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Prolonged Hypercarbia in the Awake Newborn Piglet: Effect on Brain Blood Flow and Cardiac Output

机译:清醒的新生仔猪长期高碳血症:对脑血流量和心输出量的影响

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In adults, exposure to prolonged hypercarbia results in a normalization of the extravascular brain pH associated with a reduction in brain blood flow (BBF). Following prolonged hypercarbia, sudden normalization of the arterial PCO2 also produces a change in the extravascular brain pH to an alkaline state, resulting in a marked decrease in BBF. We examined these physiologic phenomena in newborn subjects by exposing seven awake, spontaneously breathing newborn piglets to 4 h of sustained hypercarbia (PaCO2: 60-70 mm Hg) followed by a 45-min normocarbic period. Total and regional BBF, cardiac output (radionuclide-labeled microsphere method), arterial blood pressure, plasma catecholamine and lactate concentrations, blood gases, oxygen contents, and hematocrits were measured during a baseline period, at ?, 2, and 4 h of sustained hypercarbia and ? and ? h following an abrupt onset of normocarbia. The initial 2.5-fold increase in total BBF during hypercarbia persisted for 2 h and at 4 h decreased significantly below the level of the 30-min hypercarbic measurement, although the values still remained 2-fold above the baseline values. Brain tissue pH was reduced at the onset of hypercarbia, remaining unchanged throughout the hypercarbic period. Both total BBF and brain tissue pH returned to baseline values following the return to normocarbia. Changes in regional BBF were similar to that of total BBF with the exception of the boundary zone (periventricular area in the frontoparietal region of the cerebrum, adjacent to the caudate nucleus) and the parietal area (site of the brain tissue pH electrode), where a significant decrease from the peak hyperemia was not observed. Choroid plexus blood flow demonstrated a small initial increase over normocarbic baseline values. Plasma bicarbonate concentrations did not change during the studies. Following the onset of hypercarbia, heart rate and cardiac output increased significantly whereas plasma lactate concentrations decreased significantly. There was also an increase in the percentage of cardiac output distributed to the brain. The increase in cardiac output persisted throughout the hypercarbic period and returned to baseline levels during normocarbia. Mean arterial blood pressure increased significantly at the 4-h hypercarbic period and this increase persisted during normocarbia. We conclude that in newborn piglets 1) hypercarbia resulted in cerebral hyperperfusion, accompanied by marked fall in brain tissue
机译:在成年人中,暴露于长时间的高碳酸血症会导致与脑血流量(BBF)减少相关的血管外脑pH正常化。长时间的高碳酸血症后,动脉PCO2的突然正常化还会使血管外脑的pH值变为碱性,从而导致BBF明显降低。我们通过将七个清醒的,自发呼吸的新生仔猪暴露于持续4h的持续高碳血症(PaCO2:60-70 mm Hg),然后进行45分钟的正碳代谢期,来检查新生受试者的这些生理现象。在基线期,持续第2、4和4小时内,测量了总的和区域的BBF,心输出量(放射性核素标记的微球法),动脉血压,血浆儿茶酚胺和乳酸浓度,血气,氧含量和血细胞比容高碳血症和?和? h在常态卡比卡突然发作之后。高碳酸血症期间总BBF最初的2.5倍增加持续了2 h,而在4 h时则明显低于30分钟高碳酸血症测量的水平,尽管该值仍比基线值高2倍。高碳酸血症发作时脑组织pH降低,在整个高碳酸血症时期保持不变。总血脑红蛋白和脑组织pH值均恢复正常水平后恢复至基线值。除了边界区域(大脑的前顶叶区域的脑室区域,邻近尾状核)和顶区域(脑组织pH电极的位置)以外,区域BBF的变化与总BBF的变化相似。没有观察到充血高峰的明显减少。脉络丛的血流量显示出比正常含碳量基线值略有增加。在研究期间血浆碳酸氢盐浓度没有变化。高碳酸血症发作后,心率和心输出量显着增加,而血浆乳酸浓度显着降低。分配给大脑的心输出量百分比也有所增加。在高碳酸血症的整个过程中,心输出量的增加持续存在,并在正常碳酸血症期间恢复到基线水平。在高碳酸血症的4小时内,平均动脉血压显着升高,并且这种升高在正常碳酸血症期间持续存在。我们得出结论,在新生仔猪中1)高碳血症导致脑灌注过多,并伴有脑组织明显下降

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