A new strategy to establish a hepatopulmonary syndrome model in rats by inducing abdominal compartment syndrome in the presence of cirrhosis / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To find a practical method to establish hepatopulmonary syndrome (HPS) in rats for use as an experimental model system.</p><p><b>METHODS</b>Forty male Sprague-Dawley rats were equally divided into a normal group (injected subcutaneously with 3 mL/kg of olive oil for 12 weeks), abdominal compartment syndrome (ACS) group (injected subcutaneously with 3 mL/kg olive oil for 12 weeks, followed by an intraperitoneal injection of 4% succinylated gelatin and maintenance of 20 mmHg abdominal pressure for 3 h), cirrhosis group (injected subcutaneously with 40% carbon tetrachloride (CCl4) in olive oil twice weekly for 12 weeks, with first dose doubled), and an ACS+ cirrhosis (HPS model) group (CCl4-induced, followed by the intraperitoneal injection with succinylated gelatin and 3 h of 20 mmHg abdominal pressure). The mice were sacrificed to perform blood gas analysis and to assess lung pathology. Comparisons between two groups were carried out by non-parametric analysis, and multiple comparisons were carried out by the Kruskal-Wallis H test.</p><p><b>RESULTS</b>Blood gas analyses showed significant differences in the values of pH for the normal group (7.41+/-0.04), the ACS group (7.22+/-0.06), the cirrhosis group (7.53+/-0.04), and the HPS model group (7.47+/-0.02) (P less than 0.05). The ACS group and the HPS model group showed significantly different values of partial pressure of oxygen (PaO₂; 58.57+/-5.41 and 58.20+/-3.19 mm Hg) and of alveolar-arterial oxygen difference (AaDO₂; 83.86+/-28.49 and 84.80+/-11.82 mm Hg) than the normal group and the cirrhosis group (PaO₂: 86.67+/-1.37 and 85.00+/-2.53 mm Hg; AaDO₂: 38.17+/-9.20 and 37.00+/-6.23 mm Hg) (P less than 0.05). Pathological analysis of the lungs from the ACS group revealed widened alveolar septa, different-sized alveolar spaces, reduced lung capacity, edema and hemorrhage in some of the alveolar cavities, and telangiectasia in the alveolar walls. The lungs from the cirrhosis group also showed widened alveolar septa, different-sized alveolar spaces, and reduced lung capacity, but were distinct in the features of inflammatory cell infiltration, and hyperemia in the pulmonary vessels. The lungs from the HPS model group showed all of the features of both the lungs from the ACS and cirrhosis groups, but also showed macrophage accumulation and microthrombi in the pulmonary vessels.</p><p><b>CONCLUSION</b>Inducing ACS in the setting of CCL4-induced cirrhosis in a rat generates pathological features that adequately mirror those of HPS and may represent a useful experimental model for in vivo studies of HPS.</p>

Lung expression of tissue factor mRNA and its significance in a rat model of hepatopulmonary syndrome / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To determine the lung expression of tissue factor (TF) mRNA in hepatopulmonary syndrome (HPS) using a rat model system and to investigate the potential significance of its differential expression.</p><p><b>METHODS</b>Forty male Sprague-Dawley rats were used to establish models of cirrhosis (n = 20) and HPS (n = 20). Blood gas analysis was used to investigate the effects of each model on pulmonary function. Effects on the expression of TF mRNA in lung were determined by qRT-PCR and on lung pathology by histological analysis.</p><p><b>RESULTS</b>The HPS rats showed significantly lower PaO2 than the cirrhosis rats (58.20 +/- 3.19 mmHg vs. 85.00 +/- 2.53 mmHg, P less than 0.05) but significantly higher TF mRNA expression in lung (0.77 +/- 0.22 vs. 0.33 +/- 0.14, P less than 0.05). TF mRNA expression was negatively correlated with the value of PaO2 (r = -0.565, P less than 0.05). The lungs of the cirrhosis rats showed widened alveolar intervals, diversified sizes of alveolar spaces, reduced lung capacity, inflammatory cell infiltration, and hyperemia in the pulmonary vessels. The lungs of the HPS rats showed all of the same changes but also with accumulated macrophages and micro-thrombosis in the pulmonary vessels. Among the HPS rats, those with micro-thrombosis in pulmonary vessels showed a greater increase in TF mRNA expression than those without (0.68 +/- 0.17 vs. 0.40 +/- 0.12, P less than 0.05).</p><p><b>CONCLUSION</b>The expression of TF mRNA in lung of hepatopulmonary syndrome model rats was elevated and might increase the incidence of thromboembolism in the lung.</p>

Application of serum total IgE, tryptase and chymase in the identification of death caused by drug anaphylactic shock / 法医学杂志

OBJECTIVE@#To explore the application value of serum total IgE, tryptase and chymase in the identification of death caused by drug anaphylactic shock.@*METHODS@#The general information from 235 cases of non-drug anaphylactic shock and 32 cases of drug anaphylactic shock were analyzed. The serum IgE level had been detected in the cases. Ten cases caused by coronary disease and 10 cases caused by sudden manhood death syndrome were selected from non-drug anaphylactic shock cases for the control group. Expressions of tryptase and chymase in the lung and heart were detected using immunohistochemistry method. The number and IOD of positive mast cells were counted.@*RESULTS@#In the drug anaphylactic shock group, the IgE value of 18 samples (56.25%) was significantly higher than the normal upper limit of 120 IU/mL. In the non-drug anaphylactic shock group, the IgE value of 67 samples (28.51%) was higher than 120 IU/mL. The expressions of tryptase and chymase were significantly increased in lung and myocardial tissue in drug anaphylactic shock group (P < 0.05).@*CONCLUSION@#Tryptase and chymase are more superior than that of the serum total IgE in the diagnosis of death caused by drug anaphylactic shock, and are more suitable in forensic practice.