Jakob S M, Merasto-Minkkinen M, Tenhunen J J, Heino A, Alhava E, Takala J
Department of Anesthesiology and Intensive Care, Kuopio University Hospital, Finland.
Shock. 2000 Aug;14(2):123-7. doi: 10.1097/00024382-200014020-00008.
Arterial blood lactate increases as a result of poor tissue perfusion. In splanchnic hypoperfusion, increased hepatic lactate uptake may delay increases in arterial blood lactate. We hypothesized that during isolated reduction of mesenteric blood flow, maintaining systemic blood volume and flow by fluid resuscitation may prevent systemic hyperlactatemia and therefore mask splanchnic ischemia. In a randomized study, 7 pigs were subjected to 4 h of splanchnic hypoperfusion by reducing the superior mesenteric artery blood flow to 4 +/- 0.8 mL/kg min [mean +/- standard deviation (SD)]. Seven pigs served as controls. Fluid was administered in order to keep the pulmonary artery occlusion pressure at 5 to 8 mm Hg. Cardiac output, portal vein, superior mesenteric, and hepatic arterial blood flow were measured every 30 min. Arterial, mixed venous, hepatic, portal, and mesenteric venous blood lactate, and jejunal mucosal pCO2 were measured at baseline and thereafter at 30-min intervals. The initial decrease in portal venous blood flow in the ischemic animals was subsequently counterbalanced by increasing hepatic arterial blood flow from 2 +/- 1 mL x kg(-1) x min(-1) at baseline to 11 +/- 4 mL x kg(-1) x min(-1) [after 4 h of ischemia; mean +/- standard deviation (SD), P = 0.02]. Jejunal mucosal- and mesenteric vein-arterial pCO2 gradients increased in the ischemic group from 11 +/- 8 mm Hg to 73 +/- 5 mm Hg (P = 0.02), and from 10 +/- 4 mm Hg to 44 +/- 8 mm Hg, respectively (P = 0.02). Mesenteric and portal venous lactate increased in the ischemic animals from 1.1 +/- 0.3 mmol/L to 4.2 +/- 1.0 mmol/L (P = 0.02), and from 1.0 +/- 0.2 mmol/L to 1.6 +/- 0.3 mmol/L, respectively (P = 0,03). While mesenteric lactate production and hepatic lactate uptake increased in parallel in the ischemic animals from 5 +/- 6 micromol x kg(-1) x min(-1) to 14 +/- 5 micromol x kg(-1) x min(-1) (P = 0.04), and from 14 +/- 7 micromol x kg(-1) x min(-1) to 24 +/- 6 micromol x kg(-1) x min(-1), respectively (P = 0.02), hepatic venous and arterial lactate, and apparent splanchnic lactate uptake and extraction did not change. We conclude that the hepatic lactate uptake increases in response to hepatic lactate influx. Systemic hyperlactatemia and increased hepatic venous lactate concentrations are late consequences of mesenteric hypoperfusion if hypovolemia is prevented. The net exchange of lactate across the splanchnic region does not reflect hepato-portal lactate kinetics in this animal model of intestinal hypoperfusion.
由于组织灌注不良，动脉血乳酸水平会升高。在内脏低灌注时，肝脏乳酸摄取增加可能会延迟动脉血乳酸水平的升高。我们假设，在单纯降低肠系膜血流期间，通过液体复苏维持全身血容量和血流可能会预防全身性高乳酸血症，从而掩盖内脏缺血。在一项随机研究中，7头猪通过将肠系膜上动脉血流降至4±0.8毫升/千克·分钟[平均值±标准差（SD）]，经历4小时的内脏低灌注。7头猪作为对照。给予液体以使肺动脉闭塞压维持在5至8毫米汞柱。每30分钟测量心输出量、门静脉、肠系膜上动脉和肝动脉血流。在基线时以及此后每隔30分钟测量动脉血、混合静脉血、肝血、门静脉血和肠系膜静脉血中的乳酸，以及空肠黏膜pCO₂。缺血动物门静脉血流最初的减少随后被肝动脉血流增加所抵消，肝动脉血流从基线时的2±1毫升·千克⁻¹·分钟⁻¹增加到11±4毫升·千克⁻¹·分钟⁻¹[缺血4小时后；平均值±标准差（SD），P = 0.02]。缺血组空肠黏膜与肠系膜静脉 - 动脉的pCO₂梯度分别从11±8毫米汞柱增加到73±5毫米汞柱（P = 0.02），以及从10±4毫米汞柱增加到44±8毫米汞柱（P = 0.02）。缺血动物肠系膜和门静脉乳酸分别从1.1±0.3毫摩尔/升增加到4.2±1.0毫摩尔/升（P = 0.02），以及从1.0±0.2毫摩尔/升增加到1.6±0.3毫摩尔/升（P = 0.03）。在缺血动物中，肠系膜乳酸生成和肝脏乳酸摄取并行增加，从5±6微摩尔·千克⁻¹·分钟⁻¹增加到14±5微摩尔·千克⁻¹·分钟⁻¹（P = 0.04），以及分别从14±7微摩尔·千克⁻¹·分钟⁻¹增加到24±6微摩尔·千克⁻¹·分钟⁻¹（P = 0.02），而肝静脉和动脉乳酸，以及表观内脏乳酸摄取和提取没有变化。我们得出结论，肝脏乳酸摄取会随着肝脏乳酸流入而增加。如果预防了血容量不足，全身性高乳酸血症和肝静脉乳酸浓度升高是肠系膜低灌注的晚期后果。在这个肠道低灌注动物模型中，乳酸跨内脏区域的净交换并不能反映肝门静脉乳酸动力学。
