Cerebral anoxia: effect of deep hypothermia and pH.
Cerebral anoxia: effect of deep hypothermia and pH.
复制标题
脑缺氧：深低温和 pH 值的影响。
作者：
W. Norwood;C. R. Norwood;A. Castañeda
深低温停循环有助于婴儿先天性心脏畸形的修复。根据经验，低温对中枢神经系统(CNS)的缺血性损伤具有保护作用。大脑的Q10O2仅为2.2，因此代谢率的降低并不能完全解释低温的保护作用。由于H2O的离解热很高(约7kcal/摩尔)，其pH与温度有关(25℃时为7.0，20℃时为7.4)，低温可能部分通过影响氢离子浓度而起到保护作用。中枢神经系统对缺血的敏感性的一个表现是微循环受阻[无复流损害(NRL)]，表现为在循环停止一段时间后向脑循环中注入碳黑。大脑切片上灰色背景下的白色病变(NRL)随着停搏时间的增加而增大。45只杂种犬在37℃或20℃的体外循环(CPB)中接受不同时间的氮气缺氧，研究了缺氧与循环骤停、脑温度和脑细胞外pH对NRL的影响。对照组包括常温体外循环，无缺氧和常温体外循环，缺氧，等摩尔氯化钠输注。通过对脑切片照片的平面测量对NRL进行量化。这些结果证实了NRL可被低温所减弱，并提示：(1)NRL是一种缺氧而不是停滞的循环功能，因为在37℃下用氮气灌流不能保护大脑(即NRL不仅仅与“临界重新开放压”有关)；(2)NRL部分地与细胞外pH有关。
Deep hypothermic circulatory arrest facilitates repair of congenital cardiac anomalies in infants. It is known empirically that hypothermia protects against central nervous system (CNS) ischemic damage. The Q10O2 is only 2.2 for brain and thus a decrease in metabolic rate does not fully account for protective effects of hypothermia. Since enthalpy of dissociation of H2O is high (approximately 7 kcal/mole), its pH is temperature dependent (7.0 at 25 degrees C, 7.4 at 20 degrees C) and hypothermia may in part protect by its influence on hydrogen ion concentration. A manifestation of CNS susceptibility to ischemia is an obstruction of the microcirculation [no-reflow lesion (NRL)] demonstrated by infusion of carbon black into the cerebral circulation after a period of circulatory arrest. White lesions (NRL) against a gray background on cut section of brain increase in size with increasing time of arrest. The effect of anoxia versus circulatory arrest, brain temperature, and extracellular brain pH on NRL was studied in 45 mongrel dogs, subjected to varying periods of N2-induced anoxia on cardiopulmonary bypass (CPB) at 37 degrees C or 20 degrees C. In some studies jugular venous pH was adjusted by infusion of NaHCO3 or HCl. Control groups included normothermic CPB without anoxic and normothermic CPB, anoxia, and equimolar NaCl infusion. NRL was quantified by planimetry of photographs of cut sections of brain. These results confirm that NRL is abated by hypothermia and suggest that (1) NRL is a function of anoxia and not arrested circulation since perfusion with N2 at 37 degrees C does not protect the brain (i.e., NRL is not solely related to "critical reopening pressure") and (2) NRL is in part a function of extracellular pH.