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  • 11
    Electronic Resource
    Electronic Resource
    Low-dose tacrolimus (FK506)-based immunosuppressive protocol in living donor renal transplantation (1998)
    Springer
    Transplant international 11 (1998), S. S60 
    Details
    ISSN: 1432-2277
    Keywords: Key words Tacrolimus ; FK506 ; Renal transplantation ; Low-dose
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In order to avoid the side effects of tacrolimus (FK506), a low-dose FK506-based regimen was started from 1 June 1991. The dose was adjusted to maintain the FK506 whole blood trough level at 15–20 ng/ml for 7 days postoperatively, at 10–15 ng/ml for 2 months, and under 10 ng/ml thereafter. The graft survival rates at 3 years and 5 years were 87.8 and 82.3 % (FK506) vs 86.8 and 86.8 % [cyclosporine (CyA)]. The incidence of acute rejection within the first 90 days was 31.6 % in the FK506 group which was lower than the 57.1 % of the CyA group (P = 0.0585). Grades of acute rejection episodes over IIA in the FK506 group were 20 %, which was lower than the 37 % in the CyA group. The mean oral dosages of FK506 were 0.061 and 0.04 mg/kg per day at 3 and 5 years, respectively. The incidence of new onset diabetes was 27.8 % in the FK506 group and 17.1 % in the CyA group. However, insulin therapy was withdrawn in all patients of the FK506 group within 5 months. The percentage of patients who required an antihypertensive agent was 28.6 % and 40 % in the FK506 group and 73.2 % and 88 % in the CyA group at 1 and 3 years, respectively (P 〈 0.05). Nephrotoxicity was seen in 20 % of the FK506 group and 14.3 % of the CyA group. Hypercholesterolemia was less frequent in the FK506 group than the CyA group. The FK506-based regimen described here is a protocol with the potential to reduce its adverse effects. The whole blood concentration of FK506 should be monitored and blood levels maintained in the range of 5–10 ng/ml after 90 postoperative days for optimal efficacy and minimal toxicity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001470050427
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  • 12
    Electronic Resource
    Electronic Resource
    The mechanism of protection from 5 (N-ethyl-N-isopropyl)amiloride differs from that of ischemic preconditioning in rabbit heart (1997)
    Springer
    Basic research in cardiology 92 (1997), S. 339-350 
    Details
    ISSN: 1435-1803
    Keywords: Key words Ischemic preconditioning – Na+/H+ exchange – 5-(N-ethyl-N-isopropyl)amiloride (EIPA) – protein kinase C
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We investigated the effects of 5-(N-ethyl-N-isopropyl)amiloride (EIPA) on infarction in isolated rabbit hearts and cardiomyocytes. Thirty min of regional ischemia caused 29.6 ± 2.8 % of the risk zone to infarct in untreated Krebs buffer perfused hearts. Treatment with EIPA (1 μM) for 20 min starting either 15 min before ischemia or 15 min after the onset of ischemia significantly reduced infarction to 5.4 ± 2.0 % and 7.0 ± 1.0 %, respectively (p 〉 0.01 versus untreated hearts). In both cases salvage was very similar to that seen with ischemic preconditioning (PC) (7.1 ± 1.5 % infarction). Unlike the case with ischemic preconditioning, however, protection from EIPA was not blocked by 50 μM polymyxin B, a PKC inhibitor, or 1 μM glibenclamide, a KATP channel blocker. Forty-five min of regional ischmia caused 51.0 ± 2,9 % infarction in untreated hearts. Ischemic preconditioning reduced infarction to 23.4 ± 3.1 % (p 〉 0.001 versus untreated hearts). In these hearts with longer periods of ischemia pretreatment with EIPA reduced infarction similarly to 28.8 ± 2.1 % (p 〉 0.01 versus untreated hearts). However, when EIPA was combined with ischemic PC, no further reduction was seen (23.8 ± 3,5 % infarction) To further elucidate the mechanism of EIPA's cardioprotective effect, this agent was also examined in isolated rabbit cardiomyocytes. Preconditioning caused a delay of about 30 min in the progressive increase in osmotic fragility that occurs during simulated ischemia. In contrast, EIPA had no effect on the time course of ischemia induced osmotic fragility. Furthermore, EIPA treatment did not alter the salutary effect of ischemic preconditioning when the two were combined in this model. We conclude that Na+/H+ exchange inhibition limits myocardial infarction in the isolated rabbit heart by a mechanism which ist quite different from that of ischemic preconditioning. Despite the apparently divergent mechanisms, EIPA's cardioprotective effect could not be added to that of ischemic or metabolic preconditioning in these models.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00788946
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  • 13
    Electronic Resource
    Electronic Resource
    The mechanism of protection from 5 (N-ethyl-N-isopropyl)amiloride differs from that of ischemic preconditioning in rabbit heart (1997)
    Springer
    Basic research in cardiology 92 (1997), S. 339-350 
    Details
    ISSN: 1435-1803
    Keywords: Ischemic preconditioning ; Na+/H+ exchange ; 5-(N-ethyl-N-isopropyl)amiloride (EIPA) ; protein kinase C
