Microtubule stabilization with paclitaxel does not protect against infarction in isolated rat hearts.

摘要: New Findings What is the central question of this study? The microtubule network disrupted during myocardial ischaemia–reperfusion injury. It was suggested that prevention disruption with paclitaxel might reduce cardiac infarct size; however, effects on infarction have not been studied. What main finding and its importance? Paclitaxel caused a reduction in cardiomyocyte hypercontracture ischaemia–reperfusion. However, it induced greater increase cytosolic calcium, which may explain lack effect against we seen isolated rat hearts. The large perfusion pressure by model clinical implications, because detrimental drug were reported after application. Microtubules play major role transmission mechanical forces within myocardium maintenance organelle function. intracellular We assessed injury cardiomyocytes Isolated submitted to normoxia (1 h) or 45 min simulated ischaemia (pH 6.4, 0% O2, 37°C) reoxygenation, without treatment stabilizer, (10−5 m), inhibitor polymerization, colchicine (5 × 10−6 m). Simulated leads before onset ischaemic contracture. Paclitaxel attenuated both incidence hypercontracture, whereas mimicked reoxygenation. In normoxic hearts, concentration-dependent decreases heart rate left ventricular developed increases pressure. Despite protection pretreatment did modify size (60.37 ± 2.27% control hearts versus 58.75 ± 10.25, 55.44 ± 10.32 50.06 ± 10.14% 10−6, 3 × 10−6 10−5 m paclitaxel) 60 min global reperfusion Lack correlated higher calcium levels treated (2.32 ± 0.15 1.13 ± 0.16 a.u. presence absence 10−6 m paclitaxel, respectively, P < 0.05), but changes aortic reactivity. conclusion, stabilization reduces does protect