Soon-Shiong P, Cox K L, Rosenquist G L, Iwahashi-Hosoda C, Carr H
Am J Surg. 1985 Jan;149(1):163-6. doi: 10.1016/s0002-9610(85)80027-1.
Some investigators have reported that patients with gallstones empty their gallbladders more rapidly than do healthy subjects. This may contribute to the formation of lithogenic bile. To date, cholecystokinin is considered the prime mediator of gallbladder contraction. Evidence exists that cholecystokinin may not be the major hormone accounting for gallbladder emptying. The purpose of this study was to demonstrate the existence of this noncholecystokinin substance in healthy persons and to compare its concentration with that in patients with cholesterol gallstones. Fasting serum levels from 15 healthy human subjects (8 women and 7 men, mean age 32 +/- 8 years) and 10 patients with cholesterol gallstones (5 women and 5 men, mean age 48 +/- 16 years) were studied. Using rabbit in vitro gallbladder bioassay and cholecystokinin-8 as standards, serum bioactivity was measured and expressed as cholecystokinin-8 equivalent bioactivity. The effectiveness of serum to contract the gallbladder was tested before and after removal of cholecystokinin from the serum. Cholecystokinin was removed from the serum samples by affinity chromatography with Sepharose 4B beads coated with cholecystokinin 5135 antibody. Gallbladder contractility from this treated serum thus reflects the action of a noncholecystokinin stimulant. The cholecystokinin-8 bioactivity equivalents in untreated samples from healthy subjects and from patients with gallstones were 2.9 +/- 0.3 and 7.6 +/- 0.7 ng/ml, respectively. The fact that bioactivity of serum persisted after removal of cholecystokinin in both groups of subjects provides evidence that a noncholecystokinin stimulant of gallbladder contraction exists. This substance is found in significantly higher concentrations in the fasting serum of patients with gallstones compared with healthy subjects. This finding may explain, at least in part, the increased gallbladder emptying rate in patients with gallstones and may account for the reduced bile salt pool size and, thus, formation of lithogenic bile.
一些研究者报告称，胆结石患者胆囊排空比健康受试者更快。这可能促使致石性胆汁的形成。迄今为止，胆囊收缩素被认为是胆囊收缩的主要介质。有证据表明，胆囊收缩素可能并非导致胆囊排空的主要激素。本研究的目的是证实健康人存在这种非胆囊收缩素物质，并将其浓度与胆固醇结石患者的浓度进行比较。研究了15名健康受试者（8名女性和7名男性，平均年龄32±8岁）和10名胆固醇结石患者（5名女性和5名男性，平均年龄48±16岁）的空腹血清水平。以兔离体胆囊生物测定法并以胆囊收缩素-8作为标准品，测定血清生物活性并表示为胆囊收缩素-8等效生物活性。在从血清中去除胆囊收缩素之前和之后，测试血清使胆囊收缩的有效性。通过用包被有胆囊收缩素5135抗体的琼脂糖4B珠进行亲和层析，从血清样本中去除胆囊收缩素。经处理的血清的胆囊收缩力因此反映了非胆囊收缩素刺激物的作用。健康受试者和胆结石患者未经处理样本中的胆囊收缩素-8生物活性当量分别为2.9±0.3和7.6±0.7 ng/ml。两组受试者在去除胆囊收缩素后血清生物活性仍然存在，这一事实证明存在一种非胆囊收缩素的胆囊收缩刺激物。与健康受试者相比，在胆结石患者的空腹血清中发现这种物质的浓度明显更高。这一发现至少可以部分解释胆结石患者胆囊排空率增加的原因，并可能解释胆盐池大小减小以及因此导致致石性胆汁形成的原因。
