“刘”但是带教过我们生理实验，我以为他是在职研究生。
上实验的时候警告那个生理多导记录仪很贵，说坏一个，自己一个月的工资也赔不起。
后来，聊天的时候，我们同学问他知道山医有个破格提副高，又破格提正高的“宋刚”教授么？ 他说，“没听说啊！”大家晕倒！（后来基本证实了我的猜想，1992 – 1995， 山东医科大学生理学专业医学硕士）
不过现在他现在已经成为山医生理主力了，发了狂多Chin J Physiol，应该快是博导了。
刚才看了一下，竟然是医学院副院长了！
肃然起敬！
(刚刚看到马春红博士也是副院长了，再起敬一次！）
1: Am J Physiol Gastrointest Liver Physiol. 2007 Jan 4; [Epub ahead of print]
Vagal modulation of intestinal afferent sensitivity to systemic
lipopolysaccharide (LPS) in the rat.
Liu CY, Mueller MH, Grundy D, Kreis ME.
Department of Physiology, Medical School of Shandong University, Jinan,
Shandong, China.
Introduction: The CNS modulates inflammation in the gastrointestinal tract via
efferent vagal pathways. We hypothesized that these vagal efferents receive
synaptic input from vagal afferents, representing an autonomic feedback
mechanism. The consequence of this vago-vagal reflex for afferent signal
generation in response to LPS was examined in the present study. Methods:
Different modifications of the vagal innervation or sham procedures were
performed in anesthetized rats. Extracellular mesenteric afferent nerve
discharge and systemic blood pressure were recorded in vivo before and after
systemic administration of LPS (6 mgkg(-1) iv). Results: Mesenteric afferent
nerve discharge increased dramatically following LPS which was unchanged when
vagal efferent traffic was eliminated by acute vagotomy. In chronically
vagotomized animals to eliminate both vagal afferent and efferent traffic, the
increase in afferent firing 3.5 min after LPS was reduced to 3.2+/-2.5
impsec(-1) above baseline compared to 42.2+/-2.0 impsec(-1) in controls
(p<0.001). A similar effect was observed following perivagal capsaicin to
eliminate vagal afferent traffic only. LPS also caused a transient hypotension
(< 10 min), a partial recovery and then persistent hypertension which was
exacerbated by all 3 procedures. Mechanosensitivity was increased 15 minutes
following LPS but had recovered 30 min in all subgroups except for chronic
vagotomy. Conclusion: Discharge in capsaicin-sensitive mesenteric vagal
afferents is augmented following systemic LPS. This activity through a
vago-vagal pathway helps to attenuate the effects of septic shock. The
persistent hypersensitivity to mechanical stimulation after chronic vagal
denervation suggests that the vagus exerts a regulatory influence on spinal
afferent sensitization following LPS. Key words: autonomic innervation,
electrophysiology, mesenteric, vagus nerve, visceral hypersensitivity.
PMID: 17204546 [PubMed - as supplied by publisher]
2: Chin J Physiol. 2006 Aug 31;49(4):199-203.
Sexual differences of the inhibitory effect of ethanol on gastrointestinal
motility: in vivo and in vitro studies.
Liu KJ, Wang SL, Xie DP, Liu PY, Wang PS, Liu CY.
Department of Physiology, Medical School of Shandong University, Jinan 250012,
Shandong, P.R. China.
Female brain is more sensitive to the acute exposure of ethanol. This study
aimed to investigate the sexual difference of the ethanol-induced inhibition of
gastrointestinal motility. Wistar rats were fasted and allowed drinking water
only 12 - 18 h before the experiments. In the in vivo experiments, by using an
oral radiochromium motility marker, the liquid gastric emptying and intestinal
transit was measured 30 min after ethanol treatment. In the in vitro study,
strips of stomach and duodenum smooth muscle were suspended in organ baths
containing Krebs solution, and their isometric contractions were also examined.
