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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Basic research in cardiology 81 (1986), S. 336-341 
    ISSN: 1435-1803
    Keywords: 133Xe washout ; border zones ; myocardial ischemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We measured the functional overlap between the left arterior descending (LAD) and the rest of the coronary arteries in the dog heart. The measurements were performed by loading only the field of the LAD with133Xe gas via a close-arterial injection during normal perfusion. The LAD perfusion was then interrupted and blood was allowed to flow retrograde from the distal LAD segment. This caused a condition of extremely low flow in the tissue perfused by the LAD. Examination of the washout kinetics revealed two distinct compartments. The slow compartment accounted for 97% of the injected Xenon and was assumed to represent the central ischemic field of the LAD. The fast component accounted for only 3% of the injected tracer and was assumed to include all regions of admixture between the LAD and other coronary vessels at the lateral borders. Thus, less than 3% of the LAD's field functionally communicates with the rest of the coronary circulation.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Basic research in cardiology 91 (1996), S. 35-37 
    ISSN: 1435-1803
    Keywords: Ischemic preconditioning ; adenosine ; ST segment ; protein kinase C
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Basic research in cardiology 83 (1988), S. 128-136 
    ISSN: 1435-1803
    Keywords: collateral blood flow ; ischemia ; 133Xe washout
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The relationship between the collateral perfusion of ischemic myocardium and the size of the ischemic zone was examined in open-chest anesthetized dogs. Proximal and distal segments of the left anterior descending coronary artery were cannulated and perfused extracorporally from the carotid artery. By occluding one or both of these perfusion lines, three different sized ischemic zones were made in each heart. Collateral perfusion to each ischemic zone was measured by the133Xe washout method. Blood flow density (flow per unit volume tissue) to the ischemic zone was lowest when both coronary segments were occluded, as opposed to occluding either single segment in each heart (0.17±0.03 vs. 0.28±0.005 ml/min/cm3, p〈0.01 by the paired t-test). A significant correlation could not be demonstrated between the ischemic zone size and the collateral flow when the data from all dogs were pooled (r=0.19, p〉0.05). These findings demonstrate that collateral perfusion of ischemic myocardium is inversely related to ischemic zone size in any given heart, but ischemic zone size is actually a minor determinant of collateral flow when compared to the large individual variability of coronary collateralization present in the dog population.
    Type of Medium: Electronic Resource
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  • 4
    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
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