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001			76368
003			ES-MaUEC
005			20230207040221.0
007			cr nn 008mamaa
008			100301s2006 gw | s |||| 0|eng d
020			_a9783540329671
024	7		_a10.1007/3-540-32967-6 _2doi
040			_aES-MaUEC
050		4	_aQM562 _b.V37 2006 EB
082	0	4	_a615
100	1		_aMoncada, Salvador _eeditor literario _96572 _0comprobar BNE19900113959
245	0	4	_aThe Vascular Endothelium I _cedited by Salvador Moncada, Annie Higgs
246	3		_aWith contributions by numerous experts
260			_aBerlin, Heidelberg _bSpringer International Publishing _c2006
300			_a1 recurso en línea (IX, 339 p.)
336			_aTexto (visual) _btxt _2rdacontent
337			_aelectrónico _bc _2rdamedia
338			_arecurso electrónico _bcr _2rdacarrier
490	1		_aHandbook of Experimental Pharmacology _x0171-2004 _v176/I
505	0		_aNormal Endothelium -- Functional Ultrastructure of the Vascular Endothelium: Changes in Various Pathologies -- Development of the Endothelium -- Transport Across the Endothelium: Regulation of Endothelial Permeability -- Calcium Signalling in the Endothelium -- Eicosanoids and the Vascular Endothelium -- Nitric Oxide and the Vascular Endothelium -- Angiotensin, Bradykinin and the Endothelium -- Endothelin -- Transport Across the Endothelium: Regulation of Endothelial Permeability.
520			_aIt was with great pleasure that I accepted the invitation of Springer to edit this book. My association with the vascular endothelium covers a large part of my scientific career and, as with any good long-standing relationship, it has had moments of great excitement and periods of laborious construction. It has sometimes been difficult but has never given me cause for despondency. Indeed, in the last quarter of a century, research on the vascular endothelium has been very productive and its results have contributed, arguably more than any others, to unravelling the mystery of cardiovascular disease, its origin, its development, its complications and its prevention or treatment once it has developed. I am very happy that Annie Higgs agreed to join me in this task. Over the years we have collaborated closely and, as always, she has shouldered the brunt of the work and has made sure that things get done to everybody{u2019}s satisfaction. We have also been fortunate in that the scientists who have made some of the most significant contributions in the field agreed to write chapters; as a result, we have produced two volumes which is a good representation of our knowledge in early 2006. We are, however, aware that the field has expanded beyond all expectation and that there may have been some oversight in the covering of a specific area or some aspect of it. This is compounded by the speed at which knowledge is being generated, with more than 4,100 papers concerning the endothelium published in 2005. These volumes are organised in such a way that the early chapters discuss the structure, development and function of the normal vascular endothelium. The subsequent chapters consider conditions that lead to disruption of vascular physiology, while the later chapters deal with specific pathologies and their treatment. The final chapter describes various gene-therapy strategies for the treatment of vascular pathologies. Interestingly, although this field of research can now be considered mature, it continues to generate a great deal of new information at a time when some of its fruits are having a direct impact on clinical medicine. This is clearly exemplified in the contents of most of the chapters. The concept of endothelial dysfunction, although mooted many years ago, has come to the fore and has been very useful in defining a situation which may exist long before the overt signs of vascular diseases can be identified. Although VI Preface endothelial dysfunction is likely to comprise a variety of disturbances, it is interesting that these days it is almost exclusively measured as a decrease in nitric oxide (NO)-dependent vascular dilatation, either induced by suitable pharmacological agonists or by increases in blood flow. Oxidative stress, which is associated with the genesis of endothelial dysfunction, is a loose term used to define an imbalance between the release of oxygen-derived free radicals and the anti-oxidant systems of the body. Many years ago our work established that reactive oxygen species are important in reducing the local concentrations of both prostacyclin and NO. It is now clear that free radicals also affect other homeostatic systems in the vasculature. However, many things remain to be clarified, especially the origin of oxidative stress in early disease
650		7	_aFisiología humana _0comprobar BNE19900979803 _2embne _9140024
700	1		_aHiggs, Annie _eeditor literario _985398 _0Local
856	4	0	_uhttps://go.openathens.net/redirector/universidadeuropea.es?url=https://link.springer.com/book/10.1007/3-540-32967-6 _zAcceso a este recurso digital (usuarios Universidad Europea de Madrid)
901			_ai9783540329671
907			_a.b12819864 _b10-10-17 _c01-10-14
942			_2lcc _cLE
945			_aQM562 .V37 2006 EB _g1 _ieBOOK _j0 _lmae _o- _pEUR0.00 _q- _r- _sb _t15 _u0 _v0 _w0 _x0 _y.i11549087 _z06-04-17
988			_aEBOOK, EBSPRINGERrevisando
998			_am _a_alco _a_vill _b22-07-17 _cm _dz _ei _feng _ggw _h4