Armstead W M, Kurth C D
Department of Anesthesia, University of Pennsylvania, Philadelphia.
J Neurotrauma. 1994 Oct;11(5):487-97. doi: 10.1089/neu.1994.11.487.
The present study was designed to characterize the influence of early developmental changes on the relationship among systemic arterial pressure, cerebral hemodynamics, and cerebral oxygenation during the first 3 h following percussion brain injury. Anesthetized newborn (1-5 days old) and juvenile (3-4 weeks old) pigs equipped with a closed cranial window were connected to a percussion device consisting of a saline-filled cylindrical reservoir with a metal pendulum. Brain injury of moderate severity (1.9-2.3 atm) was produced by allowing the pendulum to strike a piston on the cylinder. Mean arterial blood pressure increased after brain injury in juveniles (68 +/- 4 to 93 +/- 2 mm Hg within 3 min, n = 6), whereas it decreased after injury in newborns (70 +/- 3 to 51 +/- 3 mm Hg within 3 min, n = 6). Fluid percussion brain injury decreased pial artery diameter more in newborns (132 +/- 5 to 110 +/- 5 microns within 10 min, n = 5) than in juveniles (141 +/- 3 to 133 +/- 3 microns within 10 min, n = 5). Pial arterioles constricted to a greater extent than small pial arteries following brain injury in both age groups. Within 30 sec, brain injury produced a transient increase in cerebral hemoglobin O2 saturation (27 +/- 4%, n = 5) that was reversed to a profound decrease in cerebral hemoglobin O2 saturation (45 +/- 2%, n = 5) in the newborn as measured by near infrared spectroscopy. In contrast, brain injury produced modest increases in hemoglobin O2 saturation (10 +/- 1%, n = 5), followed by mild desaturation (4 +/- 1%, n = 5) in juveniles. Additionally, regional cerebral blood flow was reduced within 10 min of injury in both newborn and juvenile pigs and remained depressed for 180 min in newborns. In contrast, cerebral blood flow returned to control values within 180 min in juveniles. These data show that the effects of comparable brain injury level were very different in newborn and juvenile pigs. Further, these data suggest that reductions in cerebral blood flow following brain injury are more dependent on changes in reactivity of arterioles. Finally, these data suggest that the decrease in cerebral oxygenation, an index of metabolism, coupled with reduced cerebral blood flow, could result in profound hypoperfusion after brain injury.
本研究旨在描述在撞击性脑损伤后的最初3小时内，早期发育变化对全身动脉压、脑血流动力学和脑氧合之间关系的影响。将装有闭合式颅窗的新生（1 - 5日龄）和幼年（3 - 4周龄）麻醉猪连接到一个由充满盐水的圆柱形储液器和金属摆锤组成的撞击装置上。通过让摆锤撞击圆柱体上的活塞造成中度严重程度（1.9 - 2.3个大气压）的脑损伤。幼年猪脑损伤后平均动脉血压升高（3分钟内从68±4毫米汞柱升至93±2毫米汞柱，n = 6），而新生猪损伤后平均动脉血压降低（3分钟内从70±3毫米汞柱降至51±3毫米汞柱，n = 6）。与幼年猪（10分钟内从141±3微米降至133±3微米，n = 5）相比，新生猪的软脑膜动脉直径在撞击性脑损伤后减小得更多（10分钟内从132±5微米降至110±5微米，n = 5）。在两个年龄组中，脑损伤后软脑膜微动脉的收缩程度均大于小软脑膜动脉。在30秒内，脑损伤使脑血红蛋白氧饱和度短暂升高（27±4%，n = 5），通过近红外光谱测量，新生猪随后脑血红蛋白氧饱和度大幅下降（45±2%，n = 5）。相比之下，脑损伤使幼年猪的血红蛋白氧饱和度适度升高（10±1%，n = 5），随后轻度降低（4±1%，n = 5）。此外，新生猪和幼年猪在损伤后10分钟内局部脑血流量均减少，新生猪的脑血流量在180分钟内持续降低。相比之下，幼年猪的脑血流量在180分钟内恢复到对照值。这些数据表明，在新生猪和幼年猪中，同等程度的脑损伤产生的影响差异很大。此外，这些数据表明，脑损伤后脑血流量的减少更依赖于微动脉反应性的变化。最后，这些数据表明，作为代谢指标的脑氧合降低，再加上脑血流量减少，可能导致脑损伤后严重的灌注不足。
