功能磁共振监测家兔失血性休克早期脑代谢及脑血流的变化

Variations of brain metabolism and cerebral blood flow of rabbits measured by functional magnetic resonance imaging in the early stage of hemorrhagic shock

目的:采用功能磁共振波谱成像(MRS)及灌注成像(PWI)观察家兔失血性休克早期脑部能量代谢及脑部血流的变化。方法:对9只新西兰家兔行右侧股动脉置管,10 min内释放40%血容量制造失血性休克模型(维持平均动脉压40 mm Hg),分别于休克前(T0)及休克30 min(T1)、90 min(T2)、150 min(T3)监测心率、平均动脉压等,并行动脉血气分析。使用Achieva 3.0 T磁共振扫描仪分别行磁共振氢质子波谱(1H MRS)及磁共振磷谱(31P MRS),测定乙酰天门冬氨酸/肌酸(NAA/Cr)、乳酸/肌酸(Lac/Cr)及磷酸肌酸/无机磷酸(Pcr/Pi)、磷酸一酯(PME);同时行PWI,测定局部脑血流量(r CBF)、局部脑血容量(r CBV)及血流平均通过时间(MTT)。结果:随着时间从T0~T3,家兔代谢性酸中毒加深,脑部Pcr/Pi降低(P<0.05),PME升高(P<0.05),NAA/Cr及Lac/Cr则无明显变化(P>0.05);r CBF、r CBV及MTT均明显增加(P<0.05)。结论:失血性休克早期家兔已出现脑组织代谢紊乱,表现为无氧代谢增加,此时脑血流量增加,但血流速度减慢。

Objective： To investigate the variations of brain metabolism and brain blood flow of rabbits in the early stage of hemorrhagic shock with the use of magnetic resonance spectroscopy （MRS） and perfusion weight imaging （PWI）. Methods： A catheter was placed in the right femoral artery of nine New Zealand rabbits. The models of hemorrhagic shock were established by bloodletting in 10 minutes, and approximate 40% of systemic blood was released in each rabbit, maintaining its mean arterial pressure（MAP） at the level of 40 mmHg. The heart rate and mean arterial blood pressure were monitored before shock （T0）, and 30 minutes （T1） ,60 minutes （T2） and 150 minutes（ T3 ） after shock and arterial blood gas analysis was performed. Using Achieva 3. 0 T MRI, brain phosphocreatine/inorganic phosphate （ Pcr/Pi ） and phosphomonoester （ PME ） were measured by 31p magnetic resonance spectroscopy （ 31p MRS ）, and N- acetylaspartate/ Creatine （NAA/Cr） and Lactate/Creatine （Lac/Cr） were measured by proton magnetic resonance spectroscopy （Xn MRS）. Regional cerebral blood flow （rCBF） , regional cerebral blood volume （rCBV） and mean transit time（MTT） were determined by peffusion weight imaging （PWI）. Results： From TO to T3, Pcr/Pi continuously decreased and PME continuously increased （P 〈 0.05 ）. NAA/Cr and Lac/Cr were stable （ P 〉 0.05 ） , while rCBF, rCBV and MTr were increased significantly （ P 〈0. 05 ）. Conclusion： During the early stage of hemorrhagic shock, metabolism disorder occurs as cerebral anaerobic metabolism increases, during which rCBV and rCBF elevate and blood flow velocity decreases.