In remote ischemic conditioning(RIC), several cycles of ischemia and reperfusion render distant organ and tissues more resistant to the ischemia-reperfusion injury. The intermittent ischemia can be applied before the ...In remote ischemic conditioning(RIC), several cycles of ischemia and reperfusion render distant organ and tissues more resistant to the ischemia-reperfusion injury. The intermittent ischemia can be applied before the ischemic insult in the target site(remote ischemic preconditioning), during the ischemic insult(remote ischemic perconditioning) or at the onset of reperfusion(remote ischemic postconditioning). The mechanisms of RIC have not been completely defined yet; however, these mechanisms must be represented by the release of humoral mediators and/or the activation of a neural reflex. RIC has been discovered in the heart, and has been arising great enthusiasm in the cardiovascular field. Its efficacy has been evaluated in many clinical trials, which provided controversial results. Our incomplete comprehension of the mechanisms underlying the RIC could be impairing the design of clinical trials and the interpretation of their results. In the present review we summarize current knowledge about RIC pathophysiology and the data about its cardioprotective efficacy.展开更多
Despite repeated attempts to develop a unifying hypothesis that explains the clinical syndrome of heart failure(HF),no single conceptual paradigm for HF has withstood the test of time. The last model that has been dev...Despite repeated attempts to develop a unifying hypothesis that explains the clinical syndrome of heart failure(HF),no single conceptual paradigm for HF has withstood the test of time. The last model that has been developed,the neurohormonal model,has the great virtue of highlighting the role of the heart as an endocrine organ,as well as to shed some light on the key role on HF progression of neurohormones and peripheral organs and tissues beyond the heart itself. However,while survival in clinical trials based on neurohormonal antagonist drugs has improved,HF currently remains a lethal condition. At the borders of the neurohormonal model of HF,a partially unexplored path trough the maze of HF pathophysiology is represented by the feedback systems. There are several evidences,from both animal studies and humans reports,that the deregulation of baro-,ergo- and chemo-reflexes in HF patients elicits autonomic imbalance associated with parasympathetic withdrawal and increased adrenergic drive to the heart,thus fundamentally contributing to the evolution of the disease. Hence,on top of guidelinerecommended medical therapy,mainly based on neurohormonal antagonisms,all visceral feedbacks have been recently considered in HF patients as additional potential therapeutic targets.展开更多
文摘In remote ischemic conditioning(RIC), several cycles of ischemia and reperfusion render distant organ and tissues more resistant to the ischemia-reperfusion injury. The intermittent ischemia can be applied before the ischemic insult in the target site(remote ischemic preconditioning), during the ischemic insult(remote ischemic perconditioning) or at the onset of reperfusion(remote ischemic postconditioning). The mechanisms of RIC have not been completely defined yet; however, these mechanisms must be represented by the release of humoral mediators and/or the activation of a neural reflex. RIC has been discovered in the heart, and has been arising great enthusiasm in the cardiovascular field. Its efficacy has been evaluated in many clinical trials, which provided controversial results. Our incomplete comprehension of the mechanisms underlying the RIC could be impairing the design of clinical trials and the interpretation of their results. In the present review we summarize current knowledge about RIC pathophysiology and the data about its cardioprotective efficacy.
文摘Despite repeated attempts to develop a unifying hypothesis that explains the clinical syndrome of heart failure(HF),no single conceptual paradigm for HF has withstood the test of time. The last model that has been developed,the neurohormonal model,has the great virtue of highlighting the role of the heart as an endocrine organ,as well as to shed some light on the key role on HF progression of neurohormones and peripheral organs and tissues beyond the heart itself. However,while survival in clinical trials based on neurohormonal antagonist drugs has improved,HF currently remains a lethal condition. At the borders of the neurohormonal model of HF,a partially unexplored path trough the maze of HF pathophysiology is represented by the feedback systems. There are several evidences,from both animal studies and humans reports,that the deregulation of baro-,ergo- and chemo-reflexes in HF patients elicits autonomic imbalance associated with parasympathetic withdrawal and increased adrenergic drive to the heart,thus fundamentally contributing to the evolution of the disease. Hence,on top of guidelinerecommended medical therapy,mainly based on neurohormonal antagonisms,all visceral feedbacks have been recently considered in HF patients as additional potential therapeutic targets.
