Kawata H, Fackler J C, Aoki M, Tsuji M K, Sawatari K, Offutt M, Hickey P R, Holtzman D, Jonas R A
Department of Surgery, Children's Hospital, Boston, MA 02115.
J Thorac Cardiovasc Surg. 1993 Oct;106(4):671-85.
A miniature piglet model that replicates clinical hypothermic (14 degrees C nasopharyngeal) circulatory arrest and low-flow (50 ml/kg per minute) bypass was used to study carotid blood flow with electromagnetic flow probe, cerebral blood flow by microsphere injection, cerebral metabolic rate by arteriovenous oxygen and glucose extractions, lactate production by cerebral arteriovenous difference, and cerebral edema. Data from five animals that underwent circulatory arrest and five animals that underwent low-flow bypass (aged 28.8 +/- 0.4 [mean +/- standard error of the mean] days) were analyzed. The duration of circulatory arrest and low-flow bypass was 1 hour. In a parallel study with the same animal model, phosphorus 31 magnetic resonance spectroscopy was used to assess cerebral phosphocreatine, nucleoside triphosphate (adenosine triphosphate), and intracellular pH. Five animals (aged 31.8 +/- 1.1 days) underwent circulatory arrest, and five underwent low-flow bypass. A brief phase of hyperemic carotid blood flow was seen immediately after the onset of reperfusion in the circulatory arrest group but not in the low-flow group. In the circulatory arrest and low-flow bypass groups, cerebral blood flow (percentage of baseline 71.2% +/- 8.3% and 69.1% +/- 5.8%, respectively), cerebral oxygen consumption (45.6% +/- 10.0%, 44.5% +/- 7.6%), and cerebral glucose consumption (31.5% +/- 30.7%, 83.5% +/- 24.2%) remained depressed after 45 minutes of reperfusion and rewarming to normothermia. However, after 3 more hours of pulsatile normothermic reperfusion, cerebral oxygen consumption and cerebral glucose consumption had returned to baseline. Phosphocreatine, adenosine triphosphate, and pH were maintained at or above baseline levels throughout low-flow bypass and throughout 3 hours of normothermic reperfusion. In contrast, both phosphocreatine and adenosine triphosphate became undetectable 32 +/- 3.7 minutes after onset of circulatory arrest. During and early after circulatory arrest, pH decreased to a minimum of 6.506 +/- 0.129 at 40 minutes after reperfusion. After 3 hours of normothermic reperfusion, phosphocreatine and adenosine triphosphate recovered to 98.6% +/- 9.0% and 90.1% +/- 13.5% of baseline, respectively, and pH was 7.087 +/- 0.051, similar to baseline (7.1755 +/- 0.041). In the low-flow bypass group, the disparity between the depressed level of cerebral oxygen consumption and normal high-energy phosphate levels may reflect incomplete cerebral rewarming or decreased energy consumption. In the circulatory arrest group, the parallel recovery of oxygen consumption and high-energy phosphates eventually achieving baseline levels suggests that the degree of hypothermia used provides adequate protection for acute cerebral recovery after 1 hour of circulatory arrest.(ABSTRACT TRUNCATED AT 400 WORDS)
使用一种微型仔猪模型，该模型可复制临床低温（鼻咽温度14摄氏度）循环骤停及低流量（每分钟50毫升/千克）体外循环，通过电磁血流探头研究颈动脉血流，经微球注射法测定脑血流量，通过动静脉氧和葡萄糖提取量计算脑代谢率，利用脑动静脉差值计算乳酸生成量，并观察脑水肿情况。分析了5只经历循环骤停的动物及5只经历低流量体外循环的动物（年龄为28.8±0.4[均值±均值标准误差]天）的数据。循环骤停和低流量体外循环的持续时间均为1小时。在一项使用相同动物模型的平行研究中，采用磷31磁共振波谱法评估脑磷酸肌酸、核苷三磷酸（三磷酸腺苷）及细胞内pH值。5只动物（年龄为31.8±1.1天）经历循环骤停，5只经历低流量体外循环。在循环骤停组再灌注开始后立即出现短暂的颈动脉充血血流期，而低流量组未出现。在循环骤停和低流量体外循环组中，再灌注45分钟并复温至正常体温后，脑血流量（分别为基线的71.2%±8.3%和69.1%±5.8%）、脑氧消耗量（45.6%±10.0%，44.5%±7.6%）和脑葡萄糖消耗量（31.5%±30.7%，83.5%±24.2%）仍处于较低水平。然而，在常温搏动性再灌注3小时后，脑氧消耗量和脑葡萄糖消耗量恢复至基线水平。在整个低流量体外循环及常温再灌注3小时期间，磷酸肌酸、三磷酸腺苷和pH值维持在或高于基线水平。相比之下，循环骤停开始后32±3.7分钟，磷酸肌酸和三磷酸腺苷均无法检测到。在循环骤停期间及之后早期，pH值在再灌注40分钟时降至最低6.506±0.129。常温再灌注3小时后，磷酸肌酸和三磷酸腺苷分别恢复至基线的98.6%±9.0%和90.1%±13.5%，pH值为7.087±0.051，与基线（7.1755±0.041）相似。在低流量体外循环组中，脑氧消耗降低水平与正常高能磷酸盐水平之间的差异可能反映了脑复温不完全或能量消耗减少。在循环骤停组中，氧消耗与高能磷酸盐的平行恢复最终达到基线水平，这表明所采用的低温程度为循环骤停1小时后的急性脑恢复提供了充分的保护。（摘要截选至400字）
