Chronic coronary artery disease and heart failure are associated with subsequent worsening of the cardiac pump function.Numerous studies within the past few years have been demonstrated,that the intracoronary stem cel...Chronic coronary artery disease and heart failure are associated with subsequent worsening of the cardiac pump function.Numerous studies within the past few years have been demonstrated,that the intracoronary stem cell therapy has to be considered as a safe therapeutic procedure in heart disease.Transplantation of autologous bone marrow cells or precursor cells improved cardiac function after myocardial infarction and in chronic coronary heart disease.The age of infarction seems to be irrelevant to regenerative potency of stem cells,since stem cells therapy in old infarctions(many years old)is almost equally effective in comparison to previous infarcts.Further indications are non-ischemic cardiomyopathy(dilative cardiomyopathy)and heart failure due to hypertensive heart disease.展开更多
We have reviewed the role of nitric oxide synthase(NOS)isoforms and nitric oxide(NO)in the normal heart and in heart failure.NO is a highly reactive siganaling molecule produced normally in the heart and is an importa...We have reviewed the role of nitric oxide synthase(NOS)isoforms and nitric oxide(NO)in the normal heart and in heart failure.NO is a highly reactive siganaling molecule produced normally in the heart and is an important modulator of myocardial function.NOS catalyzes the conversion of L-arginine to L-citrulline and NO.In the heart,three NOS isoforms are present:neuronal NOS(nNOS),and endothelial NOS(eNOS),are constitutively present enzymes in distinct subcellular locations within cardiomyocytes,whereas inducible NOS(iNOS)is absent in the healthy heart,but its expression is induced by inflammation and immune responses.In the tissue,NO has two main effects:(i)it stimulates the activity of guanylate cyclase,and(ii)nitrosylates tyrosine residues in proteins and thiol-groups of cysteine in proteins.Changes in subcellular compartmentalization of NOS isoforms lead to the increased NO synthesis,reduction of the specificity of its effects,disruption of calcium homeostasis,electromechanical uncoupling and myocardial contractile failure.展开更多
文摘Chronic coronary artery disease and heart failure are associated with subsequent worsening of the cardiac pump function.Numerous studies within the past few years have been demonstrated,that the intracoronary stem cell therapy has to be considered as a safe therapeutic procedure in heart disease.Transplantation of autologous bone marrow cells or precursor cells improved cardiac function after myocardial infarction and in chronic coronary heart disease.The age of infarction seems to be irrelevant to regenerative potency of stem cells,since stem cells therapy in old infarctions(many years old)is almost equally effective in comparison to previous infarcts.Further indications are non-ischemic cardiomyopathy(dilative cardiomyopathy)and heart failure due to hypertensive heart disease.
文摘We have reviewed the role of nitric oxide synthase(NOS)isoforms and nitric oxide(NO)in the normal heart and in heart failure.NO is a highly reactive siganaling molecule produced normally in the heart and is an important modulator of myocardial function.NOS catalyzes the conversion of L-arginine to L-citrulline and NO.In the heart,three NOS isoforms are present:neuronal NOS(nNOS),and endothelial NOS(eNOS),are constitutively present enzymes in distinct subcellular locations within cardiomyocytes,whereas inducible NOS(iNOS)is absent in the healthy heart,but its expression is induced by inflammation and immune responses.In the tissue,NO has two main effects:(i)it stimulates the activity of guanylate cyclase,and(ii)nitrosylates tyrosine residues in proteins and thiol-groups of cysteine in proteins.Changes in subcellular compartmentalization of NOS isoforms lead to the increased NO synthesis,reduction of the specificity of its effects,disruption of calcium homeostasis,electromechanical uncoupling and myocardial contractile failure.
