Department of Surgery, University of Louisville, Louisville, Kentucky, USA.
Department of Physiology and Biophysics, University of Louisville, Louisville, Kentucky, USA; Division of General Internal Medicine, Mayo Clinic, Rochester, Minnesota, USA.
Nutrition. 2014 Mar;30(3):313-8. doi: 10.1016/j.nut.2013.08.006. Epub 2013 Dec 17.
Total hepatic blood flow (HBF) via the hepatic artery and portal vein is highly dependent on gastrointestinal perfusion. During postprandial hyperemia, intestinal blood flow depends on nutrient composition, gastrointestinal location, and time. Immune-enhancing diets (IEDs) containing n-3 polyunsaturated fatty acids (PUFAs) selectively augment blood flow in the ileum at 60-120 min via a bile-dependent mechanism. My colleagues and I hypothesized that liver blood flow would be similarly affected by IEDs containing n-3 PUFAs.
Mean arterial blood pressure, heart rate, and effective HBF (galactose clearance) were measured in anesthetized male Sprague-Dawley rats after gastric gavage of either a control diet (CD, Boost, Novartis) or an IED (Impact, Nestle Nutrition), with or without bile-duct ligation (BDL), and with or without supplemental bile (bovine, dried, unfractionated). Significance was assessed by 2-way ANOVA for repeated measures with the Tukey-Kramer honestly significant difference test.
Compared with baseline levels, a CD increased HBF (peak at 40 min , *P < 0.05) whereas an IED increased HBF in two distinct peaks at 40 min (*P < 0.05) and 120 min (*P < 0.05), but BDL prevented both the early (CD and IED, †P < 0.05) and late peaks (IED, †P < 0.05). Bile supplementation in the CD + BDL or IED + BDL groups restored neither the CD peak nor the early or late IED peaks.
HBF during absorptive intestinal hyperemia is modulated by a mechanism that requires an intact enterohepatic circulation. The early peaks at 40 min (CD or IED) were prevented by BDL, even though fat absorption in the proximal gut occurs by bile-independent direct absorption. Bile supplementation with the diet (CD + BDL or IED + BDL) was insufficient to restore HBF hyperemia, which implies that a relationship exists between intestinal and hepatic blood flow that is not solely dependent on bile-mediated intestinal fat absorption and bile recirculation.
通过肝动脉和门静脉的总肝血流量(HBF)高度依赖于胃肠道灌注。在餐后充血期间,肠道血流取决于营养成分、胃肠道位置和时间。含有 n-3 多不饱和脂肪酸(PUFA)的免疫增强饮食(IED)通过依赖于胆汁的机制选择性地在 60-120 分钟内增加回肠的血液流量。我的同事和我假设,含有 n-3 PUFAs 的 IED 也会类似地影响肝血流量。
在麻醉雄性 Sprague-Dawley 大鼠中,通过胃内灌胃给予对照饮食(CD,Boost,诺华)或 IED(Impact,雀巢营养),并在有或没有胆管结扎(BDL)的情况下,以及在有或没有补充胆汁(牛,干燥,未分级)的情况下,测量平均动脉血压、心率和有效 HBF(半乳糖清除率)。采用重复测量的 2 因素方差分析和 Tukey-Kramer 诚实显著差异检验评估显著性。
与基线水平相比,CD 增加了 HBF(峰值在 40 分钟,*P < 0.05),而 IED 在 40 分钟(*P < 0.05)和 120 分钟(*P < 0.05)时增加了两个明显的 HBF 峰值,但 BDL 阻止了早期(CD 和 IED,†P < 0.05)和晚期(IED,†P < 0.05)峰值。在 CD + BDL 或 IED + BDL 组中补充胆汁既不能恢复 CD 峰值,也不能恢复早期或晚期 IED 峰值。
吸收性肠道充血期间的 HBF 受到一种需要完整的肠肝循环的机制调节。BDL 甚至阻止了 40 分钟时的早期峰值(CD 或 IED),尽管近端肠道的脂肪吸收是通过不依赖胆汁的直接吸收发生的。饮食中补充胆汁(CD + BDL 或 IED + BDL)不足以恢复 HBF 充血,这意味着肠道和肝脏血流之间存在一种关系,这种关系不仅仅依赖于胆汁介导的肠道脂肪吸收和胆汁再循环。