1.Role of VE-cadherin/catenins complex in microvascular permeability during inflammation
Hongkai GAO ; Youdai CHEN ; Zongguang ZHOU
Chinese Journal of Pathophysiology 1986;0(04):-
VE-cadherin forms VE-cadherin/catenins complex by interacting with catenins,and VE-cadherin/catenins complex is an important component of adherens junctions(AJ). During inflammation ,different kinds of factors can increase the microvascular permeability eventually by causing the disassembly of VE-cadherin/catenins complex.
2.Dynamic changes of the serum pro-and anti-inflammatory cytokines and its significance in assessing clinical condition for sepsis patients
Minghua SU ; Xuanling FENG ; Lei DENG ; Yi LI ; Junying LI ; Youdai CHEN
Chongqing Medicine 2015;(4):467-469
Objective To investigate the dynamic change of pro‐and anti‐inflammatory eytokines of sepsis patients and its signif‐icance in clinical condition .Methods Forty‐three sepsis patients from 2010 to 2011 were divided into the survival group and the death group .Morning serum samples were collected on the first ,third ,firth and seventh day morning ;ELISA method was used to quantify the serum level of TNF‐α,IL‐1 ,IL‐4 and IL‐10 .The severity of patient′s condition was assessed according to the APACHEⅡsystem .Results In the early stage ,TNF‐α and IL‐1 in of both group increased and reached the peak on the third day ;then there was a gradual decline .Test in the same time point showed that the indexes of death group were all higher than that of survival group (P<0 .05) .IL‐4 of the two groups reached its peak on the fifth day and then declined ,and in the same time point ,indexes of death group were much more higher than that of survival group (P<0 .05) .IL‐10 of the survival group reached its peak on the fifth day and then declined;in the death group ,IL‐10 level kept increasing and maintained high ,there was no significant difference among the serum levels of the third ,fifth and seventh day(P>0 .05) .The APACHE Ⅱ of the survival group declined significantly while in death group it kept increasing and stay high .Conclusion Pro‐inflammatory eytokines(TNF‐α,IL‐1) ascended earlier than anti‐in‐flammatory eytokines(IL‐4 ,IL‐10) ,and the serum level of IL‐10 keep high level prompt the poor prognosis .
3.Clinical study of the central venous catheter specialized for continuous drainage of exudates from severe acute pancreatitis (SAP) in patients with seroperitoneum
Junying LI ; Yun DONG ; Xiaohong ZANG ; Youdai CHEN ; Jun ZHENG ; Minghua SU
Chinese Journal of Emergency Medicine 2013;22(10):1096-1099
Objective To investigate the application of the central venous catheter (CVC) specialized for drainage intervention in severe acute pancreatitis (SAP) patients.Methods Sixty-two severe acute pancreatitis patients with seroperitoneum were randomly (random number) assigned into two groups:the drainage group (n =31) and the control group (n =31).All patients were treated with conventional internal medicine therapy.Patients of drainage group were treated with continuous peritoneal drainage by using the central venous catheter.The intra-abdominal pressure (IAP),lactic acid (LAC),and procalcitonin (PCT) were detected before and 12 h,24 h,48 h,72 h,5 days after intraperitoneal drainage.The symptoms of abdomen pain,abdomen distention,resume of bowel movement and the rate of MODS were observed.Results All patients with drainage got catheter successfully inserted.Compared with the control group,the IAP,LAC and PCT decreased significantly in the patients of drainage group.And the duration of abdomen pain,abdomen distention and resume of bowel movement function in the drainage group were shorter and the rate of MODS was lower.Conclusions Application of CVC specialized for intraperitoneal drainage is a safe and effective method for the treatment of pancreatitis with seroperitoneum.It is worthwhile to be widely used in clinic.
4.On PACAP-aggravated experimental acute pancreatitis.
Youdai CHEN ; Zongguang ZHOU ; Youqin CHEN ; Zhao WANG ; Hongkai GAO ; Xuelian ZHENG
Journal of Biomedical Engineering 2004;21(6):964-969
The role of PACAP (pituitary adenylate cyclase activating polypeptide), a peptidergic transmitter, in the pathogenesis of acute pancreatitis is not yet clear. This experiment was conducted to examine the action of exogenous PACAP on rat pancreas and on the course of experimental acute pancreatitis. The results showed that 5-30 microg/kg of PACAP slightly raised the serum amylase level, induced pancreatic edema (23.88% +/- 2.532%-25.86% +/- 1.974% of experiment groups versus 29.21% +/- 5.657% of control group), inflammatory cell infiltration, vacuolization of acinar cells, and occasionally fatty and parenchymal necroses. 15-30 microg/kg of PACAP aggravated cerulein-induced acute pancreatitis; the pancreatic edema became more marked (13.45% +/- 2.045%-17.66% +/- 4.652% of expreiment groups versus 21.83% +/- 3.013% of cerulein group, P<0.05), the serum amylase level became higher; and ascites, pancreatic bleeding, fatty and parenchymal necroses, and extensive vacuolization of acinar cells appeared. For sodium taurocholate-induced pancreatitis, 5-10 microg/kg of PACAP mildly attenuated the pancreatic edema, reduced the serum amylase level (1986.91 +/- 710.97-2944.33 +/- 1182.47 IU/L vs 3690.87 +/- 2277.99 IU/L, P<0.05), whereas it caused multifocal hemorrhage and prominent necrosis in pancreas. Except the cerulein-induced pancreatitis groups, other groups were found to have reduced pancreatic functional capillary density (FCD); when pancreatic edema was taken into consideration and calibrated FCD was introduced (FCD weighted against pancreatic wet/dry ratio), all groups revealed increases in pancreatic functional capillaries when compared with normal control. In conclusion, PACAP is proinflammatory in the pathogenesis of acute pancreatitis, PACAP plus cerulein can induce acute hemorrhagic/necrotizing pancreatitis, and the action of PACAP on cerulein-induced panceatitis may differ from that on sodium taurocholate-induced one. In this experiment, pancreatic FCD was underestimated due to pancreatic edema.
