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
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 352 (1995), S. 424-428 
    ISSN: 1432-1912
    Keywords: Balloon injury ; Carotid artery ; Fibrates ; Neointima ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The inhibition of neointima formation by drugs is a major goal to prevent restenosis following angioplasty. In the present study, the effect of etofibrate on blood lipids and vessel wall was investigated using a balloon injury rat model. Two weeks after ballooning the common carotid artery neointima formation was quantified by morphometric measurement of the neointimal area and cellularity in vessel cross sections, and by fluorometric evaluation of the DNA content. Etofibrate (160 mg/kg/day) had no effect on plasma triglyceride levels, but reduced serum cholesterol by about 25%. The injury-induced increase of both the neointimal area and the DNA-content was significantly inhibited by 47% (P 〈0.005) and 34% (P 〈0.05), respectively, in the drug-treated animals in comparison to the untreated control rats. The ratio of neointima and media was significantly (P 〈 0.001) reduced from 152.9 ± 11.6% (controls) to 82.84 ± 12.59% in the etofibrate-treated group. The cellularity (numerical profile and volume density of nuclei) in the neointima was similar in both groups. In conclusion, injury-induced neointima formation is reduced in etofibrate-treated animals, which could be due to an inhibition of smooth muscle cell proliferation.
    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
    Naunyn-Schmiedeberg's archives of pharmacology 352 (1995), S. 424-428 
    ISSN: 1432-1912
    Keywords: Key words Balloon injury ; Carotid artery ; Fibrates ; Neointima ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The inhibition of neointima formation by drugs is a major goal to prevent restenosis following angioplasty. In the present study, the effect of etofibrate on blood lipids and vessel wall was investigated using a balloon injury rat model. Two weeks after ballooning the common carotid artery neointima formation was quantified by morphometric measurement of the neointimal area and cellularity in vessel cross sections, and by fluorometric evaluation of the DNA content. Etofibrate (160 mg/kg/day) had no effect on plasma triglyceride levels, but reduced serum cholesterol by about 25%. The injury-induced increase of both the neointimal area and the DNA-content was significantly inhibited by 47% (P〈0.005) and 34% (P〈0.05), respectively, in the drug-treated animals in comparison to the untreated control rats. The ratio of neointima and media was significantly (P〈0.001) reduced from 152.9±11.6% (controls) to 82.84±12.59% in the etofibrate-treated group. The cellularity (numerical profile and volume density of nuclei) in the neointima was similar in both groups. In conclusion, injury-induced neointima formation is reduced in etofibrate-treated animals, which could be due to an inhibition of smooth muscle cell proliferation.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Pharmaceutical research 13 (1996), S. 457-461 
    ISSN: 1573-904X
    Keywords: nicanartine ; lipoprotein ; oxidation ; plasma binding
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract Purpose. The aim of this study is to investigate the plasma protein binding of nicanartine and to measure its antioxidant effect on lipoproteins. Methods. The blood binding was studied with an erythrocyte partitioning method and the lipoprotein oxidation with the conjugated dienes method. Results. Nicanartine was 24.7% LDL (low density lipoprotein)-bound and 29.2% AAG (alphal-acid glycoprotein)-bound. Nicanartine delayed but did not stop the oxidation of the three density classes of lipoprotein HDL (high density lipoprotein), LDL, VLDL (very low density lipoprotein). The addition of AAG to LDL in the conjugated dienes method decreased the nicanartine fraction bound to LDL and decreased its antioxidant effect. The decrease of nicanartine LDL-bound fraction and the decrease in antioxidant effect were not parallel. Conclusions. This suggested that (a) AAG-bound nicanartine dissociated to equilibrate the decrease in LDL-bound nicanartine consummed by oxidation, or (b) the oxidation conditions could involve chemical modifications of nicanartine and therefore modify its affinity for AAG.
    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...