不同缺氧条件下大鼠肝细胞能量代谢变化

目的：观察缺氧对大鼠肝细胞能量代谢的影响。方法：利用体外培养的肝细胞缺氧模型，模拟创伤后的缺血、缺氧环境，以正常生长的大鼠肝细胞为对照，采用生物化学的方法，分析氧的不同浓度及缺氧时间下肝细胞内ATP、ADP、AMP以及能荷的变化。结果：与正常对照组相比，缺氧肝细胞内ATP含量下降，4h达到最低水平，以后逐渐回升，其中O2浓度为15%组16h与正常对照无显性差异。ADP和AMP的变化与ATP相反，与正常对照相比，缺氧后水平增高，4h达到高峰，以后逐渐下降，16h仍未能完全恢复正常水平。能荷及ATP/ADP比值的变化与AMP相似。结论：缺氧后肝细胞能量代谢明显受到影响，呈现出双相变化的趋势，ATP和能荷水平先降低，后增高。     

异氟醚对缺氧或复氧肝细胞能量平衡的保护作用

目的观察异氟醚对不同缺氧时间以及复氧后肝细胞能量平衡的保护作用。方法将新鲜分离肝细胞置于krebs缓冲液中，密封容器中通人O2／CO2或N2／CO2(95％：5％)制造有氧或缺氧环境，加或不加异氟醚。实验分六组：有氧组、有氧加异氟醚组、缺氧组、缺氧加异氟醚组、缺氧后复氧组、缺氧后复氧加异氟醚组，观察配对各组用异氟醚后的变化。用高效液相技术测肝细胞内ATP、ADP、AMP水平并计算总腺苷酸和反映ATP供需平衡的能荷(=[ATP 1／2ADP]／[ATP ADP AMP])。结果(1)缺氧30min肝细胞中能荷、ATP的下降与AMP的升高被异氟醚部分逆转，而被复氧完全逆转。(2)缺氧90min肝细胞能荷、总腺苷酸明显下降，复氧可部分提高能荷而不提高总腺苷酸，异氟醚对缺氧和复氧期间的能荷、总腺苷酸均有部分逆转作用。结论临床当量的异氟醚对长期和短期缺氧肝细胞均有能量保护作用，并有效改善复氧后的能量失衡状况。     

维拉帕米和Na+-K+通道阻滞剂对低温保存成人肝细胞能量代谢的影响

目的：研究维拉帕米及Na^ -K^ 通道阻滞剂四乙基胺,奎尼丁和阿米洛利对低温保存成人肝细胞能量代谢的影响和对细胞的保护作用。方法：用胶原酶消化法制备成人肝细胞,置于分别加入维拉帕米,四乙基胺＋奎尼丁＋阿米洛利,四乙基胺＋奎尼丁＋阿米洛利＋维拉帕米的保存液中保存,高效液相色谱仪检测各组肝细胞中ATP,ADP及AMP的含量,结果：在维拉帕米实验组,ATP水平在实验过程中始终高于低温保存对照组,前4个小时ADP平衡升高,以后逐渐减低,AMP呈缓慢升高趋势,至12h达峰值;总腺苷酸含量总体呈下降趋势,但平台期延长,下降缓慢,能量转换率的变化与总腺苷酸含量相似,在加用维拉帕米和Na^ -K^ 通道阻滞剂的联合用药组,ATP缓慢降低到初期的50％以下,ADP初期缓慢上升,4h后逐渐下降,AMP呈缓慢上升趋势;总腺苷酸含量和能量转换率均较维拉帕米组高,提示细胞的活性保持良好。结论：在低温存存成人肝细胞时加入维拉帕米和Na^ -K^ 通道阻滞剂可降低肝细胞的能量消耗,它们对细胞的保护具有协同作用。     