Amylases
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blood
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Animals
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Capillaries
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pathology
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Ceruletide
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Disease Models, Animal
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Male
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Pancreas
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blood supply
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Pancreatitis, Acute Necrotizing
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chemically induced
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enzymology
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pathology
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Rats
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Rats, Wistar
5.Role of 6% hydroxyethylstarch 130/0.4 and furosemide in the treatment of acute pancreatitis.
Jiandong WANG ; Youdai CHEN ; Yun DONG ; Weijian HU ; Ping ZHOU ; Li CHANG ; Shiyan FENG ; Jian LIN ; Yu ZHAO
Journal of Biomedical Engineering 2010;27(5):1138-1145
This study was conducted to observe the effects of intravenously administered 6% hydroxyethylstarch 130/ 0.4 solution and furosemide on the outcome of acute pancreatitis patients. Patients admitted to our center from October 16, 2007 through August 31, 2009 were given intravenous infusions of 6% hydroxyethylstarch 130/0. 4 solution (1 000-2 000 ml administered for an adult) soon after admission. At the same time, furosemide was administered as intravenous bolus, trying to maintain a fluid balance. The dose level of hydroxyethylstarch was gradually lowered from the second day after admission. A total of 135 patients (54% of patients with a Ranson's score > or = 3 and 61% with a Balthazar CT score > or = D) were treated with our protocol. Only 4% and 7% patients developed pancreatic and systemic complications respectively; only 1 patient underwent necrosectomy. The in-hospital mortality rate was 4%. It was estimated that, on the average, 18. 3% of blood volume was lost on admission. Our study suggest that intravenously administered 6% hydroxyethylstarch 130/0. 4 solution and furosemide might be beneficial for patients with acute pancreatitis. Plasma extravasation is a central event of acute pancreatitis. The reversal of hypovolemia is crucial for the success in treatment of acute pancreatitis.
Acute Disease
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Adolescent
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Adult
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Aged
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Aged, 80 and over
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Child
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Child, Preschool
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Female
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Furosemide
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administration & dosage
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Humans
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Hydroxyethyl Starch Derivatives
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administration & dosage
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Hypovolemia
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prevention & control
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Infant
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Infusions, Intravenous
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Injections, Intravenous
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Male
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Middle Aged
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Pancreatitis
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drug therapy
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Young Adult
6.A sharp rise in portal vein pressure, not arterial constriction, initiates bile salt-induced pancreatic microcirculatory disturbance.
Youdai CHEN ; Huaiqing CHEN ; Yunman TANG ; Qiufen TU ; Dongxia GE ; Chang YU ; Congxun JIANG ; Shiping LIAO ; Ron WANG
Journal of Biomedical Engineering 2007;24(6):1280-1285
It was reported that pancreatic arteries constricted during the early phase of bile salt-induced acute pancreatitis (AP), leading to pancreatic microcirculatory disturbance. We conducted this experiment to verify whether the above-mentioned finding was true. AP was induced with intraductal injection of taurodeoxyholate. Small pancreatic artery pressure in dogs was recorded. Functional capillaries were counted and calibrated by multiplying wet weight of pancreas. Pancreatic perfusion was measured with Laser Doppler flowmeter. Pancreatic arterioles of rats dilated during the initial 20 min of AP, and pancreatic arterial pressure declined during the early phase of AP in dogs (from 104.5 +/- 4.8 mmHg to 54.6 +/- 5.6 mmHg). The hematocrit of blood from inferior vena cava was significantly lower than that of portal vein at 5 min after pancreatitis induction. The "true" pancreatic functional capillary density increased. The early pancreatic microcirculatory disturbance coincided with a marked increase of portal vein pressure (PVP) as high as 9.18 +/- 0.78 mmHg. Reduction of PVP to baseline level was followed by a marked increase of pancreatic perfusion (by 1.4-fold). Arterial dilatation, but not constriction, occurred during the early phase of bile salt-induced AP. The pancreatic microcirculatory disturbance was due to a marked rise in PVP that greatly reduced the pressure difference in the pancreatic blood vessels and increased plasma extravasation which led. to local hemoconcentration.
Animals
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Bile Acids and Salts
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adverse effects
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Hypertension, Portal
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complications
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Male
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Microcirculation
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drug effects
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physiology
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Pancreas
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blood supply
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Pancreatitis
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etiology
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physiopathology
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Portal Pressure
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Portal Vein
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physiopathology
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Rats
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Rats, Sprague-Dawley