Association between the expression of ve-cadherin and mesentery microcirculation blood flow of sepsis CASP rats and its clinical significance / 国际外科学杂志

Objective To monitor the association between the expression of ve-cadherin and mesentery microcirculation blood flow of sepsis CASP rats,Analysis the relationship of each other.Methods Based on the standard criteria,we established sepsis CASP rats,and the rats were divided into several groups according to the gauge of the vein detained needle in the ascending colon,every group has six rats.The groups consisted of Sepsis A group 22 G(0.9 mm× 25 mm,33 ml/min),sepis B group 20 G(1.1 mm ×32 mm,54 ml/min),sepsis C group 18 G(1.3 mm ×32 mm,80 ml/min),sepsis D group 14 G(2.0 mm ×45 mm,270 ml/min),in addition we established the control group.Real-time observation was performed by microscope on the 6 h's blood velcocity of each sepsis CASP rats group.Then we applied the immunohistochemistry to quantitatively analyze the expression of ve-cadherin of each group.Results The blood velcocity of the mesentery microcirculation in control group was (583.21 ±52.39) μm/s,it was higher compared with the sepsis D group(213.30 ±52.39) μm/s (P ＜0.05),the blood velocity in sepsis A group was (482.71 ± 58.62) μm/s,higher compared with the sepsis D group(P ＜ 0.05).The score of the immunohistochemistry quantitative analysis of mesentery ve-cadherin in control group was 11.17 ±0.34,higher compared with the sepsis D group(5.43 ±0.43)(P ＜0.01).The score of sepsis A group was 10.07 ±0.30,higher compared with the sepsis D group(P＜0.05).Conclusions The expression of ve-cadherin of sepsis CASP rats had positive correlation with the blood velocity of the mesentery microcirculation of sepsis CASP rats,and it can indirectly reflect the degree of the sepsis.

Exogenous normal lymph alleviates microcirculation disturbances and abnormal hemorheological properties in rats with disseminated intravascular coagulation

Disturbances of the microcirculation and abnormal hemorheological properties are important factors that play an important role in disseminated intravascular coagulation (DIC) and result in organ dysfunction or failure. In the present study, we established an animal model of DIC using intravenous Dextran 500 in rats, and used exogenous normal lymph corresponding to 1/15 of whole blood volume for injection through the left jugular vein. We found that normal lymph could improve the blood pressure and survival time of rats with DIC. The results regarding the mesenteric microcirculation showed that the abnormality of the diameter of mesenteric microvessels and micro-blood flow speed in the DIC+lymph group was significantly less than in the DIC+saline group. Whole blood viscosity, relative viscosity, plasma viscosity, hematocrit (Hct), erythrocyte sedimentation rate (ESR), and electrophoresis time of erythrocytes were significantly increased in the DIC+saline group compared to the control group. The electrophoretic length and migration of erythrocytes from the DIC+saline and DIC+lymph groups were significantly slower than the control group. Blood relative viscosity, Hct, ESR, and electrophoretic time of erythrocytes were significantly increased in the DIC+lymph group compared to the control group. Whole blood viscosity, relative viscosity and reduced viscosity were significantly lower in the DIC+lymph group than in the DIC+saline group, and erythrocyte deformability index was also significantly higher than in the DIC+saline and control groups. These results suggest that exogenous normal lymph could markedly improve the acute microcirculation disturbance and the abnormal hemorheological properties in rats with DIC induced by Dextran 500.

Paradoxical effects of brain death and associated trauma on rat mesenteric microcirculation: an intravital microscopic study

OBJECTIVE: Experimental findings support clinical evidence that brain death impairs the viability of organs for transplantation, triggering hemodynamic, hormonal, and inflammatory responses. However, several of these events could be consequences of brain death-associated trauma. This study investigated microcirculatory alterations and systemic inflammatory markers in brain-dead rats and the influence of the associated trauma. METHOD: Brain death was induced using intracranial balloon inflation; sham-operated rats were trepanned only. After 30 or 180 min, the mesenteric microcirculation was observed using intravital microscopy. The expression of Pselectin and ICAM-1 on the endothelium was evaluated using immunohistochemistry. The serum cytokine, chemokine, and corticosterone levels were quantified using enzyme-linked immunosorbent assays. White blood cell counts were also determined. RESULTS: Brain death resulted in a decrease in the mesenteric perfusion to 30 percent, a 2.6-fold increase in the expression of ICAM-1 and leukocyte migration at the mesentery, a 70 percent reduction in the serum corticosterone level and pronounced leukopenia. Similar increases in the cytokine and chemokine levels were seen in the both the experimental and control animals. CONCLUSION: The data presented in this study suggest that brain death itself induces hypoperfusion in the mesenteric microcirculation that is associated with a pronounced reduction in the endogenous corticosterone level, thereby leading to increased local inflammation and organ dysfunction. These events are paradoxically associated with induced leukopenia after brain damage.

