The Asia Pacific Heart Journal最新文献

The participation of reactive oxygen species in different cardiovascular pathologic conditions is widely recognised. One of these situations is the Ischaemia-reperfusion phenomenon where the role of oxygen free radicals (OFR) has been of particular interest. Ischaemia-reperfusion is a common phenomenon in the clinical setting and is observed in thrombolytic therapy, percutaneous transluminal coronary angioplasty (PTCA) and open-heart surgery. Several experimental and clinical studies strongly suggest that antioxidants may ameliorate reperfusion injury during open-heart surgery. In this regard, the following substances have been used: mannitol, deferoxamine, vitamin E, allopurinol and coenzyme Q₁₀. In PTCA procedures, the presence of an oxidative stress after reperfusion was also shown by several authors, but up to now, only probucol demonstrated efficacy in reducing restenosis after these techniques.

Background: Minimally invasive cardiac surgery has been developed in part as a result of progress in video-assisted and endovascular surgical techniques. Port-access cardiac surgery, which provides cardiopulmonary bypass, cardioplegic arrest, myocardial protection, and ventricular decompression, permits various procedures to be performed through smaller, less invasive incisions. Methods: Proper patient selection is emphasised in order to minimise potential complications with the port-access system. For port-access coronary revascularisation procedures, a limited left anterior thoracotomy allows harvesting of the internal mammary artery and access to the target coronary arteries. The ascending aorta can be exposed for placement of vein grafts. For port-access mitral valve surgery, a limited right thoracotomy provides direct visualisation of the left atrium and the mitral valve. Results: The feasibility and efficacy of port-access coronary revascularisation and mitral valve surgery have been demonstrated in experimental and clinical settings. Peripheral cardiopulmonary bypass with cardioplegic arrest has been reproducibly achieved based on indices of cardiac function. Port-access multivessel coronary revascularisation and port-access mitral valve procedures have been performed with acceptable results. Conclusions: The port-access catheter system effectively achieves peripheral cardiopulmonary bypass, aortic occlusion, cardioplegia delivery, and left ventricular decompression. Alternative, less invasive methods of coronary revascularisation and various intracardiac procedures can be performed without a conventional median sternotomy.

Background. AQP-1, a channel-forming integral membrane protein of 28 kDa prevalent in red blood cells and renal proximal tubules, was recently shown to be expressed in rat heart.

Aims: Our purpose was to charaterise the experssion of the AQO-1 gene in rat heart with respect to cell type, developmental stage and pathophysiological condition. Methods: To determine in which heart cell type the water channel was expressed, we measured AQP-1 mRNA and protein levels and immunolocalised protein in freshly isolated myocytes from adult rats and cultured myocytes and fibroblasts from neonatal rats. Results: Northern blot analysis showed that AQP-1 mRNA is expressed in adult cardiac myocytes, neonatal myocytes, and neonatal cardiac fibroblasts of rats at levels nearly as high as those observed in rat kidney. Western blot analysis, however, detected AQP-1 protein only in purified adult and neonatal cardiac myocytes at levels markedly less than kidney. Immunohistochemistry and confocal imaging localised AQP-1 protein to the sarcolemmal membrane of myocytes. Since the expression of other membrane-spanning proteins is altered during hypertrophy, we determined the level of AQP-1 mRNA in hearts of aortic-constricted (AC) rats. The level of AQP-1 mRNA decreased progressively after AC, and was 42% less than the level in left ventricles (LVs) of sham-operated control rats after 3 days of AC. Conclusions: These data indicate that AQP-1 is expressed in cardiac myocytes of adult and neonatal rats, and its expression is modulated in the rat heart during pressure-overload hypertrophy.