Julien P, Angel A
Can J Biochem. 1981 Aug;59(8):709-14. doi: 10.1139/o81-098.
In the present study, very low density lipoprotein (VLDL, d less than 1.006) in cardiac lymph was characterized to determine its role as a metabolic substrate in the interstitial compartment. A major efferent cardiac lymph trunk was cannulated in fasting (18 h) dogs (20-27 kg). Three to five millilitres of lymph were collected over 3-4 h at 4 degrees C. Cardiac lymph VLDL concentration was 1.7 +/- 0.7 mg protein . 100 mL-1 compared with 1.8 +/- 0.8 mg protein . 100 mL-1 in plasma. The VLDL triglyceride concentration in lymph was 1.0 +/- 0.3 mg triglyceride . 100 mL-1 with triglyceride/protein ratio of 0.9 compared with plasma VLDL triglyceride of 5.0 +/- 1.6 mg . 100 mL-1 with a triglyceride/protein ratio of 5.5. Electron microscopy of VLDL revealed globular particles with a mean diameter of 388 A in lymph and 661 A in plasma. Thus, cardiac lymph VLDL are smaller and contain less triglyceride per particle than plasma VLDL. Following i.v. administration of human 125I-labelled low density lipoprotein ([125I]LDL, d 1.025-1.045), cardiac lymph/plasma LDL specific activity ratio was 0.52 +/- 0.15 (n = 3) and 0.55 +/- 0.15 (n = 4)) at 3 and 27 h, respectively. The fact that the specific activity ratio did not reach 1 at plateau suggests continuous addition of unlabelled LDL in the cardiac interstitium, presumably from VLDL precursors. These findings demonstrate that on a protein basis the concentration of VLDL in cardiac lymph equals that of plasma, and also suggests that VLDL degradation and LDL production occur in the cardiac interstitial space.
在本研究中,对心脏淋巴中的极低密度脂蛋白(VLDL,密度小于1.006)进行了特性分析,以确定其在间质区作为代谢底物的作用。在禁食(18小时)的犬(20 - 27千克)中,将一条主要的心脏淋巴输出干插管。在4℃下3 - 4小时内收集3至5毫升淋巴液。心脏淋巴中VLDL浓度为1.7±0.7毫克蛋白质·100毫升⁻¹,而血浆中为1.8±0.8毫克蛋白质·100毫升⁻¹。淋巴中VLDL甘油三酯浓度为1.0±0.3毫克甘油三酯·100毫升⁻¹,甘油三酯/蛋白质比值为0.9,而血浆VLDL甘油三酯为5.0±1.6毫克·100毫升⁻¹,甘油三酯/蛋白质比值为5.5。VLDL的电子显微镜检查显示,淋巴中的球状颗粒平均直径为388埃,血浆中为661埃。因此,心脏淋巴VLDL比血浆VLDL更小,且每个颗粒含有的甘油三酯更少。静脉注射人¹²⁵I标记的低密度脂蛋白([¹²⁵I]LDL,密度1.025 - 1.045)后,心脏淋巴/血浆LDL比活性在3小时和27小时分别为0.52±0.15(n = 3)和0.55±0.15(n = 4)。在平台期比活性未达到1这一事实表明,心脏间质中持续有未标记的LDL加入,推测来自VLDL前体。这些发现表明,以蛋白质为基础,心脏淋巴中VLDL的浓度与血浆相等,也提示VLDL降解和LDL生成发生在心脏间质空间。