Brain death and lung injury research.docVIP

 PAGE \* MERGEFORMAT 5 Brain death and lung injury research Brain death can cause a syndrome, including blood pressure, the continued volatility and, ultimately, hypotension, coagulation dysfunction, lung disease, hypothermia and electrolyte imbalances. Many experimental and clinical studies have to clarify in the brain after the death of hemodynamic, metabolic, neurological and hormonal and other physiological changes in complexity. Brain death and sympathetic, hemodynamic and inflammatory mechanisms, these mechanisms can cause lung injury. Description This article in brain death-associated lung injury are reviewed. A brain-dead on the hemodynamic stability as well as the impact of lung Hemodynamic effects of brain death can be divided into two stages, the initial stage and followed by high blood pressure normal blood pressure, low blood pressure stage. The initial phase of brain death was due to brain-dead high blood pressure caused by catecholamine release, after the death of brain catecholamine release from sympathetic nerve endings, and a high degree of activation of the adrenal medulla. Catecholamine release of volume and how much brain damage depends largely on the speed and extent of intracranial pressure, the faster, the pressure is greater the more the release of catecholamines, catecholamine-induced intracellular calcium overload may be then activated fat enzyme, protease, endonuclease and nitric oxide synthase, leading to the vital organs and functional aspects of the structural damage. In addition, a large number of the release of catecholamines can lead to dramatic changes in hemodynamics, resulting in tissue and organ damage, can cause vital organs such as lung morphological changes. High blood pressure follow-up of the normal blood pressure or low blood pressure phase is due to sympathetic nerve activity decreased due. Systolic function, diastolic function and decreased sympathetic nervous self-regulation of vascular functio