An inner abilitv of organism to protect itself can be triggered or motivated by pretreatment of brief intermittent ischemia or repetitive slight hypoxia and a POwerful defence and protection from severe injury of succ...An inner abilitv of organism to protect itself can be triggered or motivated by pretreatment of brief intermittent ischemia or repetitive slight hypoxia and a POwerful defence and protection from severe injury of successive ischemia or hypoxia can thus be achieved, The neuroprotective action exerted by preconditioning seems to be re1ated to up/down regulation of contents or activity of some known neuroactive chemicals and/or generation of some unknown antihypoxic/ischemic neuroactive chemicals or mechanisms in the brain.展开更多
The possible transduction mechanisms involved in ischemic preconditioning were reviewed briefly,Nitric oxide from the endothelium (and possible also from cardiac myocytes)by the action of bradykinin stimulates soluble...The possible transduction mechanisms involved in ischemic preconditioning were reviewed briefly,Nitric oxide from the endothelium (and possible also from cardiac myocytes)by the action of bradykinin stimulates soluble guanylate cyclase in the cytosol resulting in an elevation of cGMP. This may inhibit the inward slow Ca2+ current by stimulating a cGMP-dependent PDE’ to decrease cGMP levels. The translocation of PKC to membrane by DAG formation resulting from the activation of PLC phosphorylates a membrane protein that may link to the ATP-dependent K+ channel. The pathway may be stimulated by the adenosine A, receptors,muscarine acetylcholine M1, M3 and M5 receptors and a-adrenoceptors as well. The possible approaches for pharmacological exploitation are to minic the endogenous myocardial protective mediators by more selective and long acting analogues, to enhence these mediators by modulating their release, transport and uptake, to modulate myocardial cAMP and cGMP levels,to target guanine-nucleotide binding regulatory proteins and etc.展开更多
文摘An inner abilitv of organism to protect itself can be triggered or motivated by pretreatment of brief intermittent ischemia or repetitive slight hypoxia and a POwerful defence and protection from severe injury of successive ischemia or hypoxia can thus be achieved, The neuroprotective action exerted by preconditioning seems to be re1ated to up/down regulation of contents or activity of some known neuroactive chemicals and/or generation of some unknown antihypoxic/ischemic neuroactive chemicals or mechanisms in the brain.
文摘The possible transduction mechanisms involved in ischemic preconditioning were reviewed briefly,Nitric oxide from the endothelium (and possible also from cardiac myocytes)by the action of bradykinin stimulates soluble guanylate cyclase in the cytosol resulting in an elevation of cGMP. This may inhibit the inward slow Ca2+ current by stimulating a cGMP-dependent PDE’ to decrease cGMP levels. The translocation of PKC to membrane by DAG formation resulting from the activation of PLC phosphorylates a membrane protein that may link to the ATP-dependent K+ channel. The pathway may be stimulated by the adenosine A, receptors,muscarine acetylcholine M1, M3 and M5 receptors and a-adrenoceptors as well. The possible approaches for pharmacological exploitation are to minic the endogenous myocardial protective mediators by more selective and long acting analogues, to enhence these mediators by modulating their release, transport and uptake, to modulate myocardial cAMP and cGMP levels,to target guanine-nucleotide binding regulatory proteins and etc.