Ameliorative effect of water extract of propolis preconditioning on mesenteric microcirculation of rats subjected to small intestinal ischemia reperfusion / 中国病理生理杂志

AIM: To investigate the ameliorative effect of water extract of propolis (WEP) preconditioning on mesenteric microcirculation of rats subjected to small intestinal ischemia reperfusion (I/R). METHODS: Thirty-two male Wistar rats were randomly divided into sham, I/R and WEP (100, 200 mg/kg) preconditioning groups. Model of small intestinal I/R injury was made by clamping super mesenteric artery for 45 min followed by 120 min of reperfusion in rats. Mesenteric microcirculation was detected at the end of reperfusion. The degree of small intestinal injury was The content of soluble intercellular adhesion molecule-1 (sICAM-1) in plasma and myeloperoxidase (MPO) activity in intestinal tissue were detected using enzyme linked-immuno-sorbent assay (ELISA) and spectrophotometer, respectively. RESULTS: (1) WEP preconditioning alleviated significantly the pathologic lesion in small intestine, and wet/dry ratio, compared to those in I/R group (P<0.01). (2) The disturbance of the blood flow in microvessel induced by I/R was improved significantly by WEP. In addition, WEP preconditioning alleviated significantly the decrease in diameters of microvessels and microcirculatory blood velocity (P<0.05 vs I/R group) and inhibited the adherence of leukocytes to venule (P<0.01 vs I/R group) in a dose-dependent manner. SICAM-1 content in plasma and MPO activity in intestinal tissue were decreased in WEP preconditioning group, compared to those in I/R group (P<0.05 or P<0.01). CONCLUSION: WEP preconditioning ameliorates mesenteric microcirculation of rats subjected to small intestinal I/R through suppressing the activation of polymorphonuclear neutrophils mediated by ICAM-1.

Mesenteric microcirculatory dysfunctions and translocation of indigenous bacteria in a rat model of strangulated small bowel obstruction

PRUPOSE: Bacterial translocation has been shown to occur in critically ill patients after extensive trauma, shock, sepsis, or thermal injury. The present study investigates mesenteric microcirculatory dysfunctions, the bacterial translocation phenomenon, and hemodynamic/metabolic disturbances in a rat model of intestinal obstruction and ischemia. METHODS: Anesthetized (pentobarbital 50 mg/kg, i.p.) male Wistar rats (250-350 g) were submitted to intestinal obstruction or laparotomy without intestinal obstruction (Sham) and were evaluated 24 hours later. Bacterial translocation was assessed by bacterial culture of the mesenteric lymph nodes (MLN), liver, spleen, and blood. Leukocyte-endothelial interactions in the mesenteric microcirculation were assessed by intravital microscopy, and P-selectin and intercellular adhesion molecule (ICAM)-1 expressions were quantified by immunohistochemistry. Hematocrit, blood gases, lactate, glucose, white blood cells, serum urea, creatinine, bilirubin, and hepatic enzymes were measured. RESULTS: About 86 percent of intestinal obstruction rats presented positive cultures for E. coli in samples of the mesenteric lymph nodes, liver, and spleen, and 57 percent had positive hemocultures. In comparison to the Sham rats, intestinal obstruction induced neutrophilia and increased the number of rolling (~2-fold), adherent (~5-fold), and migrated leukocytes (~11-fold); this increase was accompanied by an increased expression of P-selectin (~2-fold) and intercellular adhesion molecule-1 (~2-fold) in the mesenteric microcirculation. Intestinal obstruction rats exhibited decreased PaCO2, alkalosis, hyperlactatemia, and hyperglycemia, and increased blood potassium, hepatic enzyme activity, serum urea, creatinine, and bilirubin. A high mortality rate was observed after intestinal obstruction (83 percent at 72 h vs. 0 percent in Sham rats). CONCLUSION: Intestinal obstruction and ischemia in rats is a relevant model for ...