Systemic administration of ethanol (2 g/kg, i.p.) significantly inhibited the
gastric emptying and intestinal transit, and the effect on female rats turned
out to be greater than that on the male rats (P < 0.05). In an in vitro study,
ethanol (0.38 x 10(-3) M - 1.34 x 10(-3) M) inhibited the motility of gastric
antrum and duodenum in rats of both sexes, but there was no sexual difference in
the inhibitory effect of ethanol on muscle strips. We concluded that sexual
difference of the ethanol-induced inhibition of gastrointestinal motility was
not resulted from the smooth muscle itself.
Publication Types:
Comparative Study
In Vitro
Research Support, Non-U.S. Gov't
PMID: 17058452 [PubMed - indexed for MEDLINE]
3: Acta Physiol (Oxf). 2006 Feb;186(2):141-9.
The inhibitory effects of oxytocin on distal colonic contractile activity in
rabbits are enhanced by ovarian steroids.
Xie D, Chen L, Liu C, Liu K.
Institute of Physiology, School of Medicine, Shandong University, Jinan,
Shandong, China.
xiedping@sdu.edu.cnAIMS: To study the effects of oxytocin on isolated rabbit distal colon and the
regulation of ovarian steroids by its action. METHODS: Muscle strips parallel to
either the circular or the longitudinal fibres were excised and suspended in
tissue chambers containing 5 mL Krebs solution (37 degrees C) and bubbled
continuously with 95% O(2) and 5% CO(2). The effects of oxytocin on isometric
spontaneous contractile responses were recorded. The effects of atosiban,
tetrodotoxin, Mg(2+), progesterone and oestradiol on the oxytocin-induced
response were also examined. RESULTS: Oxytocin (1, 10 and 100 nmol L(-1)) dose
dependently decreased the area under the contraction curve of distal colonic
smooth muscle strips. The oxytocin receptor antagonist atosiban blocked the
oxytocin (10 nmol L(-1))-caused responses in a dose-dependent manner.
Tetrodotoxin (10 micromol L(-1)) had no effect on the oxytocin-induced response.
Mg(2+)-free Krebs solution attenuated the oxytocin-induced response, but
oestradiol (0.1 micromol L(-1)) or progesterone (0.1 micromol L(-1)) increased
the oxytocin-induced response. CONCLUSION: These results suggest that oxytocin
inhibits the contractile motility of the distal colon, which is regulated by
Mg(2+) and ovarian steroids.
Publication Types:
Research Support, Non-U.S. Gov't
PMID: 16497191 [PubMed - indexed for MEDLINE]
4: Brain Res. 2005 Jan 25;1032(1-2):116-22.
Oxytocin microinjected into dorsal motor nucleus of the vagus excites
gallbladder motility via NMDA receptor-NO-cGMP pathway.
Liu CY, Xie DP, Liu KJ, Zhou YQ, Liu JZ.
Institute of Physiology Medical School of Shandong University Jinan 250012 P. R.
China.
liucy@sdu.edu.cnOur recent study indicated that, in the dorsal motor nucleus of the vagus (DMV),
the N-methyl-D-aspartic acid (NMDA) receptor-nitric oxide (NO)-cGMP pathway
participated in the regulation of gallbladder motility in rabbits. Oxytocin (OT)
is involved as a neurotransmitter in autonomic regulation. The aim of the
present experiments is to investigate the effect of OT microinjected into DMV on
the gallbladder motility and the involvement of NMDA receptor-NO-cGMP pathway. A
frog bladder connected with transducer was inserted into the gallbladder to
record the gallbladder pressure. Microinjection of OT (10-50 nmol/L, 100 nl)
dose dependently increased the strength of gallbladder phasic contraction. The
excitatory effect of OT (10 nmol/L, 100 nl) was completely abolished by atosiban
(10 mmol/L, 100 nl), the specific OT receptor antagonist, but was not influenced
by [deamino-Pen(1), O-Me-Tyr(2),Arg(8)]-vasopressin (10 mmol/L, 100 nl), the
V(1) receptor antagonist. Pretreatment of ketamine (10 mmol/L, 100 nl), the NMDA
receptor antagonist, suppressed the gallbladder motor response to OT; but
pretreatment of 6-Cyaon-7-Nitroquinoxaline-2,3-(1H,4H)-Dione (CNQX; 10 mmol/L,
100 nl), the non-NMDA receptor antagonist, did not affect it. Pretreatment of
L-NAME (10 mmol/L, 100 nl), the nitric oxide synthase (NOS) inhibitor, or methyl
blue (10 mmol/L, 100 nl), the guanylyl cyclase inhibitor, inhibited the
excitatory effect of OT on gallbladder motility. Hence, we deduced that the
microinjection of OT into the DMV enhanced the gallbladder motility through
binding specific OT receptors and activating the NMDA receptor-NO-cGMP pathway.
