Lalonde C, Knox J, Youn Y K, Demling R
Longwood Area Trauma Center, Brigham and Women's Hospital, Boston, MA.
Crit Care Med. 1992 Jun;20(6):789-96. doi: 10.1097/00003246-199206000-00016.
To determine the effect of a body burn on effective or nutrient liver blood flow and the relationship between blood flow and oxidant-induced lipid peroxidation.
Anesthetized sheep were given a 40% of total body surface, third-degree burn, after which animals were fluid resuscitated to return ventricular filling pressures and cardiac output to baseline values. Animals, for the 6-hr study period, were resuscitated with lactated Ringer's solution alone or lactated Ringer's solution plus 1500 mL of 5% hydroxyethyl starch or lactated Ringer's solution plus hydroxyethyl starch on which was complexed the iron chelator deferoxamine to prevent oxidant release. Effective liver blood flow was measured using the galactose infusion technique. Liver tissue lipid peroxidation was monitored using malondialdehyde content.
We found that effective liver blood flow was decreased by 50% in the 4- to 5-hr postburn period, even when animals were resuscitated to baseline cardiac output values with lactated Ringer's solution. Tissue malondialdehyde content increased in the group treated with lactated Ringer's solution from a control value of 110 +/- 7 to 202 +/- 59 nmol/g of tissue. Resuscitation with hydroxyethyl starch restored postburn effective liver blood flow to control values, but malondialdehyde content was still increased two-fold. Resuscitation with hydroxyethyl starch and deferoxamine resulted in an increase in effective liver blood flow postburn to a value 80% above controls. In addition, lipid peroxidation was prevented.
Effective liver blood flow is markedly decreased after burn injury, even with apparently adequate volume resuscitation, when using lactated Ringer's solution. Liver lipid peroxidation persists even when effective liver blood flow is maintained, indicating that the oxidant process is not solely related to blood flow. Infusion of the antioxidant deferoxamine during resuscitation not only prevents the lipid peroxidation, most likely by a nonblood-flow-related process, but also results in an increase in blood flow above normal rates, suggesting that postburn liver oxygen needs exceed normal values.
确定体表烧伤对肝脏有效血流或营养血流的影响以及血流与氧化剂诱导的脂质过氧化之间的关系。
对麻醉的绵羊进行全身40%体表面积的三度烧伤，之后对动物进行液体复苏，以使心室充盈压和心输出量恢复到基线值。在6小时的研究期间，动物分别单独用乳酸林格氏液、乳酸林格氏液加1500毫升5%羟乙基淀粉或乳酸林格氏液加与铁螯合剂去铁胺络合的羟乙基淀粉进行复苏，以防止氧化剂释放。使用半乳糖输注技术测量肝脏有效血流。使用丙二醛含量监测肝组织脂质过氧化。
我们发现，即使在用乳酸林格氏液将动物复苏至基线心输出量值时，烧伤后4至5小时肝脏有效血流仍下降了50%。用乳酸林格氏液治疗的组中，组织丙二醛含量从对照值110±7增加到202±59纳摩尔/克组织。用羟乙基淀粉复苏可使烧伤后肝脏有效血流恢复到对照值，但丙二醛含量仍增加了两倍。用羟乙基淀粉和去铁胺复苏导致烧伤后肝脏有效血流增加到比对照值高80%的值。此外，脂质过氧化得到了预防。
烧伤后肝脏有效血流显著下降，即使使用乳酸林格氏液进行了明显充足的容量复苏。即使维持了肝脏有效血流，肝脏脂质过氧化仍持续存在，这表明氧化过程不仅仅与血流有关。复苏期间输注抗氧化剂去铁胺不仅最有可能通过与血流无关的过程预防脂质过氧化，而且还导致血流增加至高于正常速率，这表明烧伤后肝脏的氧需求超过正常值。
