Kitai T, Tanaka A, Terasaki M, Okamoto R, Ozawa K, Morikawa S, Inubushi T
Second Department of Surgery, Faculty of Medicine, Kyoto University, Japan.
Life Sci. 1991;49(7):511-8. doi: 10.1016/0024-3205(91)90068-m.
The changes in hepatic energy state were assessed by 31P-nuclear magnetic resonance spectroscopy (31P-MRS) and arterial ketone body ratio (AKBR) in brain dead dogs. 31P-MRS and AKBR were measured before and at 3 hours after brain death. Wiggers' shock model was employed to compare the energy metabolism during hypotension. 1) The brain death model: Systemic blood pressure changed from 178.3/115.0 mmHg (mean) in the control period, to 259.5/162.5 mmHg during Cushing phenomenon (CU period) and to 63.3/51.7 mmHg after completion of brain death (BD period). beta-ATP/Pi increased from 1.27 +/- 0.14 (mean +/- SEM) to 1.46 +/- 0.16 in the early CU period, and then decreased to 1.11 +/- 0.15 at 60 minutes after BD, followed by a gradual increase to 1.33 +/- 0.13 at 3 hours after BD. Intracellular pH (pHi) increased alkaline to the control value. AKBR decreased from 1.10 +/- 0.26 to 0.46 +/- 0.15 in the CU period (p less than 0.05) and then increased to 1.48 +/- 0.25 after BD. 2) Wiggers' shock model: Systemic blood pressure was 190.0/112.5 mmHg in the control period, 83.8/51.3 mmHg during exsanguination (EX period) and 185.0/117.0 mmHg after retransfusion (RT period). beta-ATP/Pi decreased from 1.17 +/- 0.13 to 0.61 +/- 0.10 in the EX period (p less than 0.05) and increased to 1.37 +/- 0.08 in the RT period. The pHi deviated from 7.33 +/- 0.07 to 6.82 +/- 0.14 in the EX period (p less than 0.01) and to 7.51 +/- 0.21 in the RT period. AKBR decreased from 1.00 +/- 0.11 to 0.21 +/- 0.04 in the EX period and increased to 1.08 +/- 0.12 in the RT period. The energy metabolism of the liver was well maintained in the state of brain death in spite of remarkable hypotension, although that was not the case with Wiggers' shock model. It was suggested that the combination of 31P-MRS and AKBR was useful for the evaluation of graft liver viability.
通过31P-核磁共振波谱法(31P-MRS)和动脉酮体比(AKBR)评估脑死亡犬的肝脏能量状态变化。在脑死亡前及脑死亡后3小时测量31P-MRS和AKBR。采用维格斯休克模型比较低血压期间的能量代谢。1)脑死亡模型:全身血压在对照期为178.3/115.0 mmHg(平均值),在库欣现象期间(CU期)升至259.5/162.5 mmHg,脑死亡完成后(BD期)降至63.3/51.7 mmHg。β-ATP/Pi在CU早期从1.27±0.14(平均值±标准误)升至1.46±0.16,然后在BD后60分钟降至1.11±0.15,随后在BD后3小时逐渐升至1.33±0.13。细胞内pH(pHi)碱性升高至对照值。AKBR在CU期从1.10±0.26降至0.46±0.15(p<0.05),然后在BD后升至1.48±0.25。2)维格斯休克模型:全身血压在对照期为190.0/112.5 mmHg,放血期间(EX期)为83.8/51.3 mmHg,再输血后(RT期)为185.0/117.0 mmHg。β-ATP/Pi在EX期从1.17±0.13降至0.61±0.10(p<0.05),在RT期升至1.37±0.08。pHi在EX期从7.33±0.07偏离至6.82±0.14(p<0.01),在RT期至7.51±0.21。AKBR在EX期从1.00±0.11降至0.21±0.04,在RT期升至1.08±0.12。尽管维格斯休克模型并非如此,但尽管存在明显低血压,肝脏能量代谢在脑死亡状态下仍能良好维持。提示31P-MRS和AKBR联合应用有助于评估移植肝的活力。