Publication Types:
Comparative Study
Research Support, Non-U.S. Gov't
PMID: 15680949 [PubMed - indexed for MEDLINE]
5: Chin J Physiol. 2004 Jun 30;47(2):89-94.
Arecoline excites the colonic smooth muscle motility via M3 receptor in rabbits.
Xie DP, Chen LB, Liu CY, Zhang CL, Liu KJ, Wang PS.
Institute of Physiology, School of Medicine, Shandong University, Jinan 250012,
P R China.
xiedping@sdu.edu.cnArecoline is an effective component of areca (betel nuts, a Chinese medicine
named pinang or binglang). The purpose of this study was to investigate the
effect of arecoline on the motility of distal colon in rabbits and its
mechanisms involved. Strips of colonic smooth muscle were suspended in organ
baths containing Krebs solution, and their isometric contractions were examined.
The response of smooth muscle to arecoline in colonic strips was recorded. The
effects of atropine, gallamine and
1,1-dimethyl-4-diphenylacetoxypiperidiniumiodide (4-DAMP) on arecoline-induced
contraction were also observed. Arecoline (1 nM - 1 microM) produced a
concentration-dependent contraction in both the longitudinal and the circular
smooth muscle of rabbit colon. Atropine (10 microM) abolished the arecoline (80
nM)--induced contraction. M3 receptor antagonist, 4 - DAMP (0.4 microM),
abolished the arecoline (80 nM)--related response, whereas M2 receptor
antagonist, gallamine (0.4 microM), did not affect the effect of arecoline.
These results suggest that arecoline excites the colonic motility via M3
receptor in rabbits.
Publication Types:
In Vitro
Research Support, Non-U.S. Gov't
PMID: 15481791 [PubMed - indexed for MEDLINE]
6: Chin J Physiol. 2004 Mar 31;47(1):1-6.
Participation of caudal ventrolateral medulla in the regulation of gallbladder
motility in rabbits.
Liu FY, Liu CY, Liu JZ, Xie DP.
Department of Physiology, School of Medicine, Shanldong University, Jinan
250012, Shandong Province, PR China.
To investigate whether the caudal ventrolateral medulla (CVLM) participates in
the regulation of gallbladder motility, we studied the effects of microinjection
of L-glutamate and other agents into the CVLM on gallbladder pressure (GP) in
anesthetized rabbits. A frog bladder connected with a force transducer was
inserted into the gallbladder to record the change of GP. Microinjection of
L-glutamate into the CVLM decreased GP, While micnoinjection of
gamma-amino-butyric acid (GABA) increased GP. Microinjection of ketamine, a
noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist, into CVLM
increased GP, while microinjection of
6-cyano-7-nitroquinoxaline-2,3-(1H,4H)-dione (CNQX), a competitive
(+/-)-a-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)/kainate
receptor antagonist, had no significant effect on GP. The effects of L-glutamate
was abolished by ketamine, but not by CNQX. Intravenous injection of
phentolamine or transection of the spinal cord eliminated the effects of
L-glutamate on GP. These results indicate that [1] CVLM participated in the
regulation of gallbladder motility; [2] endogenous L-glutamate in CVLM is
involved in the regulation mediated by NMDA receptors, the output of which is
sent through sympathetic nerve and alpha-adrenergic receptors.
Publication Types:
Research Support, Non-U.S. Gov't
PMID: 15239588 [PubMed - indexed for MEDLINE]
7: Neurogastroenterol Motil. 2004 Jun;16(3):347-53.
Microinjection of glutamate into dorsal motor nucleus of the vagus excites
gallbladder motility through NMDA receptor - nitric oxide - cGMP pathway.
Liu CY, Xie DP, Liu JZ.
Department of Physiology, Medical School of Shandong University, Jinan, China.
liucy@sdu.edu.cnWe have reported that both glutamate and nitric oxide (NO) participated in the
regulation of gallbladder motility in dorsal motor nucleus of the vagus (DMV).
The aim of this study is to investigate the type of receptor in DMV that
mediates the excitatory effect of glutamate on gallbladder motility and the
correlation between the glutamate and NO. A frog bladder connected with a force
transducer was inserted into the gallbladder to record the change of gallbladder
pressure. Glutamate (65 mmol L(-1), 100 nL) microinjected into DMV significantly
increased the strength of gallbladder phasic contraction. This effect was
abolished by ketamine (180 mmol L(-1), 100 nL), the specific N-methyl-d-aspartic
acid (NMDA) receptor antagonist, but was not influenced by
6-cyaon-7-nitroquinoxaline-2,3-(1H,4H)-dione (CNQX) (180 mmol L(-1), 100 nL),
the non-NMDA ionotropic receptor antagonist. N(G)-nitro-l-arginine-emthyl
(l-NAME) (1 mol L(-1), 100 nL), the nitric oxide synthase (NOS) inhibitor,
reversed the excitatory effect of glutamate on gallbladder motility.
Microinjection of sodium nitroprusside (SNP), the NO donor, into DMV enhanced
the gallbladder motility, and this effect was not modulated by ketamine.
Microinjection of NMDA (5 mmol L(-1), 100 nL) increased the strength of
gallbladder phasic contraction, and this effect was attenuated by methylene blue
(100 mmol L(-1), 100 nL), the soluble guanylate cyclase inhibitor. These results
suggest that glutamate regulate the gallbladder motility through the NMDA
receptor - NO - cGMP pathway in DMV.
Publication Types:
Research Support, Non-U.S. Gov't
PMID: 15198657 [PubMed - indexed for MEDLINE]
8: Chin J Physiol. 2003 Sep 30;46(3):95-101.
Erratum in:
Chin J Physiol. 2003 Dec 31;46(4):194.
Endogenous oxytocin excites phasic contraction of gallbladder in rabbits through
oxytocin receptor.
Liu CY, Liu JZ, Xie DP, Liu PY, Wang PS.
Institute of Physiology, Medical School of Shandong University, Jinan, Shandong,
PR China.
liucy@sdu.edu.cnThese experiments were performed to study the effect of oxytocin (OT) and it's
specific receptor on gallbladder motility in rabbits. The fasted New Zealand
white rabbits (2.0-2.5 kg) were anaesthetized by urethane (1 g/kg). The
gallbladder pressure was recorded continuously to monitor the gallbladder
motility. Systemic OT (0.01, 0.02, 0.04 mg/kg, iv) did not affect the
gallbladder pressure, but dose-dependently increased the frequency of phasic
contraction. Five min after OT administration (0.04 mg/kg, iv), the strength of
phasic contraction increased to 0.23 +/- 0.08 mmHg/min (P < 0.01, n = 6). The
gallbladder motility returned to normal 15 min later after OT treatment.
Intravenous injection of atosiban (0.04 mg/kg, iv), an OT receptor antagonist,
decreased the strength of gallbladder phasic contraction but did not affect
gallbladder pressure. Pretreatment of atosiban (0.04 mg/kg, iv) completely
abolished the systemic OT effect on gallbladder. Vasopressin (VP) (0.1 - 0.5
IU/kg, iv) dose-dependently decrease the gallbladder pressure but did not affect
the phasic contraction. MK-329 (0.4 mg/kg, iv), the CCK-A receptor antagonist,
L-365, 260 (0.4 mg/kg, iv), the CCK-B receptor antagonist and atropine (0.2
mg/kg, iv), the M receptor antagonist, did not affect the OT effect on
gallbladder motility. We suggest that endogenous OT regulates gallbladder phasic
contraction through specific OT receptor. This effect is independent of the
peripheral CCK and M receptors.
