In order to explore the mechanism of hemodynamic changes caused by high binary tract pressure, we established an animal model of high binary tract pressure, in which the disturbance of hemodynamics developed. The cerv...In order to explore the mechanism of hemodynamic changes caused by high binary tract pressure, we established an animal model of high binary tract pressure, in which the disturbance of hemodynamics developed. The cervical or abdominal vague nerve was then blocked. It was observed that when the binary tract pressure was increased to 16 kpa and kept for 1h, the arterial blood pressure and cardiac output decreased immediately and parallelly (P<0. 05). When the cervical or abdominal vague nerve were blocked or the pressure of the binary tract was decreased to zero, both indices returned to normal immediately (P>0. 05). The change of cardiac output lags a little behind that of arterial blood pressure. It suggests that the signal of binary tract pressure increase can be sent to the cardiovascular center through vague nerve, and the balance between sympathic and parasympathic nerve was broken, which led to the weakening of cardiac contraction and decrease of cardiac output. Due to the peripheral effects of vague nerve, hemodynamic resistance of vessels decreased, which brought about redistribution of peripheral blood flow. Both were the causes of hemodynamic disturbances. After the blood pressure decreased markedly, it showed a jump to normal state when cervical vague nerve was blocked. And the amplitude of diastolic blood pressure restored more than that of systolic blood pressure. This suggests that the cardiac output and peripheral blood resistance are important factors that cause the decrease of blood pressure.展开更多
In order to explore the effect of binary tract pressure on Oddi's sphincter and the mechanism of development of high pressure of binary tract during acute obstructive and suppurative cholangitis (AOSC), house rab...In order to explore the effect of binary tract pressure on Oddi's sphincter and the mechanism of development of high pressure of binary tract during acute obstructive and suppurative cholangitis (AOSC), house rabbits were used to establish model of high binary pressure in acute binary duct caecus. It was observed that when the pressure of the acute binary tract was increased to 8 kpa,the electric activity of Oddi's sphincter was obviously enhanced, the pressure of Oddices sphincter increased remarkably (P <0. 05), and even constant spasm appeared with accompanying increase of discharge frequency of the right greater splanchnic nerves (P <0. 05) and progressive decrease of mean arterial pressure.However, when lidocaine of 0. 6 % was used to block the right celiac plexus, no above-mentioned reaction happened when the binary tract pressure was increased again. The results indicated that the acute binary tract obstruction might induce the contraction or spasm of Oddi's sphincter and bring about a vicious cycle. Its mechanism is related to splanchnic nerves reflection and it is one of important factors in the development of AOSC course.展开更多
BACKGROUND: Biliary cancers are more common in females, and previous studies have suggested that Helicobacter pylori (H. pylori) exists in the biliary system. However, the effects of H. pylori infection and estrogen o...BACKGROUND: Biliary cancers are more common in females, and previous studies have suggested that Helicobacter pylori (H. pylori) exists in the biliary system. However, the effects of H. pylori infection and estrogen on the biological behaviors of human biliary epithelium mucosa remain unknown. The present study aimed to clarify their effects on the proliferation, apoptosis, migration and oxidative DNA damage of a human intrahepatic biliary epithelial cell (HIBEC) line in vitro. METHODS: HIBECs were co -cultured with 17 beta-estradiol (at 10(-9) mol/L, 10(-7) mol/L, and 10(-5) mol/L) and H. pylori (at MOI=0.5:1, 1:1, and 2:1) and continuously passaged until the 15th generation (approximately 45 days). Then, the following assays were performed. HIBEC proliferation was measured using the CCK-8 assay, plate clone-formation assay and by determining Ki-67 expression with immunocytochemistry; cell apoptosis and migration were investigated using Annexin-V/PI and transwell assays, respectively; and reactive oxygen species (ROS) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) production were detected by flow cytometry and immunofluorescence staining combined with confocal laser scanning microscopy, respectively. The results were the basis for evaluating the level of oxidative stress and the related DNA damage in HIBECs. RESULTS: HIBECs maintained a normal morphology and vitality when treated with 17 beta-estradiol (at 10(-9) mol/L) and H. pylori (at MOI=0.5:1 and 1:1). 17 beta-estradiol at 10(-7) mol/L and 10(-5) mol/L and H. pylori at MOI=2:1, by contrast, caused cell death. Compared with controls, HIBECs treated with 17 beta-estradiol (10(-9) mol/L) and H. pylori (MOI=1:1) had a higher up-regulation of proliferation, Ki-67 expression, clone formation, migration activity and the expression of ROS and 8-OHdG and exhibited a down-regulation of apoptosis. The above effects were further increased when 17 beta-estradiol and H. pylori were combined (P<0.05). CONCLUSIONS: H. pylori and 17 beta-estradiol, separately or in combination, promoted cell proliferation and suppressed apoptosis of HIBECs in vitro. The above phenomena might be related to oxidative stress and its subsequent DNA damage with H. pylori and 17 beta-estradiol.展开更多
