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Di Napoli P et al.  
Ischaemic preconditioning of rat myocardium: effects on postischaemic coronary endothelium hyperpermeability and microcirculatory damage

Journal of Clinical and Basic Cardiology 1998; 1 (1): 37-42

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Fig. 1: Preconditioning - koronare Mikrozirkulation Fig. 2: Preconditioning - koronare Mikrozirkulation Fig. 3: Preconditioning - koronare Mikrozirkulation Fig. 4: Preconditioning - koronare Mikrozirkulation Fig. 5: Preconditioning - koronare Mikrozirkulation Fig. 6: Preconditioning - koronare Mikrozirkulation

Keywords: Endothelendotheliale PermeabilitätMikrozirkulationPräkonditionierungReperfusionsschadenendothelial permeabilityendotheliumischaemia-reperfusion damagemicrocirculationpreconditioning

Short cycles of ischaemia followed by reperfusion may exert a protective effect on ischaemic myocardial injury. Several pathophysiological mechanisms have been postulated to explain this phenomenon termed preconditioning (P). The aim of this study was to evaluate the effects of P on postischaemic endothelial hyperpermeability, an important factor involved in reperfusion injury and coronary microcirculatory alteration. Isolated Wistar male rat (250?300 g) hearts were subdivided into three groups: Group A: control hearts subjected to 20 min global normothermic ischaemia; Group B: hearts subjected to preconditioning (three phases of 3 min ischaemia, each one followed by 2 min Langendorff reperfusion) before ischaemia; Group C: hearts subjected to preconditioning and hypertonic reperfusion in order to increase the effects on postischemic interstitial fluid accumulation (osmotic forces balance). A 65 min working heart reperfusion was also performed to assess functional response. Haemodynamic data, reperfusion arrhythmias, heart weight changes (as wet weight/dry weight ratio, ww/dw), myocardial enzyme release, microcirculation permeability changes (FITC-albumin diffusion) and ultrastructural morphometry have been evaluated. In Group B, a significant reduction of reperfusion injury (functional recovery, enzyme release, arrhythmias and ultrastructural morphometry) was detected, compared with Group A. In Group C this reduction was significantly more evident than in groups A and B. In Groups B and C, a significant reduction in myocardial reperfusion oedema (ww/dw: A: 5.9 ± 0.5; B: 4.9 ± 1.1, p < 0.02 vs A; C: 4.4 ± 0.6, p < 0.01 vs A) and FITC-albumin diffusion (A: 32.8 ± 5.9 % area; B: 16.3 ± 6.1 % area, p < 0.01 vs A; C: 13.3 ± 4.5 % area, p < 0.01 vs A), especially in perimyocytic space was also observed. Data show that preconditioning may reduce endothelial postischaemic dysfunction (vascular permeability and ultrastructural alterations) and reperfusion interstitial oedema. The importance of fluid diffusion within the interstitium in the development of reperfusion damage is supported by better postischaemic recovery in Group C, in which interstitial oedema was reduced by altering intravascular osmotic load. J Clin Basic Cardiol 1998; 1: 37-42.
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