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  • 1
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The roles of ATP-sensitive K+ channels (KATP channels) in ischaemic or pharmacological preconditioning in the rabbit heart remain unclear. Infarct limitation by ischaemic preconditioning was abolished by the KATP channel blocker glibenclamide under ketamine/xylazine anaesthesia, but not under anaesthesia induced by pentobarbital. Infarct limitation by the KATP channel opener pinacidil was detected under ketamine/xylazine anaesthesia, but not under pentobarbital anaesthesia. Thus, these effects appear to be anaesthetic dependent.2. In the present study, we examined whether nicorandil (a KATP channel opener nitrate) exhibits cardioprotective actions under halothane anaesthesia, another commonly used volatile anaesthetic. Control animals were subjected to 40 min coronary occlusion and 120 min reperfusion. Before 40 min ischaemia, the nicorandil group received nicorandil (100 μg/kg per min, i.v., for 10 min), the 5′ preconditioning (PC) group received 5 min ischaemia/20 min reperfusion, the 2.5′PC group received 2.5 min preconditioning ischaemia/20 min reperfusion, the nicorandil + 2.5′PC group received both nicorandil and 2.5 min ischaemia/20 min reperfusion, the nicorandil + 2.5′PC + 5-hydroxydecanoate (5HD) group received both nicorandil and 2.5 min ischaemia/20 min reperfusion in the presence of 5-hydroxydecanoate (5HD; a KATP blocker) and the 5HD group received 5 mg/kg, i.v., 5HD alone. Myocardial infarct size in control (n = 7), nicorandil (n = 5), 5′PC (n = 8), 2.5′PC (n = 5), nicorandil + 2.5′PC (n = 5), nicorandil + 2.5′PC + 5HD (n = 5) and 5HD (n = 4) groups averaged 44.4±3.6, 41.7±5.7, 17.8±3.2,* 34.1±4.8, 21.3±4.2,* 39.1±5.6 and 38.9±5.0% of the area at risk, respectively (*P 〈 0.05 vs control).3. Thus, nicorandil alone did not have an infarct size- limiting effect in halothane-anaesthetized rabbits. However, the results suggest that even when nicorandil alone does not demonstrate a direct cardioprotective effect, it may enhance ischaemic preconditioning via KATP channels.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-7241
    Keywords: candesartan cilexetil ; angiotensin II AT1 receptor antagonist ; essential hypertension ; cardiac hypertrophy ; magnetic resonance imaging ; echocardiography
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Using cine magnetic resonance imaging (MRI) and echocardiography, we investigated the effects of candesartan cilexetil, a specific angiotensin II type 1 (AT1) receptor antagonist, on left ventricular (LV) mass and hemodynamics in patients with essential hypertension. Ten patients (four men and six women) with essential hypertension received candesartan cilexetil 2–8 mg/day orally for 8–12 weeks. After drug administration, systolic blood pressure (BP) decreased from 178.9 ± 17.2 mmHg (mean ± SD) to 150.2 ± 14.3 mmHg (P 〈 0.0001) and diastolic BP from 101.4 ± 6.5 mmHg to 87.8 ± 11.9 mmHg (P = 0.0021). Both MRI and echocardiography revealed a significant decrease in LV mass index (LVMI) after candesartan cilexetil. MRI indicated that LVMI decreased from 111.3 ± 31.3 g/m2 to 102.6 ± 32.1 g/m2 (P = 0.0484) and echocardiography that LVMI decreased from 123.9 ± 31.1 g/m2 to 115.8 ± 31.4 g/m2 (P = 0.0316). Total systemic vascular resistance decreased significantly during treatment with candesartan cilexetil in both MRI and echocardiography assessment, from 1847.2 ± 636.3 dynes·s·cm−5 to 1540.4 ± 432.0 dynes·s·cm−5 (P = 0.0034) on MRI and from 1820.4 ± 318.8 dynes·s·cm−5 to 1659.0 ± 317.7 dynes·s·cm−5 (P = 0.0060) on echocardiography. These findings suggest that candesartan cilexetil 2–8 mg/day orally for 8–12 weeks is beneficial in the regression of cardiac hypertrophy in patients with essential hypertension.
    Type of Medium: Electronic Resource
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