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  • 1
    Electronic Resource
    Electronic Resource
    Analogs of UK 14,304 as α"2-adrenoceptor agonists. Twist and agent polarity as design elements.
    Amsterdam : Elsevier
    Bioorganic & Medicinal Chemistry Letters 4 (1994), S. 459-462 
    Details
    ISSN: 0960-894X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology , Medicine
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0960-894X(94)80016-2
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  • 2
    Electronic Resource
    Electronic Resource
    Myocardial stretch induced by increased left ventricular diastolic pressure preconditions isolated perfused hearts of normotensive and spontaneously hypertensive rats (1997)
    Springer
    Basic research in cardiology 92 (1997), S. 410-416 
    Details
    ISSN: 1435-1803
    Keywords: Stretch ; non-ischemic stress ; post-ischemic dysfunction ; isolated perfused heart ; spontaneously hypertensive rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective: The aim of our study was to determine whether myocardial stretch (non-ischemic stress) could precondition isolated perfused hearts of both normotensive Wister-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR).Methods: The perfused hearts in Langendorff mode were subjected to 30 min of global no-flow ischemia followed by 30 min of reperfusion. Left ventricular developed pressure (LVDP) and end-diastolic pressure (LVEDP) were measured. In the control group, LVEDP was set at 10 mmHg. In the stretch group, LVEDP was increased to 30 or 60 mmHg for 5 min before 30 min of ischemia. In the ischemic preconditioning group, the hearts were exposed to two cycles of a 5-min period of ischemia before 30 min of ischemia. Myocardial lactate contents were measured at the baseline and at the end of the 60 mmHg stretch.Results: Hemodynamic parameters of LVDP and LVEDP at 30 min of reperfusion improved in the stretch group (LVEDP at 60 mmHg) and the ischemic preconditioning group. Coronary flow did not decrease during the stretch. Recovery of the coronary flow during reperfusion was better in the stretch and ischemic preconditioning groups. Postischemic contractile function was better in WKY rats than in SHR. Myocardial lactate contents at the end of 60 mmHg stretch were negligible. Conclusions: Myocardial stretch induced by increasing LVEDP preconditioned isolated perfused hearts of both WKY rats and SHR, via mechanisms not involving myocardial ischemia during stretch.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00796215
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  • 3
    Electronic Resource
    Electronic Resource
    Myocardial stretch induced by increased left ventricular diastolic pressure preconditions isolated perfused hearts of normotensive and spontaneously hypertensive rats (1997)
    Springer
    Basic research in cardiology 92 (1997), S. 410-416 
    Details
    ISSN: 1435-1803
    Keywords: Key words Stretch – non-ischemic stress – post-ischemic dysfunction – isolated perfused heart – spontaneously hypertensive rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective: The aim of our study was to determine whether myocardial stretch (non-ischemic stress) could precondition isolated perfused hearts of both normotensive Wister-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). Methods: The perfused hearts in Langendorff mode were subjected to 30 min of global no-flow ischemia followed by 30 min of reperfusion. Left ventricular developed pressure (LVDP) and end-diastolic pressure (LVEDP) were measured. In the control group, LVEDP was set at 10 mmHg. In the stretch group, LVEDP was increased to 30 or 60 mmHg for 5 min before 30 min of ischemia. In the ischemic preconditioning group, the hearts were exposed to two cycles of a 5-min period of ischemia before 30 min of ischemia. Myocardial lactate contents were measured at the baseline and at the end of the 60 mmHg stretch. Results: Hemodynamic parameters of LVDP and LVEDP at 30 min of reperfusion improved in the stretch group (LVEDP of 60 mmHg) and the ischemic preconditioning group. Coronary flow did not decrease during the stretch. Recovery of the coronary flow during reperfusion was better in the stretch and ischemic preconditioning groups. Postischemic contractile function was better in WKY rats than in SHR. Myocardial lactate contents at the end of 60 mmHg stretch were negligible. Conclusions: Myocardial stretch induced by increasing LVEDP preconditioned isolated perfused hearts of both WKY rats and SHR, via mechanisms not involving myocardial ischemia during stretch.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00796215
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  • 4
    Electronic Resource
    Electronic Resource
    Release kinetics of cardiac troponin T in coronary effluent from isolated rat hearts during hypoxia and reoxygenation (1992)
    Springer
    Basic research in cardiology 87 (1992), S. 428-436 
    Details
    ISSN: 1435-1803
    Keywords: Troponin T (TnT) ; creatine kinase (CK) ; lactate dehydrogenase (LD) ; hypoxia ; isolatedheart
