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Resilience In The Team - Monika Huber - Bog - Springer - Plusbog.dk

Race Car Handling Optimization - Ralph Putz - Bog - Springer - Plusbog.dk

Physiology of the Fetal and Neonatal Lung - - Bog - Springer - Plusbog.dk

Physiology of the Fetal and Neonatal Lung - - Bog - Springer - Plusbog.dk

L. B. STRANG The past 25 years have seen a remarkable growth in our knowledge of lung development in its structural, physiological and biochemical dimensions. Much of the impetus for research leading to new knowledge has derived from the perception that many respiratory disorders in the newborn infant are due to defective development or maladaption of some component or components of the respiratory system. Thus, to cite one example, surfac­ tant deficiency is clearly seen to be the cause of atelectasis in hyaline mem­ brane disease; and to cite another, it is widely accepted that the mechanisms controlling patency of the ductus arteriosus and pulmonary vascular resistance also determine the right-to-Ieft or left-to-right shunting frequently observed in the course of neonatal respiratory disorders. There are, however, areas of physiological knowledge - such as those relating to respiratory control and to liquid formation and absorption - which are clearly of great relevance to lung adaptation at birth but where it has not yet proved possible to link a specific clinical state to the malfunction of a particular mechanism. In planning this symposium an attempt was made to organize the material in an orderly manner, starting with the embryonic and fetal stages of growth and development, continuing with respiratory control and the role of surfactant in lung aeration at birth, and ending with the treatment of neonatal respiratory disorders.

DKK 434.00
1

Coronary Tone in Ischemic Heart Disease - - Bog - Springer - Plusbog.dk

Coronary Tone in Ischemic Heart Disease - - Bog - Springer - Plusbog.dk

W. KUPPER Coronary artery vasoconstriction is not only the mechanism responsible for Prinzmetal's variant angina, but may also be involved in stable angina pectoris and myocardial infarction. However, the underlying patho-physiological mecha- nisms and the importance of coronary vasoconstriction in these syndromes is still largely unknown. Several hypotheses have been proposed. Sympathetic nervous activity plays a key role in the regulation of coronary blood flow, but mechanical or humoral constrictive factors may be active as well. a-adrenergic tone Adrenergic nerve fibers accompany coronary vessels of any size. The stimulation of cardiac sympathetic nerves causes an increase in coronary blood flow. If, however, chronotropic and inotropic effects of adrenergic stimulation are sup- pressed pharmacologically by beta-adrenoceptor blockade, a reduction in flow is observed. Thus, the primary effect of sympathetic stimulation on the coronary arteries is the alpha-adrenergic mediated vasoconstriction. Functionally inner- vated alpha-adrenoceptors have been documented both in large coronary con- ductance arteries and in the small resistance vessels. Animal studies and a human study have documented that a permanent constrictor tone is present on the coronary circulation both at rest and during exercise; this condition could be prevented with alpha-adrenoceptor blockade or was absent after heart transplan- tation. Therefore, alpha-adrenoceptor mediated coronary constriction is an at- tractive hypothesis as a possible pathophysiological mechanism of inappropriate coronary vasoconstriction and cororiary vasospasm.

DKK 816.00
1