a-硫辛酸对阻塞性黄疸大鼠肝细胞线粒体内能量代谢保护作用及机制

目的 探讨α-硫辛酸对阻塞性黄疸大鼠肝细胞线粒体内能量代谢的保护作用及其机制. 方法 将72只SD雄性大鼠随机分为对照组（SO组）,胆总管结扎＋0.9%氯化钠溶液组（BDL＋NS组）,胆总管结扎α-硫辛酸组（BDL＋LA组）.分别于术后7 d、14 d和2l d检测肝细胞线粒体内MDA、SOD、ATP、ADP和AMP含量并计算总腺苷酸（TAN）和能荷（EC）. 结果 BDL＋NS组各时间点肝细胞线粒体内MDA、ADP、AMP含量明显升高,而SOD、ATP、EC含量却明显降低.胆总管结扎7 d、14 d时,肝细胞线粒体内MDA含量BDL＋LA组比BDL＋NS组低,差异有统计学意义（P＜0.01）;2l d时,AMP、MDA含量BDL＋NS组和BDL＋LA中都更进一步升高,但两组比较差异无统计学意义（P＞0.05）.胆总管结扎7 d、14 d时,肝细胞线粒体内SOD含量、ATP含量BDL＋LA组比BDL＋NS组下降程度有显著性差异（7 d,P＜0.01;14 d,P＜0.05）;21 d时,两组肝细胞线粒体内SOD含量都进一步下降,但差异无统计学意义（p＞0.05）. 结论 α-硫辛酸在阻塞性黄疸早、中期有保护线粒体能量代谢作用,减轻了阻塞性黄疸时肝的损伤.     

α-硫辛酸对阻塞性黄疸大鼠肝细胞线粒体内能量代谢保护作用及机制

目的 探讨α-硫辛酸对阻塞性黄疸大鼠肝细胞线粒体内能量代谢的保护作用及其机制. 方法 将72只SD雄性大鼠随机分为对照组(SO组),胆总管结扎+0.9%氯化钠溶液组(BDL+NS组),胆总管结扎α-硫辛酸组(BDL+LA组).分别于术后7 d、14 d和2l d检测肝细胞线粒体内MDA、SOD、ATP、ADP和AMP含量并计算总腺苷酸(TAN)和能荷(EC). 结果 BDL+NS组各时间点肝细胞线粒体内MDA、ADP、AMP含量明显升高,而SOD、ATP、EC含量却明显降低.胆总管结扎7 d、14 d时,肝细胞线粒体内MDA含量BDL+LA组比BDL+NS组低,差异有统计学意义(P＜0.01);2l d时,AMP、MDA含量BDL+NS组和BDL+LA中都更进一步升高,但两组比较差异无统计学意义(P＞0.05).胆总管结扎7 d、14 d时,肝细胞线粒体内SOD含量、ATP含量BDL+LA组比BDL+NS组下降程度有显著性差异(7 d,P＜0.01;14 d,P＜0.05);21 d时,两组肝细胞线粒体内SOD含量都进一步下降,但差异无统计学意义(p＞0.05). 结论 α-硫辛酸在阻塞性黄疸早、中期有保护线粒体能量代谢作用,减轻了阻塞性黄疸时肝的损伤.     

热缺血损伤对大鼠移植肝组织能量代谢及存活期的影响

目的：探讨不同热缺血时间下大鼠肝组织能量代谢变化规律,预测供肝耐受热缺血的安全时限。方法：实验动物按供肝热缺血时间分别为0、10、15、20、30、45和60min,随机分为7组。采用反相高效液相色谱法测定单纯热缺血后肝组织能量代谢指标并进行超微结构的观察。然后按各组条件分别作原位肝移植,观察移植后24、48h各组肝组织能量代谢指标的恢复性变化,并统计生存时间。结果：供肝经受热缺血损伤后,肝组织ATP含量和EC水平远逐渐下降,其中前30min下降比较急剧,以后趋向平缓。热缺血30min内肝组织ATP含量和EC水平在肝移植再复流24h后基本得到恢复,术后大鼠仍可以获长期存活。45min组,移植肝在48h后能量代谢的功能也基本恢复,虽不足以影响术后的1周存活率,但对大鼠肝移植术后的3个月存活率影响显著。60min组,肝脏能量代谢储备功能难以恢复,大鼠术后生存天数显著降低。结论：供肝组织三磷酸腺苷（ATP）含量和能荷（EC）水平以及其移植术后恢复的潜能是衡量供肝质量的重要标准。供肝热缺血损伤的时间与肝组织能量代谢功能的恢复及术后动物生存情况密切相关。     

