Titlebook: Delayed Preconditioning and Adaptive Cardioprotection; G. F. Baxter,D. M. Yellon Book 1998 Springer Science+Business Media Dordrecht 1998

腐蚀

Silent-Ischemia

MORPH

Delayed Preconditioning Against Lethal Ischaemic Injury,g transient sublethal periods of ischaemia [1, 2]. These two studies initiated an area of research on ischaemic preconditioning of myocardium which has developed considerably in the last five years. This form of preconditioning, known variously as "delayed preconditioning", "late preconditioning", t

recede

, Role of Nitric Oxide as Trigger and Mediator,ial ischemic insult and lasts 2–3 hours, and a late (or delayed) phase, which becomes apparent 12–24 hours later and lasts for 3–4 days (reviewed in references 1 and 2). These two phases have different pathophysiology and probably different mechanisms. Since the late phase lasts much longer, it may

子女

Delayed Preconditioning Against Endothelial Dysfunction, of platelet and leukocyte function. Numerous experimental and clinical data suggest that these essential physiological functions of the endothelium are altered in various pathophysiological situations, such as hypertension, hypercholesterolaemia or diabetes. Such dysfunction can be characterised by

Carcinogenesis

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Intracellular Signalling Mechanisms in Myocardial Adaptation to Ischaemia,t is the basis of adaptive modification. Adaptation involves a number of cellular and biochemical alterations including (i) changes in metabolic homeostasis and (ii) reprogramming of gene expression. Changes in metabolic pathways are generally short-lived and reversible; the consequences of reprogra

Obstreperous

Changes in Cardiac Gene Expression After Ischaemia and Reperfusion,r promoting cell injury and death. Identifying these proteins is an important first step towards understanding the molecular mechanisms underlying the stress response. As new or elevated protein synthesis can result from increased gene expression, studies of gene transcription provide a key to ident