EFFECTS OF PH ON BRAIN ENERGETICS AFTER HYPOTHERMIC CIRCULATORY ARREST

被引:103
作者
AOKI, M
NOMURA, F
STROMSKI, ME
TSUJI, MK
FACKLER, JC
HICKEY, PR
HOLTZMAN, DH
JONAS, RA
机构
[1] CHILDRENS HOSP MED CTR,DEPT CARDIOVASC SURG,300 LONGWOOD AVE,BOSTON,MA 02115
[2] CHILDRENS HOSP MED CTR,DEPT PEDIAT,BOSTON,MA 02115
[3] CHILDRENS HOSP MED CTR,DEPT NEUROL,BOSTON,MA 02115
[4] CHILDRENS HOSP MED CTR,DEPT ANESTHESIOL,BOSTON,MA 02115
[5] MIT,CAMBRIDGE,MA 02139
[6] HARVARD UNIV,SCH MED,BOSTON,MA 02115
关键词
D O I
10.1016/0003-4975(93)90014-9
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The pH management that provides optimal organ protection during hypothermic circulatory arrest is uncertain. Recent retrospective clinical data suggest that the pH-stat strategy (maintenance of pH at 7.40 corrected to core temperature) may improve brain protection during hypothermic cardiopulmonary bypass with a period of circulatory arrest in infants. The impact of alpha-stat (group A) and pH-stat (group P) strategies on recovery of cerebral high-energy phosphates and intracellular pH measured by magnetic resonance spectroscopy (A, n = 7; P, n = 5), organ blood flow measured by microspheres, cerebral metabolic rate measured by oxygen and glucose extraction (A, n = 7; P, n = 6), and cerebral edema was studied in 25 4-week-old piglets undergoing core cooling and 1 hour of circulatory arrest at 15-degrees-C. Group P had greater cerebral blood flow during core cooling (54.3% +/- 4.7% versus 34.2% +/- 1.5% of normothermic baseline, respectively; p = 0. 001). The intracellular pH during core cooling showed an alkaline shift in both groups but became more alkaline in group A than in group P at the end of cooling (7.08 to 7.63 versus 7.09 to 7.41, respectively; p = 0.013). Recovery of cerebral adenosine triphosphate (p = 0.046) and intracellular pH (p = 0.014) in the initial 30 minutes of reperfusion was faster in group P. The cerebral intracellular pH became more acidotic during early reperfusion in group A, whereas it showed continuous recovery in group P. Brain water content postoperatively was less in group P (0.8075) than in group A (0.8124) (p = 0.05). These results suggest that compared with alpha-stat, the pH-stat strategy provides better early brain recovery after deep hypothermic cardiopulmonary bypass with circulatory arrest in the immature. animal. Possible mechanisms include improved brain cooling by increased blood flow to subcortical areas, improved oxygen delivery, and reduction of reperfusion injury, as well as an alkaline shift in intracellular pH with hypothermia in spite of a stable blood pH.
引用
收藏
页码:1093 / 1103
页数:11
相关论文
共 44 条
[1]   COOLING GRADIENTS + BRAIN DAMAGE WITH DEEP HYPOTHERMIA [J].
ALMOND, CH ;
MEYER, BW ;
SNYDER, HM ;
GRANT, SM ;
JONES, JC .
JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY, 1964, 48 (06) :890-&
[2]   HEART-MUSCLE VIABILITY FOLLOWING HYPOXIA - PROTECTIVE EFFECT OF ACIDOSIS [J].
BING, OHL ;
BROOKS, WW ;
MESSER, JV .
SCIENCE, 1973, 180 (4092) :1297-1298
[3]   EFFECTS OF METABOLIC-ACIDOSIS ON VIABILITY OF CELLS EXPOSED TO ANOXIA [J].
BONVENTRE, JV ;
CHEUNG, JY .
AMERICAN JOURNAL OF PHYSIOLOGY, 1985, 249 (01) :C149-C159
[5]  
COLES JG, 1984, CIRCULATION, V70, P96
[6]   PROTECTION BY ACIDOTIC PH AGAINST ANOXIC CELL KILLING IN PERFUSED-RAT-LIVER - EVIDENCE FOR A PH PARADOX [J].
CURRIN, RT ;
GORES, GJ ;
THURMAN, RG ;
LEMASTERS, JJ .
FASEB JOURNAL, 1991, 5 (02) :207-210
[7]  
FISK G C, 1976, Anaesthesia and Intensive Care, V4, P126
[8]   MITOCHONDRIAL DAMAGE DURING CEREBRAL-ISCHEMIA [J].
FISKUM, G .
ANNALS OF EMERGENCY MEDICINE, 1985, 14 (08) :810-815
[9]   ACIDOSIS REDUCES NMDA RECEPTOR ACTIVATION, GLUTAMATE NEUROTOXICITY, AND OXYGEN-GLUCOSE DEPRIVATION NEURONAL INJURY IN CORTICAL CULTURES [J].
GIFFARD, RG ;
MONYER, H ;
CHRISTINE, CW ;
CHOI, DW .
BRAIN RESEARCH, 1990, 506 (02) :339-342
[10]   FACTORS AND THEIR INFLUENCE ON REGIONAL CEREBRAL BLOOD-FLOW DURING NONPULSATILE CARDIOPULMONARY BYPASS [J].
GOVIER, AV ;
REVES, JG ;
MCKAY, RD ;
KARP, RB ;
ZORN, GL ;
MORAWETZ, RB ;
SMITH, LR ;
ADAMS, M ;
FREEMAN, AM .
ANNALS OF THORACIC SURGERY, 1984, 38 (06) :592-600