L-精氨酸对阻塞性黄疸大鼠肝细胞能量代谢的影响

目的　探讨L 精氨酸 (L Arg)对阻塞性黄疸大鼠肝细胞能量代谢的影响。 方法　将5 4只SD雄性大鼠随机分为假手术对照组 (SO ) ,胆总管结扎组 (BDL) ,胆总管结扎 +L 精氨酸组(BDL +L Arg)。分别于术后 7、14、2 1d 3个时间点检测肝组织三磷酸腺苷 (ATP)、二磷酸腺苷(ADP)、一磷酸腺苷 (AMP)及丙二醛 (MDA)和一氧化氮 (NO)含量。结果　BDL组各时间点肝组织ATP、总腺苷酸 (TAN )和能荷 (EC)明显降低 ,而NO、MDA含量显著增加。BDL +L Arg组在胆管结扎 7d时ATP、TAN含量较BDL组高 (P <0 .0 5 ) ,EC维持在接近正常水平。 14d时BDL +L Arg组ATP、TAN与BDL组差异无显著性 (P >0 .0 5 ) ,但EC仍未明显降低。 2 1d时两组ATP、TAN、EC及MDA含量相接近 ,NO在BDL +L Arg组明显高于BDL组 (P <0 .0 1)。 结论　L Arg在阻塞性黄疸早期可保护肝细胞能量代谢功能 ,减轻肝损伤     

钌红对严重烧伤早期心肌能量代谢的影响

目的 探讨钌红对严重烧伤早期心肌能量代谢的影响。方法 Wistar大鼠24只,随机分为正常对照组、烧伤组和烧伤钌红治疗组。烧伤组、烧伤钌红治疗组大鼠造成30％总体表面Ⅲ度烧伤,伤后30min经腹腔补液,烧伤治疗组同时于颈外静脉推注钌红(2mg/kg体重）,3h后再推注1次。伤组和烧伤治疗组动物于伤后6h活杀。测定心肌线粒体呼吸功能、Ca^2 浓度（[Ca^2 ]m)及心肌组织ATP、ADP、AMP和乳酸含量。结果 钌红治疗组[Ca^2 ]m较烧伤组显著降低,线粒体呼吸控制率（RCR）、Ⅲ态呼吸速率（ST3）明显升高,Ⅳ态呼吸速率（ST4）降低;钌红治疗组ATP含量较烧伤组升高100.4%,同时ADP、AMP含量明显低于烧伤组,且钌红治疗组乳酸仿较烧伤组降低53.5%。结论 钌红治疗可改善严重烧伤早期线粒体功能和心肌能量代谢。     

