
PubMed1984

[Neonatal risk in early manifested maternal diabetes].

Neonatal risk in 172 women with early manifested maternal diabetes mellitus (manifestation less than or equal to 18 years) has been estimated in an analysis of 10 years. We found a tendency towards an increased rate of mortality and malformations, but there are no statistic significant differences compared with the White B group as well as with the C/D-group of late manifestation. An increased risk of morbidity (rate of fetopathy , immaturity, disturbed adaptation) could be demonstrated, but it exists also in the newborns of diabetic mothers of the White group B. Using the recent literature the causes have been discussed and conclusions have been made.

Congenital Abnormalities↗
PubMed1983

[Gestation in early onset diabetes mellitus].

Report about the gestation of 172 diabetic patients with manifestation of disturbance of carbohydrate metabolism in childhood or adolescence (Group White C and D early manifestation) based on a ten years experience. Relating to age of menarche, behaviour of menstrual cycle and course of pregnancy no significant difference could be found in comparison to 454 other diabetic patients delivered in the same clinic. Only the frequency of obstetrics operations of more than 50 per cent was higher significantly.

Adolescent↗