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  • 1
    Electronic Resource
    Electronic Resource
    Effects of naftidrofuryl oxalate on microsphere-induced changes in acetylcholine and amino acid content of rat brain regions (1994)
    Springer
    Experimental brain research 99 (1994), S. 7-16 
    Details
    ISSN: 1432-1106
    Keywords: Acetylcholine ; Asparte ; Brain ischemia Glutamate ; Microsphere embolism Naftidrofuryl oxalate ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Effects of naftidrofuryl oxalate (naftidrofuryl) on neurotransmitter, acetylcholine, and amino acid content of brain regions following microsphere-induced cerebral embolism were examined to elucidate its possible therapeutic effects on ischemic brain. Rats received 900 microspheres (48 μm in diameter) via the right internal carotid artery, followed by ligation of the right common carotid artery; and histological and biochemical alterations were examined on the 3rd, 5th, and 28th days after embolism. The embolism induced increases in triphenyltetrazolium chloride-(TTC)-unstained areas and decreases in acetylcholine, glutamate, aspartate, and γ-aminobutyric acid (GABA) contents in the cerebral cortex, striatum, and hippocampus of the right hemisphere, suggesting that microsphere embolism causes severe damage to these brain regions. Hematoxylin-eosin staining of the right cortical sections after embolism showed degeneration and necrosis of nerve cells with chromatolytic nuclei and eosinophilic cytoplasm. Changes in neurotransmitters of the left hemisphere were relatively small. Treatment with naftidrofuryl of the embolized rats with stroke-like symptoms took place from postoperative day 1 to 28. Treatment resulted in a reduction in TTC-unstained areas, less morphological damage to cerebral cortex on the 3rd and 5th days, and an appreciable restoration of acetylcholine content of three brain regions of the right hemisphere throughout the experiment, but restoration of neurotransmitter amino acids was observed to a smaller degree. The results suggest that naftidrofuryl is capable of preventing the development of ischemia-induced, sustained damage to brain regions vulnerable to oxygen deficiency, particularly by improving impaired acetylcholine metabolism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00241407
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Role of cardiac renin-angiotensin system in sarcoplasmic reticulum function and gene expression in the ischemic-reperfused heart (2000)
    Springer
    Molecular and cellular biochemistry 212 (2000), S. 227-235 
    Details
    ISSN: 1573-4919
    Keywords: renin angiotensin system ; sarcoplasmic reticulum ; Ca2+-handling ; gene expression ; ischemia-reperfusion ; cardioprotection
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The aim of this study was to explore the possible participation of cardiac renin-angiotensin system (RAS) in the ischemia-reperfusion induced changes in heart function as well as Ca2+-handling activities and gene expression of cardiac sarcoplasmic reticulum (SR) proteins. The isolated rat hearts, treated for 10 min without and with 30 μM captopril or 100 μM losartan, were subjected to 30 min ischemia followed by reperfusion for 60 min and processed for the measurement of SR function and gene expression. Attenuated recovery of the left ventricular developed pressure (LVDP) upon reperfusion of the ischemic heart was accompanied by a marked reduction in SR Ca2+-pump ATPase, Ca2+-uptake and Ca2+-release activities. Northern blot analysis revealed that mRNA levels for SR Ca2+-handling proteins such as Ca2+-pump ATPase (SERCA2a), ryanodine receptor, calsequestrin and phospholamban were decreased in the ischemia-reperfused heart as compared with the non-ischemic control. Treatment with captopril improved the recovery of LVDP as well as SR Ca2+-pump ATPase and Ca2+-uptake activities in the postischemic hearts but had no effect on changes in Ca2+-release activity due to ischemic-reperfusion. Losartan neither affected the changes in contractile function nor modified alterations in SR Ca2+-handling activities. The ischemia-reperfusion induced decrease in mRNA levels for SR Ca2+-handling proteins were not affected by treatment with captopril or losartan. The results suggest that the improvement of cardiac function in the ischemic-reperfused heart by captopril is associated with the preservation of SR Ca2+-pump activities; however, it is unlikely that this action of captopril is mediated through the modification of cardiac RAS. Furthermore, cardiac RAS does not appear to contribute towards the ischemia-reperfusion induced changes in gene expression for SR Ca2+-handling proteins.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007174803993
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Attenuation of changes in sarcoplasmic reticular gene expression in cardiac hypertrophy by propranolol and verapamil (2000)
    Springer
    Molecular and cellular biochemistry 213 (2000), S. 111-118 
    Details
    ISSN: 1573-4919
    Keywords: pressure overload ; gene expression ; subcellular remodeling ; sarcoplasmic reticulum Ca2+-handling ; anti-hypertensive therapy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The effects of propranolol and verapamil on contractile dysfunction, subcellular remodeling and changes in gene expression in cardiac hypertrophy due to pressure overload were examined. Rats were subjected to banding of the abdominal aorta and then treated with either propranolol (10 mg/kg daily), verapamil (5 mg/kg daily) or vehicle for 8 weeks after the surgery. Depression of the left ventricular function in the hypertrophied heart was associated with decreases in myofibrillar and myosin CA2+ ATPase activities as well as Ca2+-pump and Ca2+-release activities of the sarcoplasmic reticulum (SR). The level of a-myosin heavy chain (α-MHC) mRNA was decreased while that of β-MHC mRNA was increased in the pressure-overloaded heart. The level of SR Ca2+-pump ATPase (SERCA2) mRNA and protein content for SERCA2 were decreased in the pressure overloaded heart. Treatment of the hypertrophied animals with propranolol or verapamil resulted in preservation of the left ventricular function and prevention of the subcellular alterations. Shift in the α- and β-MHC mRNA levels and changes in the expression in SERCA2 mRNA level and protein content were also attenuated by these treatments. The results suggest that blockade of β-adrenoceptors or voltage-dependent calcium channels normalizes the cardiac gene expression, prevents subcellular remodeling and thus attenuates heart dysfunction in rats with cardiac hypertrophy. Furthermore, both cardiac β-adrenoceptors and L-type Ca2+-channels may be involved in the genesis of cardiac hypertrophy due to pressure overload.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007120332587
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    Paper (German National Licenses)
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