Nitric oxide and deep hypothermic circulatory arrest after ischemia-reperfusion injury in the nervous system.doc

 PAGE \* MERGEFORMAT 13 Nitric oxide and deep hypothermic circulatory arrest after ischemia-reperfusion injury in the nervous system Keywords:: deep hypothermic circulatory arrest (DHCA) nitric oxide (NO) the nervous system Was first proposed in 1967, such as cardiopulmonary bypass Hikasa deep hypothermic circulatory arrest (DHCA) technology used by Okamoto and other infants with congenital heart disease in 1975, Griepp [1] applies to adults, since the major vascular surgery, greatly improved the heart and large The success rate of vascular surgery, but simply circulatory arrest more than 60 minutes, after Yi appeared nervous system complications. The occurrence of complications mainly related to DHCA cerebral ischemia and reperfusion injury, of which glutamate excitotoxicity is a major reason for damage caused by glutamate acting on N-methyl-D-aspartate (NMDA ) receptor, resulting in a large number of Ca2 influx, activating NO synthase, NO synthesis increased, and thus NO in the nervous system ischemia-reperfusion injury in gradually be taken seriously. 1, NO feature 1. NO biochemical and physiological characteristics of the physiological role of NO in the body is very extensive, the normal function of the blood circulatory system plays an important regulatory role, including: (a) regulating vascular tone. Vascular endothelial cells in the basic condition for sustainable release of NO, to maintain a basis of vascular tone; (2) regulating blood pressure. Witte et al [2] confirmed that, NO / cGMP system involved in the normal rat rhythmic fluctuations in blood pressure regulation. High dose of NOS inhibitor L-NAME (30 mg / kg body weight) the rats showed the opposite fluctuations in blood pressure rhythm; (3) regulating organ blood flow. In the whole animal, NOS inhibitors administered systemic circulation can cause coronary vasoconstriction frequently; (4) inhibit blood cell adhesion to endothelium. Can inhibit endothelial NO produced by a variety of blood