Hypoxia stimulates ventilation, but when it is sustained, a decline in the ventilatory response is seen. The mechanism responsible for this decline lies within the CNS, but still remains unknown. In this study, we attempted to elucidate the possible role of hypoxia-induced depression of respiratory neurons by comparing the ventilatory response to hypoxia in intact rats and those with denervated carotid bodies. A whole-body plethysmograph was used to measure tidal volume, frequency of breathing and minute ventilation (VE) in awake and anesthetized intact rats and rats after carotid body denervation during exposure to hypoxia (FIO2 0.1). Fifteen-minute hypoxia induced an initial increase of VE in intact rats (to 248 % of control ventilation in awake and to 227 % in anesthetized rats) followed by a consistent decline (to 207 % and 196 % of control VE, respectively). Rats with denervated carotid bodies responded with a smaller increase in VE (to 134 % in awake and 114 % in anesthetized animals), but without a secondary decline (145 % and 129 % of control VE in the 15th min of hypoxia). These results suggest that afferentation from the carotid bodies and/or the substantial increase in ventilation are crucial for the biphasicity of the ventilatory response to sustained hypoxia and that a central hypoxic depression cannot fully explain the secondary decline in VE., H. Maxová, M. Vízek., and Obsahuje bibliografii
Ventricular assist devices (VAD ) have recently established themselves as an irreplaceable th erapeutic modality of terminal heart failure. Because of the worldwide shortage of donors, ventricular assist devices play a key role in modern heart failure therapy. Some clinical data have revealed the possibility of cardiac recovery during VAD applic ation. On the other hand, both clinical and experiment al studies indicate the risk of the cardiac atrophy development, especially after prolonged mechanical unloading. Little is known about the specific mechanisms governing the unloading-induced cardiac atrophy and about the exact ultrastructural changes in cardiomyocytes, and even less is known about the ways in which possible therapeutical interventions may affect heart at rophy. One aim of this review was to present important aspects of the development of VAD- related cardiac atrophy in humans and we also review the most significant observations linking clinical data and those derived from studies using experimental mo dels. The focus of this article was to review current methods applied to alleviate cardiac atrophy which follows mechanical unloading of the heart. Out of many pharmacological agents studied, only the selective beta2 agonist clenbuterol has been proved to have a significantly beneficial effect on unloading-induced atrophy. Mechanical means of atrophy alleviation also seem to be effective and promising., M. Pokorný ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy