Combined Traditional And Modern Medicine
Copyright ©The Author(s) 1999. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Feb 15, 1999; 5(1): 61-63
Published online Feb 15, 1999. doi: 10.3748/wjg.v5.i1.61
Plasma L-ENK, AVP, ANP and serum gastrin in patients with syndrome of Liver-Qi-stagnation
Ze-Qi Chen, Guo-Lin Chen, Xue-Wen Li, Yu-Qiu Zhao, Lin-Jie Shi
Ze-Qi Chen, Guo-Lin Chen, Xue-Wen Li, Yu-Qiu Zhao, Lin-Jie Shi, Department of TCM, Affiliated Xiangya Hospital, Hunan Medical Uni-versity, Changsha 410008, Hunan Province, China
Ze-Qi Chen, male, born on 1951-10-04, in Ningxiang County, Hunan Province, graduated from Hunan Medical University in 1973, now associate professor, Deputy Chief Physician of Department of In-tegrated Chinese and Western Medicine, majoring in liver disease study in TCM (Traditional Chinese Medicine), having 30 papers published.
Author contributions: All authors contributed equally to the work.
Supported by the National Natural Science Foundation of China, No.39330240
Correspondence to: Dr. Ze-Qi Chen, Department of TCM, Affiliated Xiangya Hospital, Hunan Medical University, 141 Xiangya Road, Changsha 410008 , Hunan Province, China
Received: July 6, 1998
Revised: November 22, 1998
Accepted: December 13, 1998
Published online: February 15, 1999


AIM To investigate the pathophysiologic basis of syndrome of Liver-Qi stagnation and parame-ters for clinical differentiation.

METHODS Plasma L-ENK, AVP, ANP and serum gastrin were determined by RIA in 84 patients with neurasthenia, mastodynia, chronic gastri-tis, and chronic cholecystitis presenting the same syndrome of Liver-Qi stagnation in tr adi-tional Chinese medicine (TCM). Healthy subjects served as controls in comparison with patients having the same syndrome but with different diseases.

RESULTS Among the patients with Liver-Qi stagnation, the plasma L-ENK, ANP and gastrin levels were 38.83 ng/L ± 6.32 ng/L, 104.11 ng/L ± 29.01 ng/L and 32.20 ng/L ± 6.68 ng/L, being significantly lower than those in the healthy controls (P < 0.01, t = 3.34, 6.17, 4.48). The plasma AVP of the patient group (52.82 ng/L ± 19.09 ng/L) was significantly higher than that of the healthy contr ols (P < 0.01, t = 5.79). The above changes in patients having the same symptom complex but different diseases entities showed no significant differences, P > 0.05.

CONCLUSION The syndrome of Liver-Qi stagnation is closely related to the emotional modulatory abnormality of the brain, with decrease of plasma L-ENK, ANP and gastrin, and increase of plasma AVP as the important pathophysiologic basis.

Key Words: Syndrome of Liver-Qi stagna-tion, leucine enkephalin/ blood, arginine vaso-pressin/ blood, atrial natural polypeptide/ blood, gastrin/blood


Liver-Qi stagnation syndrome is common in liver disease. The predominant clinical manifestations were characterized by emotional alterations and digestive disturbances. In order to explore the patho-physiological basis and indexes of differentiation, we investigated the alterations of neurohumoral parameters in association with modulating emotional and digestive function.


Fifty-four patients with Liver-Qi stagnation syn-drome selected from Xiangya Hospital and several general hospitals of Hunan Province from May 1995 to October 1996 were examined for plasma L-ENK, AVP and ANP. Seven were males and 47 females. Age ranged from 14-60 years, averaging 39 ± 11.2 years. The diagnoses were mastod ynia (19), neuras-thenia (17), chronic gastritis (10), and chronic cholecystitis (8). Another 30 patients selected from Xiangya Hospital through March 1997 to October 1997 were added, they were all females, aged 20-53 years, averaging 34.7 ± 12.7 years. Mastodynia was diagnosed in eleven cases, neurasthenia in nine cases, chronic gastritis in seven, and chronic chole-cystitis in three.

The healthy controls were selected from the blood donors and employees in our hospital, all of them were negative in physical examination, blood routine, liver function test and chest fluoroscopy to rule out organic disease of heart, liver, lung, kid-ney, and nervous system diseases. L-ENK, ANP and AVP were detected in 30 cases, whereas serum gastrin was examined in 33 cases.

Differentiation and diagnosis by TCM

Based on previous criteria derived by our depart-ment[1], they were modified according to the clini-cal epidemiological survey as: hypochondrial, breast and lower abdominal pain; depression; restless and easily irritated; obstruction sensation at the phar-ynx; dysmenorrhea, amenorrhea, or irregular men-strual cycle; and the tense pulse. The patients presented with 3 or more of the above six items were considered to have Liver-Qi stagnation syndrome. (The disease entities selected including mastodynia, neurathenia, chronic gastritis, chronic cholecystitis were diagnosed according to the textbook listed criteria and diagnosed by the departments of breast disease, neurology, general surgery, and digestive medicine).

Laboratory methods

All the 4 parameters were determined by radioim-munoassay. The apparatus used was FJ-2008 P-type gamma immunocounter. Venous blood samples were collected during fasting in the morning and deter-mined subsequently. Radioimmunoassay kits for L-ENK and AVP were provided by the Department of Neurobiology of the 2nd Military Medical University, and the ANP and gastrin immunoassay kits were provided by Northern Institute of Immunoreagents, Beijing. The standard curve for L-ENK was r = 0.998, CV = 3.07%, RER 0.039; for ANP, r = 0.998, CV = 7.15%, RER = 0.035; for AVP, r = 0.998, CV = 3.15%, RER 0.039; and for gastrin, r = 1.000, CV = 3.18%, RER 0.038; all fitted the quality control criteria.

Statistical analysis

All data were expressed as -x±s. Student’s t test and F tes t were used for comparison between groups 2 and 3.


Table 1 lists the results of measurement of plasma L-ENK, AVP, ANP and serum gastrin of the Liver-Qi stagnant patients group (LQSP) and of the normal controls and Table 2 shows the results of mesure-ments in patients with different disease entities.

Table 1 The plasma L-ENK, AVP, ANP and serum gastrin levels in Liver Qi stagnation patients.
LQSP38.83 ± 6.32(40)b52.82 ± 19.09(30)b104.11 ± 29.01(32)b32.20 ± 6.68(30)b
Control45.19 ± 9.58(30)29.88 ± 10.35(30)149.50 ± 28.89(30)47.02 ± 15.64(30)
Table 2 The plasma and serum neurohumeral parameters of patients with Liver Qi stagnantion syndrome of different disease entities.
Neurathenia40.72 ± 17.18(14)42.95 ± 1078(8)110.24 ± 39.40(10)31.03 ± 7.79(9)
Mastodynia36.40 ± 21.12(10)61.31 ± 23.57(13)104.73 ± 34.43(13)33.49 ± 7.08(11)
Gas-Chole*40.87 ± 26.02(16)49.32 ± 12.85(9)99.83 ± 20.15(9)31.24 ± 4.52(10)
F value0.
P> 0.05> 0.05> 0.05> 0.05

In TCM, the function of liver is mainly dredging and storing of blood. The dredging function of the liver is extremely important in regulating the flow of Qi and blood in the body, the psychoemotion, di-gestion and absorption, water and fluid metabolism, menstruation and reproductive function. Psycho-e-motional disturbance is the main cause of Liver-Qi stagnation, and in turn, psychoemotional change is the clinical feature of Liver-Qi stagnation, such as easily irritated and arousal of angry, depression and sighing, insomnia with nightmares, even suspicious and indifferent and grieving. RIA of the psychoe-motional and digestive function related neurohu-moral parameters in this series showed that among the Liver-Qi stagnantion patients, plasma L-ENK, ANP and serum gastrin were significantly decreased and the plasma AVP increased as compared with those of the normal controls. However, between the different disease entities of various organ sys-tems in modern Western medicine observed no sig-nificant difference. It strongly indicates that these alterations are the pathophysiological basis of Liver-Qi stagnation in common. These parameters are the indexes of syndrome, rather than the indexes of the disease entity. This study preliminarily explored the relationship between Liver-Qi stagnation syndrome and the modulatory neurohumeral factors associated with psychoemotional changes.

L-ENK is an active neuropeptide, its secretory neurons are distributed in thes triatal body thala-mus, periaqua duct gray matter, and dorsal glial re-gion of spinal cord, and are the modulators of emo-tional activity within the central nervo us system[2]. Gastrin is a gastrointestinal hormone secreted by G cells distributed in pylorus and upper duodenum. Recent study reveals that some of the gastrointesti-nal peptide is also situated in CNS, the dual distribu-tion of these peptides were called as brain enteric peptide[3]. Immunohistochemical studies demonstrated that gastrin and leucine enkephalin are also presented in the brain, stomach, intestine and pancreas[4]. Enkephalin is extensively distributed in the central nervous system and the digestive tract, and its secretory cells coincided with gastrin secretory cells[5]. In this study, both plasma L-ENK and serum gastrin were sigificantly decreased in the patients with Liver-Qi stagnant syndrome, which might play an important role in the pathogenesis of psychoemotional modulation disorder and result in unstable emotional activity. Since the brain-enteric peptide secretion and release are closely related with the functional status of CNS and the vegetable ner-vous system, decreased brain-enteric peptide during Liver-Qi stagnation would certainly affect the gastric acid secretion, the intestinal, pancreatic juice, bile secretion and motility of the digestive tract, ultimately leading to digestive disturbance.

Vasopression, the antidiuretic hormone (ADH), is synthesized by the neurons of supraoptic nucleus of hypothalamus. Release of ADH is normally modulated by plasma osmotic pressure, blood volume and blood pressure; but pain, vomiting and emotional tension may promote ADH release, and antagonize the diuresis[4].

Atrial natriuretic polypeptide is mainly distributed in the brain, which is high in the hypotha-lamus and the diaphragmatic sellae region. Its secretion is influenced by physical, humoral and neural factors. Its functions include natiuresis, vasodila-tion, and decrease of blood pressiure[6]. It was re-ported that ANP significantly inhibited the release of AVP via hypothalamus neuropituitary axis, the antagonistic effect of ANP and renin-angiotensin not only existed peripherally, but also in the CNS, particularly in regulating the blood volume, elec-trolyte balance and maintenance of blood pres-sure[7]. Decrease of plasma ANP and elevation of AVP might be one of the pathophysiologic basis of the CNS regulatory dysfunction resulting in in-creased vascular tension, sodium and water reten-tion, and hypertension in Liver-Qi stagnation syn-drome. But the cause-effect relationship, the pre-cise mechanism of the elevated AVP and decreased ANP, as well as the validity of the four neuro-humeral parameters in this study as reference index-es in differentiation of the Liver-Qi stagnant syn-drome await further clarification.


Edited by Jing-Yun Ma

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