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We investigated the effects of 5-(N-ethyl-N-isopropyl)amiloride (EIPA) on infarction in isolated rabbit hearts and cardiomyocytes. Thirty min of regional ischemia caused 29.6±2.8% of the risk zone to infarct in untreated Krebs buffer-perfused hearts. Treatment with EIPA (1 μM) for 20 min starting either 15 min before ischemia or 15 min after the onset of ischemia significantly reduced infarction to 5.4±2.0% and 7.0±1.0%, respectively (p〈0.01 versus untreated hearts). In both cases salvage was very similar to that seen with ischemic preconditioning (PC) (7.1±1.5% infarction). Unlike the case with ischemic preconditioning, however, protection from EIPA was not blocked by 50μM polymyxin B, a PKC inhibitor, or 1μM glibenclamide, a KATP channel blocker. Forty-five min of regional ischemia caused 51.0±2.9% infarction in untreated hearts. Ischemic preconditioning reduced infarction to 23.4±3.1% (p〈0.001 versus untreated hearts). In these hearts with longer periods of ischemia pretreatment with EIPA reduced infarction similarly to 28.8±2.1% (p〈0.01 versus untreated hearts). However, when EIPA was combined with ischemic PC, no further reduction in infarction was seen (23.8±3.5% infarction). To further elucidate the mechanism of EIPA's cardioprotective effect, this agent was also examined in isolated rabbit cardiomyocytes. Preconditioning caused a delay of about 30 min in the progressive increase in osmotic fragility that occurs during simulated ischemia. In contrast, EIPA had no effect on the time course of ischemia-induced osmotic fragility. Furthermore, EIPA treatment did not alter the salutary effect of ischemic preconditioning when the two were combined in this model. We conclude that Na+/H+ exchange inhibition limits myocardial infarction in the isolated rabbit heart by a mechanism which is quite different from that of ischemic preconditioning. Despite the apparently divergent mechanisms, EIPA's cardioprotective effect could not be added to that of ischemic or metabolic preconditioning in these models.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00788946
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  • 14
    Electronic Resource
    Electronic Resource
    Mild Hypothermia reduces infarct size in the beating rabbit heart: A practical intervention for acute myocardial infarction? (1998)
    Springer
    Basic research in cardiology 93 (1998), S. 372-383 
    Details
    ISSN: 1435-1803
    Keywords: Key words Hypothermia – ischemic preconditioning – myocardial infarction – myocytes – rabbit
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present study describes a method for rapidly cooling the whole body via its blood pool and tests whether cooling instituted after ischemia has begun can sill limit infarction. We also evaluated whether the cardiac protection seen with cooling could be added to that from ischemic preconditioning. Recently it was reported that lowering myocardial temperature by only several degrees greatly slows the extent of myocardial infarction in the beating heart experiencing regional ischemia. To further explore the potential of hypothermia for myocardial protection, rabbits underwent either a 30-, 45- or 60-min coronary artery occlusion and 3-h reperfusion. Blood from a carotid artery was allowed to circulate through a heat exchanger immersed in ice water and return to a jugular vein until the blood temperature in the left atrium reached the target temperature of 35 or 32°C. Furthermore, to elucidate the mechanism of hypothermia's protection, we also examined its effect on isolated cardiomyocytes. Rewarming began upon reperfusion in all protocols. Cooling to 32°C before a 30-min ischemia reduced infarct size from 37.3±2.5% (n=6) of the risk zone in normothermic controls to 3.6±0.3% (n=6). When cooling was begun 10 or 20 min after the onset of ischemia infarct size was still significantly smaller [8.1±1.2% and 22.8±1.8%, respectively (n=6 in each group)]. Less but significant protection was also seen with cooling to 35°:C. Cooling caused only mild bradycardia and hypotension and no apparent arrhythmias. Forty-five min of regional ischemia caused 50.7±3.3% (n=6) of risk zone to infarct in untreated hearts. Preconditioning with 5-min ischemia/10-min reperfusion reduced infarct size to 27.5±2.5% (n=6). Cooling to 32°C starting 20 min after the onset of ischemia protected the heart (28.7±2.6% infarction, n=8), and this protection could be added to the effect from ischemic preconditioning delayed the progressive increase in osmotic fragility that occurs during simulated ischemia in an additive way, but only hypothermia delayed the appearance of contracture suggesting that different mechanisms are involved. Hence blood pool cooling was easily induced and well tolerated and protected the beating heart against infarction even when hypothermia was started after the onset of coronary occlusion. We conclude that hypothermia might be a simple and useful therapy for patients presenting with acute myocardial infarction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003950050105
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  • 15
    Electronic Resource
    Electronic Resource
    Mapping of 20 polymorphic DNA markers in the rat by somatic hybrid and linkage analysis (1996)
    Springer
    Mammalian genome 7 (1996), S. 71-73 
    Details
    ISSN: 1432-1777
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003359900018
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    Paper (German National Licenses)
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