成体大鼠心肌细胞微管解聚对线粒体分布及能量代谢的影响

目的 了解成体大鼠心肌细胞微管解聚对线粒体分布、线粒体活性及细胞能量代谢的影响. 方法 分离培养成体SD大鼠及SD大鼠乳鼠心肌细胞,按随机数字表法分为:大(乳)鼠对照组(常规培养,不加任何刺激因素)、大(乳)鼠微管解聚剂组(用含终浓度8μmol/L秋水仙碱的培养液培养,作用30 min).(1)用蛋白质印迹法检测各组大鼠和乳鼠心肌细胞聚合态β微管蛋白表达量.(2)取2组大鼠心肌细胞,用蛋白质印迹法检测细胞色素c表达量;免疫荧光染色法观察细胞聚合态β微管蛋白、电压依赖型阴离子通道(VDAC)分布情况;免疫细胞化学法检测细胞线粒体内膜电位;噻唑蓝法测量细胞活性;采用高效液相色谱法,检测细胞ATP、腺苷二磷酸(ADP)、腺苷一磷酸(AMP)含量及能荷. 结果 (1)聚合态β微管蛋白表达量:大鼠微管解聚剂组为0.52±0.07,较大鼠对照组1.25±0.12明显减少(F=31.002,P=0.000);乳鼠微管解聚剂组为0.76±0.12,较乳鼠对照组1.11±0.24显著减少(F=31.002,P=0.000),但明显高于大鼠微管解聚剂组(F=31.002,P=0.009).(2)细胞色素c表达量:大鼠对照组为0.26±0.03,明显低于大鼠微管解聚剂组(1.55±0.13,t=-24.056,P=0.000).(3)免疫荧光染色:大鼠对照组心肌细胞微管多呈线性管状、与心肌纤维平行分布;VDAC着色显示线粒体呈颗粒状与微管同向分布.大鼠微管解聚剂组微管正常排列规律被破坏,表现为免疫荧光强度减弱,微管结构不清晰、连续性丧失、粗糙;线粒体分布散乱.(4)线粒体内膜电位:大鼠对照组荧光强度为1288±84,明显高于大鼠微管解聚剂组(331±27,t=26.508,P=0.000).(5)细胞活性:大鼠对照组吸光度值为1.75±0.11;大鼠微管解聚剂组为0.81±0.07,较前者明显降低(t=17.348,P=0.000).(6)能量代谢:与大鼠对照组比较,大鼠微管解聚剂组心肌细胞ATP含量下降,ADP、AMP含量上升,ATP/ADP值与能荷均降低. 结论 在正常成体大鼠心肌细胞内,微管与线粒体分布方向一致.微管解聚后心肌细胞线粒体排列紊乱,细胞色素c从线粒体漏出,线粒体内膜电位下降、能量供应降低,细胞活性下降.     

L-精氨酸对兔缺血再灌注损伤肝脏能量代谢的影响

目的探讨L-精氨酸(L-Arg)对肝缺血再灌注损伤(HIRI)时肝细胞能量代谢的影响及其机制。方法实验兔30只,随机分为对照组(C组),模型组(HIRI组)和L-Arg干预组(L-Arg组)。在再灌注45min时,分别检测肝组织内三磷酸腺苷(ATP)、二磷酸腺苷(ADP)、一磷酸腺苷(AMP)含量,总腺苷酸量(TAN),能荷(EC),丙二醛浓度(MDA),超氧化物歧化酶活性(SOD),一氧化氮代谢产物(NO_2-/NO_3-)水平,血栓素B_2(TXB_2)和6-酮基-前列腺素F_1α(6-keto-PGF_1α)含量以及TXB_2/6-keto-PGF_1α(T/K)值。结果 L-Arg组与HIRI组比较,肝组织内ATP、NO_2-/NO_3-、6-keto-PGF_1α含量,EC和SOD活性均明显增高(P0.05或P0.01),AMP含量及T/K值显著降低(P0.05或P0.01)。结论 L-精氨酸可通过降低体内氧自由基水平,提高一氧化氮水平,纠正TXA_2与PGI_2的平衡,从而改善缺血再灌注损伤肝脏的能量代谢。     

Energy metabolism of experimental wounds at various oxygen environments.

Energy metabolism of healing tissue was studied in experimental wounds of rats chronically breathing 11% O2, air or 55% O2. Increasing oxygen supply elevated both PO2 and PCO2 in the wound tissue. At the early phases of healing hypoxic wounds contained less DNA than normoxic or hyperoxic tissues. In hypoxia the accumulation of wound collagen was clearly retarded. Furthermore, tissue taken from wounds healing in hypoxic environments and tested ex vivo in air showed decreased capacity for glucose utilization, lactate production and oxygen consumption. Concentrations of AMP, ADP and ATP in repair tissue increased as healing progressed. The more oxygen available the higher the amounts of ADP and ATP. The AMP content was not affected by changes in local oxygen tension. These results support the earlier concept that the supply of oxygen in healing tissue may be rate-limitimg. Reduction of available oxygen either by systemic hypoxia or by increased diffusion distance impedes healing.     