文摘In order to explore the mechanism of hemodynamic changes caused by high binary tract pressure, we established an animal model of high binary tract pressure, in which the disturbance of hemodynamics developed. The cervical or abdominal vague nerve was then blocked. It was observed that when the binary tract pressure was increased to 16 kpa and kept for 1h, the arterial blood pressure and cardiac output decreased immediately and parallelly (P<0. 05). When the cervical or abdominal vague nerve were blocked or the pressure of the binary tract was decreased to zero, both indices returned to normal immediately (P>0. 05). The change of cardiac output lags a little behind that of arterial blood pressure. It suggests that the signal of binary tract pressure increase can be sent to the cardiovascular center through vague nerve, and the balance between sympathic and parasympathic nerve was broken, which led to the weakening of cardiac contraction and decrease of cardiac output. Due to the peripheral effects of vague nerve, hemodynamic resistance of vessels decreased, which brought about redistribution of peripheral blood flow. Both were the causes of hemodynamic disturbances. After the blood pressure decreased markedly, it showed a jump to normal state when cervical vague nerve was blocked. And the amplitude of diastolic blood pressure restored more than that of systolic blood pressure. This suggests that the cardiac output and peripheral blood resistance are important factors that cause the decrease of blood pressure.
文摘In order to explore the effect of binary tract pressure on Oddi's sphincter and the mechanism of development of high pressure of binary tract during acute obstructive and suppurative cholangitis (AOSC), house rabbits were used to establish model of high binary pressure in acute binary duct caecus. It was observed that when the pressure of the acute binary tract was increased to 8 kpa,the electric activity of Oddi's sphincter was obviously enhanced, the pressure of Oddices sphincter increased remarkably (P <0. 05), and even constant spasm appeared with accompanying increase of discharge frequency of the right greater splanchnic nerves (P <0. 05) and progressive decrease of mean arterial pressure.However, when lidocaine of 0. 6 % was used to block the right celiac plexus, no above-mentioned reaction happened when the binary tract pressure was increased again. The results indicated that the acute binary tract obstruction might induce the contraction or spasm of Oddi's sphincter and bring about a vicious cycle. Its mechanism is related to splanchnic nerves reflection and it is one of important factors in the development of AOSC course.
基金supported by grant from the National Natural Science Foundation of China(81401932)
文摘BACKGROUND: Biliary cancers are more common in females, and previous studies have suggested that Helicobacter pylori (H. pylori) exists in the biliary system. However, the effects of H. pylori infection and estrogen on the biological behaviors of human biliary epithelium mucosa remain unknown. The present study aimed to clarify their effects on the proliferation, apoptosis, migration and oxidative DNA damage of a human intrahepatic biliary epithelial cell (HIBEC) line in vitro. METHODS: HIBECs were co -cultured with 17 beta-estradiol (at 10(-9) mol/L, 10(-7) mol/L, and 10(-5) mol/L) and H. pylori (at MOI=0.5:1, 1:1, and 2:1) and continuously passaged until the 15th generation (approximately 45 days). Then, the following assays were performed. HIBEC proliferation was measured using the CCK-8 assay, plate clone-formation assay and by determining Ki-67 expression with immunocytochemistry; cell apoptosis and migration were investigated using Annexin-V/PI and transwell assays, respectively; and reactive oxygen species (ROS) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) production were detected by flow cytometry and immunofluorescence staining combined with confocal laser scanning microscopy, respectively. The results were the basis for evaluating the level of oxidative stress and the related DNA damage in HIBECs. RESULTS: HIBECs maintained a normal morphology and vitality when treated with 17 beta-estradiol (at 10(-9) mol/L) and H. pylori (at MOI=0.5:1 and 1:1). 17 beta-estradiol at 10(-7) mol/L and 10(-5) mol/L and H. pylori at MOI=2:1, by contrast, caused cell death. Compared with controls, HIBECs treated with 17 beta-estradiol (10(-9) mol/L) and H. pylori (MOI=1:1) had a higher up-regulation of proliferation, Ki-67 expression, clone formation, migration activity and the expression of ROS and 8-OHdG and exhibited a down-regulation of apoptosis. The above effects were further increased when 17 beta-estradiol and H. pylori were combined (P<0.05). CONCLUSIONS: H. pylori and 17 beta-estradiol, separately or in combination, promoted cell proliferation and suppressed apoptosis of HIBECs in vitro. The above phenomena might be related to oxidative stress and its subsequent DNA damage with H. pylori and 17 beta-estradiol.