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A newly developed troponin T (TnT) test for the detection of myocardial cell necrosis has been reported to be very efficient in the detection of acute myocardial infarction. The aim of the present study was to determine whether cardiac TnT in coronary effluent from isolated heart perfused with albumin-free perfusion medium could be detected using the enzyme-linked immuno-sorbent assay developed by Katus et al. Isolated rat hearts were perfused according to the method of Langendorff. Coronary flow rate was measured by timed collection of the coronary perfusate that dripped from the hearts during 5 h of hypoxia (protocol A) or 4 h of hypoxia followed by 1 h of reoxygenation (protocol B). Creatine kinase (CK) and lactate dehydrogenase (LD) levels were compared with that of TnT. Myocardial adenine nucleotides were measured by HPLC. There was a strong correlation between TnT levels in albumin-free coronary effluent and TnT levels in coronary effluent diluted 1:1 with 5% bovine serum albumin (r=0.996, N=72). The coefficients of correlation between TnT and CK or LD during hypoxia and reoxygenation were 0.891 (N=88) and 0.871 (N=88), respectively. The coefficient of correlation between CK and LD was 0.993 (N=88). There were no significant differences in either the decrease of coronary flow or the increase of TnT content between the hearts in the two protocols. There was no significant correlation between ΣTnT and energy charge of adenine nucleotides. These results indicate that cardiac TnT levels can be easily measured in albumin-free coronary effluent of isolated heart preparations. Like CK and LD, TnT is a good indicator for detecting myocardial cell damage. However, the release kinetics of TnT seem to be different than those of CK and LD. After 4 h of hypoxia, 1 h of reoxygenation has no effect on coronary flow rate or release of TnT. ΣTnT did not determine energy charge at the end of hypoxia or reoxygenation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00795055
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  • 5
    Electronic Resource
    Electronic Resource
    Release kinetics and correlation with hemodynamic dysfunction of cardiac troponin T in coronary effluent from isolated rat hearts during reperfusion (1993)
    Springer
    Basic research in cardiology 88 (1993), S. 307-313 
    Details
    ISSN: 1435-1803
    Keywords: Troponin T (TnT) ; creatine kinase (CK) ; lactate dehydrogenase (LD) ; reperfusion ; isolated rat heart
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Previously, we reported that cardiac troponin T (TnT) can be detected and measured in coronary effluent from isolated rat hearts during hypoxia. The present study was designed to evaluate the release kinetics of TnT from post-ischemic rat hearts. Using the Langendorff technique, the hearts were reperfused for 4h after 20 min or 60 min of global ischemia. Coronary flow was measured by timing the collection of the coronary perfusate that dripped from the hearts, and left ventricular pressure (LVP) was monitored continuously during the experiments. The amount of TnT released in 1 min was compared with the release of creatine kinase (CK) and lactate dehydrogenase (LD). The release kinetics of CK and LD showed a monophasic pattern and the levels at 4 h after reperfusion returned to baseline levels. By contrast, the release kinetics of TnT showed a small peak followed by a larger and more sustained peak. There were good negative correlations between developed pressure of LVP and both Σ TnT and the amount of TnT released within 1 min at 4 h after reperfusion. These results indicate that the release kinetics of TnT is different from that of CK and LD during reperfusion, and further that cardiac TnT is a useful indicator of myocardial cell damage and can be used to evaluate the degree of myocardial cell damage in both the early and late phase of acute myocardial infarction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00800637
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  • 6
    Electronic Resource
    Electronic Resource
    Effects of ischemic preconditioning on the release of cardiac troponin T in isolated rat hearts (1994)
    Springer
    Basic research in cardiology 89 (1994), S. 241-249 
    Details
    ISSN: 1435-1803
    Keywords: Cardiac troponin T ; ischemic preconditioning ; left ventricular pressure ; reperfusion-induced arrhythmia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The aim of this study was to examine the effect of ischemic preconditioning on the releases of cardiac troponin T (TnT) during reperfusion in isolated rat hearts. Experiments were done on 22 rat hearts, which were perfused according to the method of Langendorff and were divided into the control group (n=14) and the preconditioning group (n=8). Double 5 min of ischemia each followed by 5 min reflow were applied as ischemic preconditioning. After 20 min of global ischemia, the releases of TnT, creatine kinase (CK), and lactate dehydrogenase (LD) in coronary effluent and the left ventricular developed pressure (LVP) were measured during 60 min of reperfusion. Ischemic preconditioning significantly suppressed the amounts of TnT released during reperfusion, as with those of CK and LD, and also improved contractile dysfunction (nine hearts in which ventricular fibrillation was sustained were excluded from the evaluation for hemodynamics), though the release kinetics of TnT was different from that of CK and LD. There were good inverse relationships between the LVP and the total amounts of TnT released during reperfusion period (Σ TnT) or TnT levels at 60 min of reperfusion. Cardiac TnT can be used as a useful biochemical marker for hemodynamics and myocardial damage after reperfusion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00795616
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