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Biomedical subjects

W Paschen

Publications and source records attributed to W Paschen.

119 records · Page 7Linked to original sources
PubMed1979

Response of platelets exposed to potassium tetraperoxochromate, an extracellular source of singlet oxygen, hydroxyl radicals, superoxide anions and hydrogen-peroxide.

When potassium tetraperoxochromate (K3CrO8) is added to platelet suspension media it decomposes to the oxygen species hydrogen peroxide, superoxide radicals, hydroxyl radicals, and singlet oxygen. K3CrO8 induces a reversible shape change and aggregation of human platelets and, in the presence of Tris or sucrose, also the release of serotonin. Its effect on shape change and aggregation is due to the long-lived species hydrogen peroxide and is abolished by indomethacin and acetylsalicylic acid. Superoxide radicals, which are formed from K3CrO8 in HEPES-containing media do not evoke a platelet response. The release of serotonin depends on an interaction of hydroxyl radicals with Tris or sucrose and is associated with excessive formation of thiobarbituric acid-reactive material from platelets. Other scavengers of hydroxyl radicals such as mannitol, dimethylsulfoxide, EDTA or histidine prevent the release and the formation of thiobarbituric acid chromogen. Interaction of hydroxyl radicals with Tris or sucrose most likely results in the generation of short-lived intermediates which may act on platelets to produce thiobarbituric acid chromogen and to promote serotonin release. These effects on platelets are not inhibited by acetylsalicylic acid or indomethacin. Therefore the highly reactive hydroxyl radical and singlet oxygen, when generated extracellularly, do not mediate their effects via the enzyme-catalyzed prostaglandin pathway, in contrast to those evoked by the less reactive hydrogen peroxide.

Blood Platelets↗
PubMed1978

Superoxide-independent platelet response to xanthine oxidase.

Xanthine oxidase (1--5 microgram/ml) from cow's milk induces shape change, aggregation, and the release reaction of human washed platelets. Xanthine oxidase plus xanthine produce superoxide radicals, which reduce nitro blue tetrazolium. Superoxide dismutase, allopurinol, or ommission of xanthine inhibits the reduction of nitro blue tetrazolium but has no influence on the platelet response to xanthine oxidase. In contrast, small amounts of plasma or apyrase from potatoes abolish the effect on platelets, but not the enzyme activity of xanthine oxidase. Comparison of two xanthine oxidase preparations shows that higher specific enzyme activity corresponds to a lesser effect on platelets. The results suggest that platelet and enzyme activities reside in different components of xanthine oxidase preparations.

Apyrase↗
PubMed1975

Problems concerning the biochemical action of superoxide dismutase (erythrocuprein).

The decay of the tetraperoxochromate- (V) complex (CrO83theta) was examined to study the substrate specificity of erythrocuprein (super-oxide dismutase). The decay of CrO83theta proved rather complex in aqueous solutions. Apart from the two known oxygen species O2theta and singlet oxygen (1 deltagO2), H2O2 and probably OH radicals were formed. No unequivocal evidence for the appearance of superoxide was obtained. The possible electron transfer from Cr5 to Fe3 (cytochrome c) was also discussed. In Tris buffer, pH 7.8, there were absolutely no signs of superoxide or OH radical formation. In fact, pulse radiolysis measurements employing a homogeneous OH source demonstrated that the Tris and OH radicals react with each other. One mol of H2O2 was generated from 1 mol of CrO83theta in Tris buffer. By contrast, only 0.5 mol H2O2 could be determined when the CrO83theta decay was carried out in 2-[4-(2-hydroxyethyl)-1-piperazinyl]-ethanesulfonic acid (HEPES) buffer, pH 7.8. The phenomenon of reducing oxidized cytochrome c could not fully be assigned to a superoxide-mediated reduction, since erythrocuprein was unable to inhibit this cytochrome c reduction efficiently. The energetic oxygen species (1deltag O2, OH etc.) appearing during the CrO83theta decay gave rise to a clearly detectable chemiluminescence. In this system, erythrocuprein was very active regardless of which buffer was used. Even in the absence of a chemiluminescent mediating agent, which might have interferred with the enzyme, erythrocuprein proved capable of inhibiting the CrO83theta-induced chemiluminescence in a rather specific way. No such specificity was seen in the presence of low molecular weight Cu-chelates including Cu(Tyr)2, Cu(Lys)2 and Cu(His)2. The ability to suppress chemiluminescence was approximately 3 orders of magnitude less pronounced than that of the native enzyme. It is presumed that erythrocuprein reacts with oxygen species other than the superoxide radical.

Animals↗
PubMedDate not supplied

Polyamines in cerebral ischemia.