Energy deficits in hepatocytes isolated from phenobarbital-treated or fasted rats and briefly exposed to halothane and hypoxia in vitro

Experimental factors implicated in the pathogenesis of halothane hepatotoxicity in the phenobarbital-hypoxia rat model were examined for direct effects on the energy status of isolated rat liver cells in vitro. Intact hepatocytes were isolated after collagenase perfusion of livers of adult male Fischer 344 rats previously treated with phenobarbital (0.1% in drinking water for 5-7 days) and/or deprived of food for 48 h. Cells were incubated in Krebs-Henseleit buffer + substrates for 10 min at steady states of energy metabolism, with extracellular PO2 constant at 32, 16, or 4 mmHg +/- 1% halothane. Fasting produced the largest energy deficits in incubated hepatocytes, regardless of phenobarbital treatment status, PO2 value, or presence/absence of halothane. The combination of hypoxic PO2 (4 mmHg) and 1% halothane shifted lactate metabolism toward lactate production, whereas hypoxia or halothane alone did not. Prior phenobarbital treatment plus hypoxia decreased adenosine triphosphate/adenosine diphosphate (ATP/ADP) and increased lactate production compared with drug treatment or hypoxia alone. We conclude that pathogenic factors that interact to produce halothane hepatotoxicity act directly and jointly on isolated liver cells to produce energy deficits within 10 min. Differences in the relative importance of pathogenic factors in vitro and in vivo suggest that short-term, direct effects on hepatocellular energy status are not solely responsible for halothane hepatotoxicity.     

Hypoxia-mediated impaired differentiation by LLC-PK1 cells: evidence based on the protein kinase C profile.

We recently reported that mild hypoxia in LLC-PK1 cells, grown in standard fashion under a still layer of overlying medium at 5% CO2/18% O2 environment, result in decreased oxidative metabolism and impaired differentiated functions in comparison to adequately oxygenated cultures maintained either under a higher oxygen (36% O2) environment or conditions of continuous rocking of the media fluid. In the present study, subcellular distribution of a regulatory enzyme protein kinase C (PKC) was examined between hypoxic still and normoxic rocked LLC-PK1 cells. Subconfluent cultures of hypoxic LLC-PK1 cells exhibited significantly lower and predominantly membrane-bound PKC activity in comparison to mostly cytosolic localization of this enzyme in normoxic rocked cells. One hour of exposure of adequately oxygenated-rocked LLC-PK1 cells with the phorbol ester TPA, a dedifferentiating agent that did not effect the cell ATP content, resulted in significant inhibition of dome formation and sodium-dependent glucose transport activity, a partial loss of pH-responsive ammoniagenesis, and almost complete translocation of protein kinase C activity from cytosol to the membrane pool; all of which resembles the behavior of hypoxic still cultured cells. In addition, acute re-oxygenation of hypoxic still cultures by rocking the media fluid for one hour resulted in an increase in cell ATP content to the cellular levels of ATP observed in normoxic rocked cells. However, all the parameters of differentiation were unaffected by re-oxygenation. These studies support the notion that hypoxia can act in some primary fashion, independent of its effects on energy metabolism, to impair cellular differentiation in LLC-PK1 cells. They also raise the possibility that activation of protein kinase C may act as an important mediator in this process.     

Changes in hepatic energy metabolism in rats with acute necrotizing pancreatitis

In this study, changes of hepatic cellular ATP, ADP, and AMP, concentrations and mitochondrial oxidative phosphorylation were investigated in rats with experimental acute necrotizing pancreatitis (ANP). It was found that energy change (ATP + 1/2 ADP)/(ATP + ADP + AMP) of the liver decreased from 0.866 to 0.806 (P less than 0.05) 24 h after ANP, and to 0.769 (P less than 0.01) at 48 h. On the other hand, mitochondrial phosphorylative activity increased to 130% and 157% over the control at 12 h and 24 h respectively, and then rapidly dropped to 62% of normal value at 48 h. Blood ketone body ratio was positively correlated with hepatic energy charge level in ANP. The authors came to the following conclusions that: (1) In ANP, mitochondrial function damage resulted in decreased hepatic energy charge, which, in turn, led to hepatocellular impairment; (2) the measurement of blood ketone body ratio was a reliable indicator by which to assess the energy status of the liver in ANP.     

