Search PubMed⌕ Search

Biomedical subjects

D W Scheuch

Publications and source records attributed to D W Scheuch.

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

Inhibition of lipoxygenase (LOX) or of cyclooxygenase (COX) improves survival of rats in endotoxin shock.

In a well defined endotoxin (ET) shock model we compared the influence of a selective LOX-inhibitor FLM 5011 and the COX-inhibitor Acetylsalicylic acid (ASA) on survival as well as on their effects on TXB2 and 6-oxo-PGF1 and on selected parameters characterizing the shock syndrome. Pretreatment with both substances reduced the lethality rate. Neither TXB2 nor the PGF1 concentration revealed a consistent trend after therapeutic intervention. None of the investigated mediators could be identified as the primary "shock mediator".

6-Ketoprostaglandin F1 alpha↗
PubMed1988

Influence of inhibitors of the eicosanoid metabolism, of antagonists of the eicosanoids and of PAF on mortality assayed in three biochemically characterized shock models.

Experiments were carried out to lower the mortality (LD70-90) of rats in ovalbumin-induced anaphylactic (DA) shock and in endotoxin-induced (ET) shock, and of mice after injection of Platelet-activating Factor (PAF shock) comparing the effects of the cyclooxygenase (COX)-inhibitors aspirin (ASA), indomethacin, of the COX-/lipoxygenase (LOX)-inhibitors nordihydroguajaretic acid (NDGA), phenidone and X 86 (analogue of BW 755c), of the inhibitor of thromboxane (TX) synthesis HOE 944, of the TX-antagonist BM 13177, of the PAF-antagonist BN 52021 and of ketotifen. Ketotifen was strongly effective in DA shock, COX- and LOX-inhibitors only slightly. Combined COX- and LOX-inhibitors and BN 52021 showed good effects in the ET shock. Ketotifen was inefficacious. All the used substances influenced the PAF shock. The shock syndromes were biochemically characterized by determination of isocitratedehydrogenase (ICDH) activity, lactate, glucose, haematocrit, numbers of thrombocytes and leucocytes, TXB2 and 6-keto-Prostaglandin(PG)F1 alpha.

Anaphylaxis↗
PubMed1987

[In vitro effects of E. coli endotoxin on the membrane permeability and substrate transport of isolated rat liver mitochondria].

Incubation of freshly isolated rat liver mitochondria with E. coli endotoxin resulted in an increased inner membrane permeability for K+ and Cl- ions. This effect was not prevented by addition of the synthetic antioxidant butylated hydroxytoluene. The carrier-mediated transport rates of phosphate, pyruvate, citrate and reducing equivalents via the malate-aspartate shuttle were not altered significantly by endotoxin. Therefore, the endotoxin-mediated impairment of mitochondrial respiration and oxidative phosphorylation could not be attributed to a decrease in transport capacities through the inner mitochondrial membrane.

Animals↗
PubMed1987

Inhibition of stimulated dopamine release from striatum slices after hemorrhagic shock in the rat. Protective effect of piracetam.

The antihypoxic effect of piracetam was studied using a hemorrhagic shock model in the rat. Different shock severity was achieved by bleeding of 35% or 50% of estimated blood volume (EBV). Hemorrhagic shock caused an inhibition of K+ induced dopamine release from striatum slices in proportion to the magnitude of hemorrhage, reflecting the degree of membrane damage in dopaminergic transmission structures. Piracetam was effective in preventing the post-hemorrhagic changes in moderate shock and accelerated restitution of post-hemorrhagic release inhibition in severe shock.

Animals↗