The present series of experiments was designed to study regional profiles of polyamines (putrescine, spermidine, and spermine) in reversible cerebral ischemia produced in rats and Mongolian gerbils. Polyamine profiles did not change during ischemia, but did following recirculation. The most prominent changes were a dramatic postischemic increase in putrescine and a marked decrease in spermine in severely damaged regions. Within a given brain structure, the postischemic putrescine levels correlated closely with the density of ischemic cell injury and the time period of cerebral ischemia. Furthermore, putrescine was already considerably increased in the CA1-subfield of the hippocampus of gerbils after 8 h recirculation, i.e., at a time when the cells are still intact. The results indicate that putrescine may be viewed as an excellent biochemical correlate of ischemic cell injury. The postischemic changes in putrescine levels are discussed in relation to the known activities of this compound.

Animals↗
PubMedDate not supplied

Regional pH and electrolyte homeostasis of cat brain after prolonged ischemia.

Following prolonged cerebral ischemia, primary electrophysiological recovery may be followed by secondary deterioration of the recovery process. It has been suggested that the secondary deterioration is caused by "late" cytotoxic brain edema. To test this hypothesis, adult normothermic cats were submitted to 1 h complete cerebral ischemia followed by 3 and 6 h recirculation, respectively. Postischemic recovery of energy metabolism was imaged by ATP-induced bioluminescence, and regional tissue pH and electrolyte content was measured in regions with and without metabolic recovery. In areas with postischemic restitution of metabolic activity, sodium gradually rose from 338 +/- 17 to 488 +/- 28 mumol/g protein and calcium from 8.81 +/- 0.35 to 18.24 +/- 0.97 mumol/g protein. Tissue potassium content decreased from 761 +/- 12 to 676 +/- 19 mumol/g protein and magnesium from 46.8 +/- 0.8 to 36.3 +/- 1.1 mumol/g protein. Tissue pH rose from 7.09 +/- 0.04 to 7.31 +/- 0.13 and 7.26 +/- 0.17 after 3 and 6 h recirculation, respectively. In areas without metabolic recovery, electrolyte disturbances were even more pronounced and pH--after transient alkalization--fell to 6.82 +/- 0.12. These data demonstrate that during the later phase of postischemic recirculation, progressive disturbances of electrolyte homeostasis create a preedematous situation that has to be considered for preventing delayed postischemic complications.

Adenosine Triphosphate↗
PubMedDate not supplied

Pial arterial pressure in cats following middle cerebral artery occlusion. II. Relationship to regional disturbance of energy metabolism.

Focal cerebral ischemia was produced in 16 cats by occluding the left middle cerebral artery (MCA) for 120 min. Cortical blood flow and pial artery pressure were determined prior to vascular occlusion and after 15, 60 and 120 min. At the end of the experiments (after 120 min MCA occlusion) heads were frozen in situ with liquid nitrogen. Cooled brains were cut into 0.5 cm thick slices. From these slices twenty-micron sections passing through the territory of the MCA were prepared in a cryostat and used in the pictorial presentation of glucose and ATP. NADH-fluorescence was recorded from the tissue slice, immersed in liquid nitrogen. In addition, tissue samples were taken from regions of interest and used for quantitative determination of biochemical substrates. In all but two animals permanent MCA occlusion led to disturbances in the energy-producing metabolism, as indicated by reduction in glucose and ATP, and increase in lactate. The regions exhibiting bright NADH-fluorescence were much smaller than those in which ATP was absent. In 6 animals NADH-fluorescence was not increased but even decreased in areas with disturbed energy-producing metabolism. A close correlation was obtained after comparing cortical blood flow measured 15 min after MCA occlusion with the area of ATP-depletion at the end of the experiments. However, the size of ATP-depletion did not correlate with flow measured 60 or 120 min after MCA occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Regional cerebral blood flow, glucose metabolism, protein synthesis, serum protein extravasation, and content of biochemical substrates in stroke-prone spontaneously hypertensive rats.

Stroke-prone spontaneously hypertensive rats with arterial blood pressure above 210 mmHg were taken for the present study after appearance of neurological symptoms. Regional cerebral blood flow, glucose metabolism, and protein synthesis rate were evaluated on the same brain section by means of triple-labelled autoradiographic techniques. Consecutive sections were used in the pictorial presentation of glucose, ATP, and serum protein extravasation. In addition, NADH-fluorescence was recorded. Two different patterns of hypertension-induced brain lesions could be distinguished: in two animals sharply demarcated cysts were visible in the cortical grey matter. In these animals no regional inhomogeneities of flow and metabolism were present remote from the infarct. In contrast, in three animals cysts were located in the white matter, leading to pronounced hemodynamic and metabolic disturbances throughout the brain. It is concluded that edema-induced brain swelling was the main cause for reduction in blood flow and metabolism.

Adenosine Triphosphate↗