Publication Types:
Research Support, Non-U.S. Gov't
PMID: 14672277 [PubMed - indexed for MEDLINE]
9: Chin J Physiol. 2002 Sep 30;45(3):101-7.
Nucleus raphe obscurus participates in regulation of gallbladder motility
through vagus and sympathetic nerves in rabbits.
Xie YF, Liu CY, Liu JZ.
Institute of Physiology, Medical School of Shandong University, Jinan, Shandong
250012, People's Republic of China.
The aim of the present study is to investigate if the nucleus raphe obscurus
(NRO) participate in regulating the gallbladder motility in rabbits. Rabbits
were fasted for about 20-24 hours. After anesthetization with urethane, an
incision was made at the middle of the abdomen and the gallbladder was exposed.
A frog bladder connected with force transducer was inserted into the gallbladder
through a small incision at the funds to record gallbladder motility (tonic
contraction and phasic contraction). Glutamate and other chemicals were
microinjected into NRO through a vitreous tube attached to a microsyringe. We
found both the tonic contraction and phasic contraction of the gallbladder were
enhanced after the glutamate was injected into NRO. GABA inhibited gallbladder
motility if administrated in the same way. Microinjection of ketamine, NMDA
(N-methyl-D-aspartate) receptor antagonist, into NRO inhibited the phasic
contraction of gallbladder. Administration of CNQX
(6-cyano-7-nitroquinoxaline-2, 3-dione), a non-NMDA receptor antagonist,
enhanced the gallbladder tonic contraction. Pretreatment of ketamine into NRO
attenuated the effect of glutamate, while pretreatment of CNQX had no effect on
it. Intravenous injection of atropine or vagotomy completely abolished the
effect of glutamate on gallbladder phasic contraction, while intravenous
injection of phentolamine or transecting the spinal cord at T3-4 inhibited that
on tonic contraction. Intravenous injection of propranolol did not influence the
glutamate effect. These results suggested that glutamate in NRO participates in
regulating the motility of the gallbladder through NMDA receptor. When excited,
the NMDA receptors in NRO enhance the phasic contraction of the gallbladder
through vagus nerve and peripheral M-receptors, and enhance the tonic
contraction of the gallbladder through sympathetic nerve and peripheral
alpha-receptors. GABA in NRO is also involved in the regulation of gallbladder
motility.
Publication Types:
Research Support, Non-U.S. Gov't
PMID: 12817712 [PubMed - indexed for MEDLINE]
10: World J Gastroenterol. 2003 Jan;9(1):165-8.
Effect of oxytocin on contraction of rabbit proximal colon in vitro.
Xie DP, Chen LB, Liu CY, Liu JZ, Liu KJ.
Department of Physiology, School of Medicine, Shandong University, Jinan 250012,
Shandong Province, China.
AIM: To investigate the effects of oxytocin (OT) on isolated rabbit proximal
colon and its mechanism. METHODS: Both longitudinal muscle (LM) and circular
muscle (CM) were suspended in a tissue chamber containing 5 mL Krebs solution
(37 degrees ), bubbled continuously with 950 mL x L(-1) O(2) and 50 mL x L(-1)
CO(2). Isometric spontaneous contractile responses to oxytocin or other drugs
were recorded in circular and longitudinal muscle strips. RESULTS: OT (0.1 U x
L(-1)) failed to elicit significant effects on the contractile activity of
proximal colonic smooth muscle strips (P>0.05). OT (1 to 10 U x L(-1)) decreased
the mean contractile amplitude and the contractile frequency of CM and LM.
Hexamethonium (10 micromol x L(-1)) partly blocked the inhibition of oxytocin (1
U x L(-1)) on the contractile frenquency of CM.
N(omega))-nitro-L-arginine-methylester (L-NAME, 1 micromol x L (-1)),
progesterone (32 micromol x L(-1)) and estrogen (2.6 micromol x L(-1)) had no
effects on OT-induced responses. CONCLUSION: OT inhibits the motility of
proximal colon in rabbits. The action is partly relevant with N receptor, but
irrelevant with that of NO, progesterone or estrogen.
Publication Types:
In Vitro
Research Support, Non-U.S. Gov't
PMID: 12508375 [PubMed - indexed for MEDLINE]
11: Chin J Physiol. 2002 Mar 31;45(1):19-24.
Anatomical and functional study of localization of originating neurons of the
parasympathetic nerve to gallbladder in rabbit brain stem.
Li AJ, Liu JZ, Liu CY.
Department of Physiology, School of Medicine, Shandong University, Jinan, PR
China.
The present study was to investigate the localization of preganglionic
parasympathetic neurons of gallbladder in brain stem by anatomical and
functional approaches. Male or female rabbits (n = 11) were anesthetized with
sodium pentobarbital (30 mg/kg, i.v.). Cholera toxin B conjugated to horseradish
peroxidase (CB-HRP) was injected into the gallbladder wall. Four days later,
animals were re-anesthetized and perfused transcardially with paraformaldehyde
solution in a 0.1 M phosphate buffer. The rabbit brain was then frozenly
sectioned. The sections were processed for HRP label and stained with neutral
red. Another group of rabbits (n = 54) were anesthetized by urethane (1 g/kg)
after fasting for 18-24 hours, Gallbladder pressure (GP) was measured by
inserting a frog bladder filled with normal saline into the gallbladder.
Myoelectrical activity of the sphincter of Oddi (SO) was induced by a pair of
copper electrodes. A glass tube (30 microm tip diameter) connected with a
microsyringe was directed to the dorsal vagal complex (DVC) for microinjection.
Majority of retrogradely labeled cells was found bilaterally in dorsal motor
nucleus of the vagus nerve (DMV) throughout the length, except the rostral and
caudal part. These cells were distributed in subnuclei parvicellularis or
mediocellularis of DMV. Some labeled perikarya located in the medial subnucleus
of the solitary tract (mNTS). Thyrotropin-releasing hormone (TRH, 1.3 mmol/L,
0.2 microl) microinjected into the rostral portion of the DVC (including DMV and
NTS) enhanced the motility of gallbladder and SO. Microinjection of TRH at the
middle part of DVC seldom induces excitatory effects on the gallbladder or SO.
TRH microinjected into the caudal portion of the DVC elicited weaker response of
gallbladder and SO than rostral portion. Our results indicated that DMV is one
of the most important original nuclei of gallbladder's vagus nerves and mNTS may
be also involved in the control of gallbladder's parasympathetic activity.
Neurons that innervate the gallbladder distribute at most part of DVC, and are
relatively dense at rostral and caudal position of DMV.
Publication Types:
Research Support, Non-U.S. Gov't
PMID: 12005348 [PubMed - indexed for MEDLINE]
12: World J Gastroenterol. 2002 Apr;8(2):338-41.
Effects of progesterone on gastric emptying and intestinal transit in male rats.
Liu CY, Chen LB, Liu PY, Xie DP, Wang PS.
Department of Physiology, School of Medicine, Shandong University, Jinan 250012,
Shandong Province, China.
liucy@sdu.edu.cnAIM: To study the dose-dependent of progesterone (P) effect and the interaction
between the oxytocin (OT) and P on gastrointestinal motility. METHODS: In order
to monitor the gastric emptying and intestinal transit, the SD male rats were
intubated via a catheter with normal saline (3 ml/kg) containing Na(2)(51)CrO(4)
(0.5 microCi/ml) and 10% charcoal. OT was dissolved into normal saline and P was
dissolved into 75% alcohol. RESULTS: Low does of P (1 mg/kg, i.p.) enhanced the
gastric emptying (75+/-3%, P<0.05) and high dose of P (5 mg/kg, i.p.) inhibit it
(42+/-11.2%, P<0.01). P (1 mg/kg) increased the intestinal transit (4.2+/-0.3,
P<0.05) while the higher dose (10-20 mg/kg) had no effect. OT (0.8 mg/kg, i.p.)
