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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 274 (1972), S. 229-237 
    ISSN: 1432-1912
    Keywords: Rat Folic Acid Reductase ; Pregnancy ; Fetus ; Newborns ; Trimethoprim
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The folic acid reductase activity in various organs of adult rats was studied in comparison to pregnant females (20th day of gestation) and fetal rats. The enzyme activities in the tissues of pregnant rats were in general about 30% higher than in normal adults. Fetal rats also possess the ability to catalyze the reduction of dihydrofolic acid, but it is evident that the liver and kidney have a considerably reduced capacity to form tetrahydrofolate. The folic acid reductase activity in liver and kidney rises for 10 days after birth and then declines to normal enzyme levels by the 4th week of life. Further studies concerning the interaction between trimethoprim and folic acid reductase in adult rats demonstrate that an oral dose of 5 or 50 mg/kg results in about a 30% increase of folic acid reductase activity in liver and kidney. The experiments suggest that there is a stimulation of enzyme synthesis following trimethoprim administration; because, the trimethoprim induced increase of the reductase activity is blocked by the administration of either puromycin or actinomycin D.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 278 (1973), S. 227-230 
    ISSN: 1432-1912
    Keywords: Trimethoprim ; Rat Folic Acid Reductase ; Pregnancy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The increased level of folic acid reductase activity in rats during the perinatal period is inhibited following the oral administration of 5 or 50 mg/kg Trimethoprim. When the enzyme activity was tested in vitro, the highest sensitivity to the antimetabolite was displayed by the liver reductase isolated from rats the 20th day of pregnancy, the lowest was observed in the foetal liver extract. It is proposed that the stimulated reductase activity during the pregnancy is caused by a newly synthesized, Trimethoprim-sensitive enzyme form. The results of the in vitro experiments could contribute to the suggested hypothesis.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Basic research in cardiology 91 (1996), S. 50-52 
    ISSN: 1435-1803
    Keywords: Myocardial ischemia ; reperfusion ; myocarial infarction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: In conclusion 1)Despite certain similarities between ischemic preconditioning and myocardial hibernation, these two cardioprotective phenomena are different in nature. 2) Intermittent reperfusion inbetween the preconditioning and the sustained ischemic period is not necessary for infarct size reduction by ischemic preconditioning.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1435-1803
    Keywords: Greggphenomenon ; regionalfunction ; stunnedmyocardium ; myocardialoxygenconsumption ; reperfusion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The “Gregg phenomenon” implies that myocardial function and oxygen consumption ( $$M\dot VO_2 $$ ) increase when coronary perfusion is enhanced within or above the autoregulatory range. We have recently demonstrated that the “Gregg phenomenon” has no significance for regional myocardial function and $$M\dot VO_2 $$ in anesthetized swine in situ. There is, however, some evidence that the “Gregg phenomenon” may exist within stunned myocardium. To test whether coronary hyperperfusion increases regional myocardial function and $$M\dot VO_2 $$ in stunned myocardium, in six anesthetized swine the left anterior descending coronary artery (LAD) was cannulated and perfused at constant pressure (CAP) using an extracorporal circuit. The coronary vein which parallels the LAD was cannulated to allow measurement of regional $$M\dot VO_2 $$ and regional systolic wall thickening (WT%) of the anterior myocardium was assessed using sonomicrometry. Blood flow (CBF) to the LAD was increased by increasing CAP within the extracorporal circuit or by intracoronary adenosine infusion (150 μg/min). In normal myocardium, increasing CBF from 71.4 ± 19.7 (SD) to 156.7 ± 48.8 ml/min/100 g by increasing CAP from 100 ± 10 to 190 ± 10 mm Hg or increasing CBF from 75.1 ± 29.1 to 189.2 ± 45.8 ml/min/100 g by intracoronary adenosine infusion did not increase WT% (34.3 ± 12.2 % vs 32.1 ± 10.6 % and 32.3 ± 10.7 % vs 30.1 ± 13.2 %, respectively). $$M\dot VO_2 $$ was not changed during enhanced CAP (6.94 ± 1.05 vs 8.10 ± 1.08 ml/min/100 g) and during intracoronary adenosine infusion (6.67 ± 1.45 vs 7.30 ± 2.23 ml/min/100 g). Twenty min of hypoperfusion followed by 30 min of reperfusion depressed WT% by 47 % (p 〈 0.05). However, $$M\dot VO_2 $$ was only decreased by 23 % (NS). In the stunned myocardium, increasing CBF from 62.1 ± 36.4 to 157.1 ± 60.0 ml/min by increasing CAP was not associated with an increase in WT%. $$M\dot VO_2 $$ , however, increased from 5.14 ± 1.07 to 8.88 ± 1.83 ml/min/100 g (p 〈 0.05). Comparable results were achieved when CBF was increased from 60.3 ± 28.7 to 176.9 ± 48.5 ml/min by intracoronary adenosine infusion. WT% was unaffected, while $$M\dot VO_2 $$ increased from 4.69 ± 0.92 to 9.46 ± 3.39 ml/min/100 g (p 〈 0.05). Thus, increasing coronary perfusion within or above the autoregulatory range increases $$M\dot VO_2 $$ in stunned myocardium, but without a simultaneous increase in regional myocardial function.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Basic research in cardiology 90 (1995), S. 294-296 
    ISSN: 1435-1803
    Keywords: Myocardial ischemia ; reperfusion ; inotropic reserve calcium antagonists ; ACE inhibitors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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