Alterations in biochemical functions during hyperthermic isolation-perfusion of the human liver.
Alterations in biochemical functions during hyperthermic isolation-perfusion of the human liver.
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人肝脏高温隔离灌注过程中生化功能的变化。
DOI：
10.1016/0022-4804(86)90058-2
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发表时间：
1986
期刊：
影响因子：
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通讯作者：
R. Petroff
中科院分区：
文献类型：
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作者：
J. Skibba;E. Quebbeman;J. Kalbfleisch;Joy C. Sonsalla;R. Petroff
采用隔离-灌注技术对8例肝癌患者的肝脏进行热疗（42 ~ 42.5°）。在灌注过程中通过测量多种灌注液成分来评估肝功能完整性。7次灌注的数据可用于分析。在灌注过程中，灌注液乳酸，丙酮酸，葡萄糖，尿素，钾，碱性磷酸酶，SGOT和LDH增加。除钾外，其他各组分均显著增加（P< 0.05）。乳酸在整个灌注过程中从3.8 ± 1.0 mM积累到4 h时的7.6 ± 3.5 mM，丙酮酸在灌注的前3 h从0.14 ± 0.06 mM增加到0.80 ± 0.37 mM，然后下降到4 h时的0.54 ± 0.24 mM，L/P（乳酸/丙酮酸）比在灌注期间在前2小时降低至<10，但在灌注结束时升高至正常范围内。L/P比值明显降低（P< 0.05）。最初，灌流液葡萄糖浓度从4.5 ± 0.8 mM迅速升高至2 h时的20.7 ± 5.4 mM，此后无显著变化。尿素从0.64 ± 0.22 mM上升到1.92 ± 0.76 mM，灌流钾从灌流时的7.0 ± 1.0 mM上升到2 h时的8.3 ± 1.7 mM，然后下降。SGOT、LDH和碱性磷酸酶在灌注期间分别从21 ± 15、142 ± 48和16 ± 6增加至176 ± 22、472 ± 53和52 ± 42。灌注液中的总酮体在90 min时从0.08 ± 0.05 mM增加到0.89 ± 0.49 mM，然后下降到约0.58 ± 0.46 mM。在整个灌注时间内，B/A（3-羟基丁酸/乙酰乙酸）比值保持在1.0附近。灌注液酶的升高表明热灌注引起的肝损伤。高乳酸血症与灌流液丙酮酸和降低L/P比的显着上升，表明丙酮酸脱氢酶的活性可能降低或从线粒体到胞质溶胶的还原当量转移失败。数据表明，在42-42.5°灌注4小时后，肝功能完整性得以维持。
Hyperthermia (42–42.5°) was applied to the liver of eight patients with cancer in the liver by a technique of isolation-perfusion. Hepatic functional integrity was assessed during perfusion through measurement of multiple perfusate constituents. Data from seven perfusions were available for analysis. During perfusion there was an increase in perfusate lactate, pyruvate, glucose, urea, potassium, alkaline phosphatase, SGOT, and LDH. All increases in these constituents were significant (P< 0.05) except for potassium. Lactate accumulated throughout the perfusion from an initial level of 3.8 ± 1.0 mMto 7.6 ± 3.5 mMat 4 hr. Pyruvate increased over the first 3 hr of perfusion from 0.14 ± 0.06 mMto 0.80 ± 0.37 mMbefore declining to 0.54 ± 0.24 mMat 4 hr. The L/P (lactate/pyruvate) ratio decreased during perfusion to <10 in the first 2 hr, but rose to within normal limits by the end of perfusion. The decreases in L/P ratios were significant (P< 0.05). Initially there was a rapid rise in perfusate glucose concentrations from 4.5 ± 0.8 mMto 20.7 ± 5.4 mMat 2 hr with nonsignificant changes thereafter. Urea levels increased from 0.64 ± 0.22 mMto 1.92 ± 0.76 mM. Perfusate potassium increased from the initial level of 7.0 ± 1.0 mMduring perfusion to 8.3 ± 1.7 mMat 2 hr before declining. SGOT, LDH, and alkaline phosphatase increased during perfusion from 21 ± 15, 142 ± 48, and 16 ± 6 to 176 ± 22, 472 ± 53 and 52 ± 42, respectively. Total ketone bodies in the perfusate increase from 0.08 ± 0.05 mMto 0.89 ± 0.49 mMat 90 min and decrease to about 0.58 ± 0.46 mM. The B/A (3-hydroxybutyrate/acetoacetate) ratio remained near 1.0 throughout the perfusion time. The rise in perfusate enzymes was indicative of hepatic damage from hyperthermic perfusion. Hyperlactatemia with a marked rise in perfusate pyruvate and a decreased L/P ratio suggested a possible decrease in the activity of pyruvate dehydrogenase or failure of transfer of reducing equivalents from the mitochondria to the cytosol. The data indicate that hepatic functional integrity was maintained during perfusion after 4 hr at 42–42.5°.