inhibited the gastric emptying (23.5+/-9.8%, P<0.01). The inhibitory effects of
P(20 mg/kg) (32+/-9.7%, P<0.05) and OT (0.8 mg/kg) on gastric emptying enhanced
each other when the two chemicals were administrated simultaneously (17+/-9.4%,
P<0.01). CONCLUSION: Low dose of P increased GI motility while high dose of P
decreased it. During the later period of pregnancy, elevated plasma level of OT
may also participate in the gastrointestinal inhibition.
Publication Types:
Research Support, Non-U.S. Gov't
PMID: 11925620 [PubMed - indexed for MEDLINE]
13: World J Gastroenterol. 1998 Jun;4(3):238-241.
Effects of octreotide on gallbladder pressure and myoelectric activity of Oddi
sphincter in rabbits.
Zhou JH, Liu CY, Zhang RH, Wang HR, Liu KJ.
Department of Physiology, Shandong Medical University, Jinan 250012, Shandong
Province,China.
AIM:To observe the effect of octreotide (OT) and somatostatin (SS) on
gallbladder pressure and myoelectric activity of SO in rabbits.METHODS:Male
rabbits fasted for 15h-18h and anesthetized with urethane. The mean gallbladder
pressure (GP) and myoelectric activity of SO were simutaneously measured with a
frog bladder connected to a transducer and a pair of copper
electrodes.RESULTS:After injection of OT (10&mgr;g/kg, iv), the GP decreased in
2min and reached the lowest value in about 60min (P < 0.01, n = 19), and
completely or partially returned to the normal level in 120min. The frequency of
myoelectric activty of SO was reduced, even disappeared in 2min (P < 0.01, n =
19) and returned to normal in about 20min. Injection of SS (10&mgr;g/kg, iv)
also decreased GP and myoelectric activity of SO (P < 0.01, n = 7); Before and
after injection of OT or SS, injection of CCK-8 (100ng or 200ng) caused similar
increase in myoelectric activity of SO and GP (P >0.05). Before and after
injection of OT, there were no significant differences in increases of
myoelectric activity of SO and GP caused by electric stimulation of dorsal motor
nucleus of vagus (P >0.05).CONCLUSION:OT and SS decreased GP and myoelectric
activity of SO, demonstrating that effects of OT were similar to those of SS.
Intravenous injection of OT did not affect the increase of myoelectric activity
of SO and GP caused by CCK-8 or electric stimulation of dorsal motor nucleus of
vagus.
PMID: 11819285 [PubMed - as supplied by publisher]
14: World J Gastroenterol. 1998 Apr;4(2):162-164.
TRH microinjection into DVC enhances motility of rabbits gallbladder via vagus
nerve.
Liu CY, Liu JZ, Zhou JH, Wang HR, Li ZY, Li AJ, Liu KJ.
Department of Physiology, Shandong Medical University,Jinan 250012, Shandong
Province, China.
AIM:To investigate the effects of TRH in DVC on motility of the gallbladder in
rabbits.METHODS:fter fasted for 15h-18h, rabbits were anesthetized with urethane
(1.0g/kg).Gallbladder pressure (GP) was measured by a frog bladder perfused with
normal saline.RESULTS:After microinjection of TRH (8.8nmol,1&mgr;l) into DVC,GP
was raised and the frequency of phasic contraction of gallbladder (FPCGB)
increased. All the doses of TRH (0.13, 0.25, 0.50, 0.80, 1.30nmol, 1&mgr;l)
injected into DVC could excite the motility of gallblader. As the dose of TRH
was enlarged, the amplitude and duration of the reaction increased. Effects of
TRH in DVC on motility of the gallbladder could be completely abolished by
atropine (0.2mg/g, i.v.) or vagotomy, but could not be inhibited by phentolamine
iv (1.5mg/g) or propranolol iv (1.5mg/g)or by transecting the spinal
cord.CONCLUSION: Thyrotropin-releasing hormone in DVC can excite motility of
gallbladder. This effect was mediated by vagus nerves and peripheral M receptor.
