Library

X
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
    Longitudinal Changes in Myocardial Basic Fibroblast Growth Factor (FGF-2) Activity Following Coronary Artery Ligation in the Dog
    Amsterdam : Elsevier
    Journal of Molecular and Cellular Cardiology 26 (1994), S. 683-690 
    Details
    ISSN: 0022-2828
    Keywords: Angiogenesis ; Coronary occlusion ; Myocardial ischemia ; Neovascularization ; Radioactive microspheres
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1006/jmcc.1994.1081
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Failure of N-2-mercaptopropionyl glycine to reduce myocardial infarction after 3 days of reperfusion in rabbits (1999)
    Springer
    Basic research in cardiology 94 (1999), S. 180-187 
    Details
    ISSN: 1435-1803
    Keywords: Key words Free radicals – N-2-mercaptopropionyl glycine – myocardial infarction – preconditioning – triphenyltetrazolium chloride
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Recent studies have repoarted that prolonged infusion of N-2-mercaptopropionyl glycine (MPG), a diffusible antioxidant, could limit infarct size in dogs. However, there are no comparable studies testing this agent in other species. We examined the efficacy of MPG in a rabbit model of infarction. Rabbit hearts were subjected to a 30-min coronary artery occlusion. Infarct size expressed as a percentage of risk zone was determined by either triphenyltetrazolium chloride (TTC) staining after 3 h of reperfusion (study 1) or by histology after 72 h of reperfusion (study 2). In study 1, 37 ± 2.6 % of the risk zone infarcted in the control group. Intravenous MPG at a rate of 100 mg/kg/h starting 15 min after the onset of ischemia and continuing until 1 h after reperfusion had no effect on infarct size (35.4 ± 3.4 % infarction). However, infusion of MPG until the end of reperfusion significantly reduced infarct size as measured with TTC to 17.2 ± 2.5 % (p 〈 0.01 vs. control group). In study 2, 48.6 ± 4.0 % of the risk zone infarcted in the control group. In the treatment group MPG was started as above and was continued for 4 h of reperfusion followed by an intramuscular injection at the termination of the intravenous infusion. No protection was seen after 72 h of reperfusion (43.8 ± 2.1 % infarction). These findings reveal that MPG at a dose and schedule that appeared to protect the dog heart could not effect sustained protection in the rabbit heart. TTC staining revealed that MPG appeared to have preserved viability for up to 3 h of reperfusion suggesting that failure may have been due to early withdrawal of the drug. Alternatively, early TTC staining may yield spurious results under conditions in which protection is dependent upon antioxidant or free radical scavenger treatment as has previously been suggested. It is concluded that MPG as administered in the previous canine studies does not limit infarct size in all species, thus raising a concern about MPG's potential efficacy in man.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003950050141
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Myocardial protection by insulin is dependent on phospatidylinositol 3-kinase but not protein kinase C or KATP channels in the isolated rabbit heart (1999)
    Springer
    Basic research in cardiology 94 (1999), S. 188-198 
    Details
    ISSN: 1435-1803
    Keywords: Key words Insulin – tyrosine kinase – protein kinase C – KATP channels – phosphatidylinositol 3-kinase – ischemic preconditioning
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Because tyrosine kinase blockade prevents protection by ischemic preconditioning (PC) in several species, activation of tyrosine kinase appears to be critical for cardioprotection. The tyrosine kinase's identity, however, is unknown. The present study tested whether activation of a receptor tyrosine kinase, the insulin receptor, could mimic PC and if the mechanism of protection was similar to that of PC. Isolated rabbit hearts were subjected to 30 min of regional ischemia and 2 h of reperfusion. Infarct size was determined by triphenyltetrazolium staining and expressed as a percentage of the area at risk. Infarct size in control hearts was 32.6 ± 2.3 %. A 5-min infusion of insulin (5 mU/ml) followed by a 10-min washout period prior to ischemia significantly reduced infarction to 14.7 ± 2.1 % (P 〈 0.05). The tyrosine kinase inhibitor genistein (50 μM) given around the insulin infusion blocked protection (28.9 ± 2.8 %). However, when present during the onset of ischemia, genistein had no effect on protection triggered by insulin (14.0 ± 2.4 %; P 〈 0.05). Inhibition of either PKC by polymyxin B (50 μM) or KATP channels by 5-hydroxydecanoate (100 μM) also failed to prevent protection by insulin (17.5 ± 3.2 % and 17.6 ± 3.0 %, respectively). However, the reduction in infarct size by insulin was significantly attenuated by wortmannin (100 nM), a selective inhibitor of phosphatidylinositol 3-kinase (P13K, 28.3 ± 2.2 %). Insulin was still able to protect the heart when given only during the reperfusion period (13.2 ± 3.4 %). PC reduced infarction to 12.8 ± 2.0 % (P 〈 0.05). In conclusion, activation of the insulin receptor reduces infarct size in the rabbit heart even when instituted upon reperfusion. However, the mechanism of protection is quite different from that of PC and involves activation of P13K but not PKC or KATP channels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003950050142