δ阿片受体激动剂对脓毒症大鼠小肠能量代谢作用的研究

目的：探讨δ阿片受体激动剂DADLE（D—Ala^2-D—Leu^5-enkephali）对脓毒症大鼠小肠屏障功能的保护作用及其机制。方法：72只SD大鼠,分为假手术组、脓毒症组和DADLE（5mg／Kg）治疗组．每组24只。采用改良盲肠结扎穿孔方法（CLP）建立大鼠脓毒症模型,假手术组除不结扎刺穿盲肠外,其余操作同脓毒症组,DADLE治疗组模型建立后立即按5mL/kg剂量静脉注射浓度为0．5mg／mL的DALDE。于手术后4、8、12h处死大鼠,测定小肠黏膜组织中ATP、ADP、AMP含量;制备肠上皮细胞线粒体,测定各组大鼠线粒体呼吸控制率（RCR）、磷氧比（P／O）和肠道氧摄取率（Oext）;观察并比较各组小肠黏膜上皮组织病理改变。结果：DADLE治疗组的小肠黏膜ATP、ADP含量较脓毒症组均有明显升高（P〈0．05）,AMP含量明显下降（P〈0．05）;DADLE治疗组小肠上皮细胞中线粒体RCR、P／O和Oext较脓毒症组均明显升高（P〈0．05）;小肠黏膜上皮组织病理学提示DADLE组的组织损伤明显轻于脓毒症组。结论：δ阿片受体激动剂DADLE对脓毒症大鼠小肠氧代谢和能量代谢的抑制状态具有一定程度的改善作用。     

The adenosine phosphate content in human sperm and their motility

Adenosine phosphoric acids (ATP, ADP, AMP) are of significance for the metabolic processes in living beings, including spermatozoa, as they are the principal donors of energy in all the reactions of biosynthesis. Besides, spermatozoa need the energy to perform a particular function-to move in the female genital tract to the ovum. It was stated that a decrease in the ATP levels reduced or ceased the translational motion of spermatozoa, therefore the investigations of adenosine phosphates in the spermatozoa were found to be mandatory. The authors studied the levels of ATP, ADP and AMP and the energy charge in the native human spermatozoa in the patients with oligo- and asthenospermia. Spermatozoa with morphologically and physiologically normal fertility were used as controls. The results obtained demonstrated that in oligospermic males the levels of ATP were slightly decreased whereas the levels of AMP significantly increased from 31.6 to 38 per cent. As a result there was a significant decrease in the ATP/ADP ratio. A more pronounced decrease in the ATP levels and an increase in the AMP levels were revealed in asthenospermic patients (12.6 and 40.5 per cent respectively. In the latter patients the ADP fraction decreased to 42.4 per cent versus 51.4 per cent in health and the energy charge underwent a more significant decrease: from 0.37 (normal) to 0.3. The results obtained are indicative of the possibility of using the aforementioned method for a comprehensive evaluation of the spermatozoan functional activity and the detection of asthenospermia-inducing mechanisms.     

热休克蛋白70对肠上皮细胞缺氧/复氧后线粒体功能及能量代谢的影响

目的 了解Ad-热休克蛋白70(HSP70)对缺氧/复氧损伤后肠上皮细胞线粒体功能及能量代谢的影响.方法 取肠上皮细胞株IEC-6分别转染Ad-HSP70腺病毒载体和空腺病毒载体,蛋白质印迹法观察HSP70的表达.取IEC-6细胞分为正常对照组(不作任何处理)、缺氧/复氧组(给予缺氧/复氧处理)、Ad-HSP70转染组(转染Ad-HSP70腺病毒载体后,给予缺氧/复氧处理).采用噻唑蓝比色法检测细胞内线粒体脱氧酶的活性,高效液相色谱分析法测定细胞能量代谢.结果 与转染空腺病毒载体相比,转染Ad-HSP70腺病毒载体可显著增加细胞HSP70的表达.缺氧/复氧组细胞内线粒体脱氢酶的活性明显低于正常对照组(P＜0.01),Ad-HSP70转染组该指标明显高于缺氧/复氧组(P＜0.01).缺氧/复氧组细胞内腺苷三磷酸含量较正常对照组显著下降,而腺苷二磷酸、腺苷-磷酸含量显著升高;Ad-HSP70转染组细胞能量指标与正常对照组相似(P＞0.05),较缺氧/复氧组有明显改善(P＜0.05或P＜0.01).缺氧/复氧组细胞能荷为0.615±0.060,明显低于正常对照组(0.748±0.012,P＜0.01)、Ad-HSP70转染组(0.736±0.028,P＜0.01).结论 Ad-HSP70腺病毒载体转染肠上皮细胞可诱导HSP70表达增加,显著提高细胞缺氧/复氧后胞内腺苷三磷酸的含量及细胞能荷,保护线粒体整体功能,提示线粒体是HSP70保护肠上皮细胞缺氧/复氧损伤的主要靶细胞器之一.     