Its physiological significance may be related to maintaining the phasic
contraction of gallbladder in interdigestive period.
PMID: 11819264 [PubMed - as supplied by publisher]
15: Auton Neurosci. 2001 Feb 20;87(1):46-51.
Effects of nitric oxide in the dorsal motor nucleus of the vagus on the
extrahepatic biliary system in rabbits.
Wang J, Liu J, Liu C.
Department of Physiology, Shandong Medical University, Jinan 250012, Shandong
Province, PR China.
To investigate whether nitric oxide (NO) in the dorsal motor nucleus of the
vagus (DMV) mediated an influence on the extrahepatic biliary system, we studied
the effects of microinjection of NO-producing drugs into DMV on the motilities
of the gallbladder (GB) and the sphincter of Oddi (SO) in anesthetized rabbits.
Microinjection of the NO precursor L-arginine into the rostral DMV produced an
increase in the GB and SO motilities, which can be counteracted by both
NG-nitro-L-arginine-methyl (L-NAME), an inhibitor of NOS, and reduced hemoglobin
(rHb), a scavenger of NO, and were eliminated by bilateral cervical vagotomy. On
the other hand, the NO donor sodium nitroprusside (SNP) was able to mimic the
excitatory effect of L-arginine. This effect can be antagonized by rHb, but not
by L-NAME, for SNP supplied exogenous NO without activating NOS. These results
indicate that NO in the DMV mediates an excitatory effect on the extrahepatic
biliary system.
Publication Types:
Research Support, Non-U.S. Gov't
PMID: 11270140 [PubMed - indexed for MEDLINE]
16: Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2000 Nov;16(4):347-9.
[The vagus nerve coordinates the motion of gallbladder and sphincter of Oddi in
the interdigestive period in rabbits]
[Article in Chinese]
Liu CY, Liu JZ, Li ZY, Liu KJ.
Department of Physiology, Shandong Medical University, Jinan 250012.
AIM: To investigate the effect of vagus nerve on coordinating the motion of
gallbladder (GB) and sphincter of Oddi (SO) in the interdigestive period in
rabbits. METHODS: Fasted for 15 h-18 h, but allowed to drink water, the rabbib
were anesthetized with urethane (1.0 mg/kg, i.v.). In order to measure GB
pressure, a frog bladder filled with normal saline was put into GB and connected
to a transducer (TP-200T). Myoelectric signals of SO was recorded by a pair of
copper electrodes. RESULTS: In the interdigestive period, phasic contractions of
GB (PCGB) and clusters of spike potentials of SO (CSPSO) was 1:1 correlated (Y =
0.962X + 0.587, r = 0.982, P < 0.01). That is, every PCGB was accompanied by one
CSPSO. Microinjection of thyrotropin-releasing hormone (TRH, 0.8 nmol, 1
microliter) or monosodium glutamate (MSG, 2 mumol, 1 microliter) into dorsal
vagal complex (DVC) enhanced the motility of GB and SO, and the 1:1 temporal
relation between PCGB and CSPSO still existed. Vagotomy or intravenous injection
of atropine inhibited the PCGB and the spike potentials of SO, and the 1:1
correlation between PCGB and CSPSO disappeared. The spike bursts of SO did not
respond to the artificial rise of gallbladder pressure. CONCLUSION: In the
interdigestive period in rabbits, gallbladder and SO contract and relax
rhythmically and simultaneously. This eoordinated motion between GB and SO is
controlled by DVC via vagus nerve and peripheral M receptors.
Publication Types:
English Abstract
Research Support, Non-U.S. Gov't
PMID: 11236698 [PubMed - indexed for MEDLINE]
