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Biomedical subjects

D W Scheuch

Publications and source records attributed to D W Scheuch.

At least 19 recordsLinked to original sources

[The behavior of trypsin-like proteases in sulcus fluid].

The present study shows results aimed at determining whether levels of a trypsin-like protease in gingival crevicular fluid are associated with disease activity as assessed by the level of gingival inflammation and probing attachment loss. Maximum enzyme level was significantly elevated by groups with gingival inflammation and periodontal destruction. In a long-time study we find a decrease of enzyme activity with clinical therapy by scaling and root planning.

Adolescent

[Agent-conditioned influence on carbohydrate metabolism and energy state in liver and lung of rats in endotoxic shock].

The pretreatment of rats with the substance LPH and LXU caused decrease of lethality in endotoxin shock and suppression of the following changes 6 hours post endotoxin: Increase of plasma ICDH activity, decrease in platelet count, decrease of the hepatic energy state and increase of the ATP content in the lung. The catabolic glucose metabolism during endotoxin shock was not influenced by LPH and LXU administration.

Adenine Nucleotides

[The effect of vitamin E on the survival rate and biochemical parameters such as isocitrate dehydrogenase, lactate and selected peptidases and proteases during endotoxic shock in the rat].

Protective effect of the investigated alpha-tocopherol solution regarding survival and changes of several biochemical parameters in rat endotoxin shock could already be demonstrated after application of the solvent (special oil HCO-60) alone. An additional effect of Vitamin E was observed only in DP IV activity and leukocyte counts.

Animals

Hormonal responses to hemorrhage and their relationship to individual hemorrhagic shock susceptibility.

The effect of differences in sympathoadrenomedullary and pituitary-adrenocortical responses of individual animals to 35% hemorrhage on severity of shock induction has been studied in unanesthetized unrestrained rats by measuring plasma concentrations of adrenaline (A), noradrenaline (NA), corticosterone (CS) and adrenocorticotropin (ACTH). The responses of A, CS and ACTH were related to the decrease of blood volume and mean arterial pressure (MAP), whereas plasma NA remained unchanged. Higher susceptibility to blood loss was characterized by more pronounced hemorrhage-induced increase in blood lactate concentration and plasma enzyme activities as well as lethal outcome of hemorrhagic shock. In animals with irreversible hemorrhagic shock, enhanced catecholamine secretion and reduced ACTH release was observed. Furthermore, a revealed direct correlation between A and blood lactate concentration and plasma enzyme activities (aspartate aminotransferase, isocitric dehydrogenase, creatine kinase, lipase and glutathione-S-transferase) may indicate its possible participation in the mechanism of shock induction. In contrast, an inverse relationship of plasma CS to the indicators of shock severity was demonstrated. In conclusion, non-optimal neuroendocrine regulation of cardiovascular adjustments to hemorrhage in shock-prone animals might cause an exaggerated compensatory activation of adrenomedullary catecholamine secretion, which in turn has been shown to exert deleterious vascular and metabolic effects. The mechanisms responsible for reduced ACTH secretion in shock-prone animals remain to be established.

Adrenal Glands

[Influence of endotoxin on the synthesis of lipoxygenase products formed from arachidonic acid by rat alveolar macrophages].

Alveolar macrophages of normal and endotoxin--treated rats were stimulated in suspension by calcium ionophore A 23187. After solid phase extraction and isocratic separation by HPLC the lipoxygenase products (Leukotriene B4, 5-hydroxyeicosatetraenoic acid and 12-hydroxyeicosatetraenioc acid) were quantified. Unlike alveolar macrophages of control animals, alveolar macrophages of endotoxin treated rats showed an increased synthesis of lipoxygenase products (Leukotriene B4: 1.6fold; 5-hydroxyeicosatetraenoic acid: 2.1fold; 12-hydroxyeicosatetraenoic acid: 1.3fold). Our results suggest that in vivo endotoxin disturbs the mechanisms of arachidonic acid liberation in alveolar macrophages.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid

[The effect of LPH on the behavior of parameters of the kallikrein-kinin system (KKS) in the early phase of experimental endotoxic shock in the rat].

The effect of a new shock-protective agent LPH on parameters of the kallikrein-kinin-system was studied in a standardized endotoxin shock model. Activation of KKS in endotoxin shock was not significantly influenced by LPH. On the other hand, LPH by itself caused activation of KKS. Decrease of kininogen level by endotoxin, however, was prevented by the pretreatment with LPH.

Animals

Effect of kallikrein-kinin system activation by factor XII f pretreatment on experimental hemorrhagic shock.

Effects of Hageman factor fragment (factor XIIf) administration on shock induction were studied in anesthetized male Wistar rats with hemorrhagic shock. Administration of factor XIIf in non-hemorrhaged rats resulted in an immediate decrease of mean arterial pressure (MAP) for 5 min and in significant increases of blood glucose, lactate and hematocrit (Hct) as well as in a strong tendency for plasma kallikreinogen (KKN) to decrease. At the beginning of bleeding (15 min after factor XIIf administration) MAP has been normalized again. During subsequent hemorrhage pretreated rats showed a sharper decrease in MAP which remained significantly lower up to 25% of estimated blood volume (EBV) and recovered more slowly to normal level after hemorrhage. Blood glucose, lactate and Hct were significantly higher in pretreated animals after hemorrhage of 30% EBV. KKN depicted significant lower values during hemorrhage and in the posthemorrhagic period. Mortality within the observation time increased from 20% (control group) to 60% (pretreated animals). The results demonstrate that prehemorrhagic kallikrein-kinin system (KKS) activation induced an increased severity of shock state with higher mortality.

Animals

Energy state, glycolytic intermediates and mitochondrial function in the liver during reversible and irreversible endotoxin shock.

Metabolites of the energy and carbohydrate metabolism and mitochondrial function in the liver were compared in rats with reversible as well as with irreversible shock. 6 h after induction of shock there was a close correlation between the severity of shock and the energy state of the liver. Only rats with irreversible shock showed a marked deterioration in parameters of the adenylate system, whereas in animals with reversible shock the energy state remained at control levels. Liver glycogen and glucose stores declined similarly in all shocked rats. The capacity of isolated liver mitochondria to produce ATP did not essentially differ in reversible and irreversible shock. Further investigations should consider the intracellular environment in evaluating the mitochondrial function in vivo during endotoxin shock.

Adenosine Diphosphate

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

[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

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