Hepatic energy charge and adenine nucleotide status in rats anesthetized with halothane, isoflurane or enflurane

Background: Volatile anesthetics are known to have varying effects on hepatic oxygen supply in vivo and have been shown to depress hepatic mitochondrial respiration and so energy charge in vitro. However, the effect of halothane, isoflurane and enflurane on hepatic adenine nucleotide status in viuo has not been evaluated.
Methods: Ninety male rats were exposed to 40% oxygen (n=22) or 40% oxygen in equipotent (1 MAC) concentrations of halothane (1%) (n=23), isoflurane (1.4%) (n=22) or enflurane (2%) (n=23) for 2 hours. All animals were then administered intraperitoneal pentobarbital and anesthesia continued and laparotomy was performed. A liver biopsy was taken for determination of hepatocellular adenosine-5-triphosphate (ATP), adenosine-5-diphosphate (ADP) and adenosine-5-monophosphate (AMP) and computation of energy charge (EC) from ((ATP+1/2 ADP)+(ATP+ADP+AMP)) and total ade nine nucleotides (TAN) from (ATP+ADP+AMP). After the biopsy the aorta was cannulated for blood sampling.
Results: Rats in each group were similar in weight, as well as acid base and blood gas status just after liver biopsy. Hepatic energy charge, ATP, ADP, AMP, and TAN levels were not different in animals receiving either halothane, isoflurane or enflurane when compared with those receiving only oxygen.
Conclusions: One MAC of anesthesia for a period of 2 hours with the described volatile anesthetic agents did not affect adenine nucleotide status in viuo in rats.     

Myocardial high-energy phosphate levels in cardiomyopathic turkeys

A congestive cardiomyopathy (CCM) model occurs in inbred broad-breasted turkeys and is manifested by reduced hatchability and a high mortality within a week of hatching. In the survivors, cardiac dilation begins by 3-4 weeks of age and further mortality occurs from chronic congestive heart failure. The mechanisms behind these changes is unknown, and, therefore, we investigated what role, if any, myocardial energy metabolism might play in these events. Ventricular myocardial samples were obtained for analysis of adenine nucleotides (ATP, ADP, AMP) and creatine phosphate (CP) in control and CCM turkeys, 1-31 days old. The adenine nucleotide energy charge (EC) was calculated using the formula EC = ATP + 1/2ADP/(ATP + ADP + AMP). We found the myocardial ATP levels and EC in CCM hearts at 1-2 days were reduced. In control turkeys, no significant age-related differences were found in myocardial high-energy phosphate compounds or in the EC. This depression in the energy metabolism of CCM turkeys may also be reflected in their poor hatchability. By 6-10 days, however, ATP levels had recovered and remained normal despite the onset of cardiac dilation and failure at 3-4 weeks of age in CCM turkeys. Because CP levels in control and CCM turkey hearts were similar in all age groups, significant ischemia did not appear to be present after hatching in CCM turkeys. Our results suggest, therefore, that an insult probably prior to hatching produced depressed myocardial energy levels in CCM turkeys and led to reduced hatchability. This early insult appears to be significant, in that late cardiac dysfunction resulted despite the recovery of myocardial ATP levels.