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Attenuation of S-T Segment elevation during repetitive coronary occlusions truly reflects the protection of Ischemic preconditioning and is not an epiphenomenon (1997)
    Springer
    Basic research in cardiology 92 (1997), S. 426-434 
    Details
    ISSN: 1435-1803
    Keywords: Key words Ischemia – preconditioning – 8-(p-sulfophenyl)theophylline – ST segments – tyramine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Attenuation of S-T segment elevation between the first and subsequent balloon inflations of a coronary angioplasty procedure has been assumed to indicate a transition to a preconditioned state, but there has been no validation of this assumption. Open-chest rabbits were instrumented with a coronary snare and epicardial electrode. The coronary artery was occluded twice for 5 min with each occlusion followed by 10 min of reflow before a final 30 min occlusion. The evolving S-T elevation was quantitated as the voltage-time integral. For the first coronary occlusion total S-T segment elevation averaged 40.8±5.4 mV·min, significantly greater than 26.2±4.6 mV·min for the second occlusion (p 〈 0.001). There was no further change during the initial 5 min of the third occlusion (42.5±4.5 mV·min). When the protection of ischemic preconditioning was blocked by intravenous infusion of 8-(p-sulfophenyl)theophylline, an adenosine receptor antagonist, attenuation of S-T segment elevation was no longer apparent. When preconditioning was pharmacologically triggered by tyramine rather than ischemia, there also was no alteration in S-T segment elevation among the 3 occlusions. Therefore, S-T elevation was diminished during the second episode of ischemia only when a transition occurred from non-preconditioned to preconditioned state between occlusions. An attenuated S-T segment is a valid marker for the presence of the preconditioned state.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00796217
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    Adenosine A1 Agonist at Reperfusion Trial (AART): Results of a Three-Center, Blinded, Randomized, Controlled Experimental Infarct Study (2000)
    Springer
    Cardiovascular drugs and therapy 14 (2000), S. 607-614 
    Details
    ISSN: 1573-7241
    Keywords: adenosine ; A1 receptor agonist ; GR79236 ; infarct size ; ischemia-reperfusion ; reperfusion injury
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Adenosine A1 receptor agonists given prior to myocardial ischemia limit ischemic injury in several species. However, the ability of adenosine receptor agonists to limit infarct size when given at reperfusion has proved controversial. We designed a three-center experimental study using a blinded, randomized treatment protocol to test the hypothesis that adenosine A1 receptor activation during early reperfusion can attenuate lethal reperfusion injury, thereby reducing infarct size. Sixty anesthetized rabbits (20 in each laboratory) underwent 30 minutes coronary artery occlusion followed by 120 minutes reperfusion. The selective adenosine A1 receptor agonist GR79236 (10.5 μg/kg, a dose shown to limit infarction in this model when given before ischemia) or vehicle were administered IV 10 minutes before reperfusion. Infarct size was assessed by tetrazolium staining and, after the randomization code was revealed, data from the three laboratories were pooled for statistical analysis. Infarct size was not modified by administration of GR79236. In the vehicle-treated group, the infarct-to-risk ratio was 28.9 ± 2.7% (n = 24) compared with 31.9 ± 2.6% (n = 26) in the GR79236-treated group (not significant). Risk zone volume was similar in the two groups (1.06 ± 0.05 cm3 vs 1.00 ± 0.05 cm3, respectively). A modest reduction in rate-pressure product was noted following the administration of GR79236, but this effect was transient. The same dose of GR79236 was found to limit infarct size when given prior to coronary artery occlusion. We conclude that A1 receptor activation does not modify lethal reperfusion injury in myocardium.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007850527878
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...