Library

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • ATP  (1)
  • Aktivierte Thrombozyten  (1)
  • Ischemic cell necrosis  (1)
  • 1
    ISSN: 1432-0533
    Keywords: Barbiturate ; Ischemic cell necrosis ; Mongolian gerbil ; Nimodipine ; Putrescine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Twenty mongolian gerbils were anesthetized (1.5% halothane) and severe forebrain ischemia was produced in 15 animals by occluding both common carotid arteries. After 5 min ischemia brains were recirculated spontaneously. Immediately after ischemia nimodipine (1.5 mg/kg) or pentobarbital (50 mg/kg) was injected intraperitoneally into five animals. Four days later animals were reanesthetized (1.5% halothane); the brains were frozen with liquid nitrogen and cut in a cryostat. Ten-micrometer-thick coronal cryostat sections were stained with cresyl violet to assess the extent of ischemic cell damage in the lateral striatum, the CA1-layer of the hippocampus, and the thalamus. In addition, tissue samples (about 4 mg each) were taken from the lateral striatum, CA1 layer of the hippocampus and the thalamus. Putrescine levels were measured in these samples using reversed-phase high performance liquid chromatography and fluorescence detection. Reversible cerebral ischemia produced a significant increase in putrescine in the lateral striatum (from 11.15±0.79 to 44.83±11.76 nmol/g,P≤0.05), the CA1 subfield of the hippocampus (from 11.27±0.64 to 41.80±3.62 nmol/g,P≤0.05) and less so in the thalamus (from 11.28±0.70 to 16.50±1.71 nmol/g). Both postischemic nimodipine and barbiturate treatment of animals markedly reduced this increase in the lateral striatum to 14.09±1.41 and 15.75±1.38 nmol/g, respectively (P≤0.05 cf. untreated animals), to 29.82±6.04 and 23.21±3.12 nmol/g in the CA1-subfield of the hippocampus (P≤0.05 barbiturate-treated cf. untreated animals), and to 11.92±1.37 and 11.76±0.64 in the thalamus (P〈0.05 barbiturate-treated cf. untreated animals). Severe neuronal necroses were apparent in the lateral striatum in four out of five animals but in none of the nimodipine- or barbiturate-treated animals. In the CA1 subfield of the hippocampus the number of necrotic cells/mm stratum pyramidale amounted to 202.1±9.8, 141.9±4.2 and 78.0±33.4 in untreated, nimodipine- or barbiturate-treated animals, respectively (P≤0.05 barbiturate-treated cf. control animals). It is suggested that putrescine, produced during recirculation following ischemia, contributes to the manifestation of ischemic cell injury. Putrescine may thus be taken as a significant biochemical correlate of ischemic cell damage.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Annals of hematology 38 (1979), S. 17-24 
    ISSN: 1432-0584
    Keywords: Aktivierte Thrombozyten ; Aggregation ; Walker Zellen ; Activated platelets ; Aggregation ; Walker cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Walker 256 carcinoma cells form irreversible aggregates with rat platelets activated by ADP or serotonin. Since serotonin induces platelet shape change but not platelet aggregation the degree of activation indicated by the disc-sphere transformation is sufficient for platelets to interact with these tumor cells. This is confirmed by experiments with spheroid washed platelets which form irreversible mixed aggregates with Walker 256 carcinoma cells without a stimulus being required. This type of tumor cells could react with platelets in vivo, provided the platelets are activated by disturbed blood flow or contact with subendothelium. Our observations can explain why other authors found no interaction between Walker 256 carcinoma cells and non-activated platelets in vitro even though platelets contributed to the formation of blood-borne metastases of this tumor.
    Notes: Zusammenfassung Walker 256 Karzinomzellen bilden irreversible Aggregate mit Ratten-Thrombozyten, die durch ADP oder Serotonin aktiviert wurden. Serotonin induziert bei Thrombozyten die Formänderung, jedoch keine Aggregation. Der Aktivierungsgrad der Thrombozyten, der durch die Scheiben-Kugel-Transformation angezeigt wird, ist demnach für die Reaktion zwischen Thrombozyten und Walker-Zellen ausreichend. Dies wird durch Versuche mit sphäroiden gewaschenen Thrombozyten bestätigt: Diese Thrombozyten bilden ohne zusätzlichen Stimulus mit Walker-Zellen irreversible Aggregate. In vivo könnten Walker-Zellen mit Thrombozyten reagieren, die durch Wirbel im Blutstrom oder durch Kontakt mit Subendothel aktiviert wurden. Unsere Beobachtungen erklären, warum andere Autoren keine Reaktion zwischen Walker 256 Karzinomzellen und nicht-aktivierten Thrombozyten in vitro messen konnten, obwohl Thrombozyten bei diesem Tumor an der Ausbildung hämatogener Metastasen beteiligt sind.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 3
    ISSN: 1573-7365
    Keywords: brain ischemia ; seizure ; glycerol ; ATP ; lactate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Glycerol, the end product of phospholipid degradation, was measured in cat brains under pathophysiological conditions known to cause activation of lipolysis, namely, bicucullineinduced seizures, permanent focal cerebral ischemia (2hr of middle cerebral artery occlusion), and global cerebral ischemia (15 min of complete cerebral ischemia with or without 2 hr of recirculation). In addition, ATP and lactate were measured in order to correlate the activation of lipid degradation with disturbances in the energy-producing metabolism. A highly significant increase in the tissue glycerol content was observed after 1 hr of bicuculline-induced seizures (from 0.29 ± 0.07μmol/g in control animals to 1.30 ± 0.06μmol/g in seizure animals;P 〈 0.001) or after 15 min of complete cerebral ischemia (from 0.29 ± 0.07 to 1.17 ± 0.14μmol/g;P 〈 0.01). Furthermore, a close correlation was found between the increase in glycerol and the increase in lactate or decrease in ATP after permanent focal ischemia. In contrast, following recirculation after complete cerebral ischemia, restoration of the energy pool did not lead to a reduction of the glycerol formed during ischemia. It is concluded that glycerol is a useful indicator of lipid degradation under pathological conditions. Since glycerol formed during vascular occlusion is trapped in brain cells, presumably owing to low glycerol kinase activity, it can be used as a stable postischemic indicator of ischemia-induced lipid degradation.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...