ObjectiveTo assess fine needle aspiration (FNAC) in the early diagnosis for auto immune thyroid disease (AITD) in adolescent.Methods Seventy-one patients, age ranging from 9 to 23 years with thyroid enlargement underwent FNAC. Their smears were classified into 4 types according to the degree of degeneration of adenoidal cell and lymphocyte invasion by HE combining with rapid staining.The results were compared with B ultrasound and serum thyroid auto antibody measurement.ResultsB ultrasound showed hyperthyroidism in 12 cases, inflammation in 53, nodule change in 5, normal in 5. Thyroid function examination demonstrated hyperthyroidism in 22 cases, hypothyroidism in 9 cases, and euthyroidism in 40 cases. Auto thyroid antibody (TGAb,TMAb) were all beyond normal range except in 1 case, and TPOAb elevated in 37 cases. FNAC identified Grave′s disease in 14, Hashimoto′s diseases typeⅠ( HT-Ⅰ) in 35 cases,HT(Ⅱ) in 13,HT(Ⅲ) in 3, and HT(Ⅳ) in 6 cases. ConclusionsFNAC contributes to early diagnosis of AITD in adolescent for its safety, simplicity, rapidity and accuracy.

Objective To study the role of vascular mediators in the pathogenesis of hepatopulmonary syndrome in rats. Methods Male Sprague-Dawley (SD) rats were divided into four groups: SO (surgical control), IHPH (intrahepatic portal hypertension), PHPH (prehepatic) and PCS (portocaval shunt). Two weeks after pathological study, arterial blood gas and the concentrations of NO, glucagon, VIP and ET-1 in plasma and lung were determined. Results Lung structural alteration of rats induced by CCl 4 was of alveolar capillary dilation and angiogenesis, thickened alveolar septa and decreased alveolar capacity. There was no inflammation, edema, fibrosis, alveolar collapse and hyaline membrane formation in lung of all rats. PaO 2 ( mm?Hg)decreased more significantly in IHPH (73.85?6.51) rats than in PHPH (972?9?1.33), PCS (95.23?2.22) and SO rats (99.05?0.75). The level of lung NO of IHPH (19.78?5.33) was significantly increased than those of PHPH (13.21?3.99) and PCS (13.89?3.16) whose level in lung homogenate increased than those of SO (8.71?1.68). There was no difference of Glu and VIP levels in lung among all rats. The level of lung ET-1 in IHPH was significantly decreased than other rats. Conclusion Increased NO levels and decreased ET-1 levels in lung of HPS rats cause alveolar dilation and angiogenesis leading to mismatched ventilation-perfusion, and decrease of PaO 2.

OBJECTIVETo investigate the expression of ET-1 mRNA in the lung of rats with hepatopulmonary syndrome.

METHODSMale Sprague-Dawley rats were divided into four groups: SO, IHPH, PHPH and PCS. Two weeks after production of rat models, all measurements were performed. Arterial blood gas was analyzed. The concentrations of NO and ET-1 in lungs were measured by using radioimmunoassay. In situ hybridization, ET-1 mRNA expressions were detected in lung tissue sections with digoxin-labeled ET-1 oligonucleotide probes. Liver and lung tissues and all the results of in situ hybridization were analyzed by one pathologist. At a magnification of 10 x 40, percent areas of positive stains were detected to indicate the expressions of ET-1 mRNA in the arteries, capillaries and branches.

RESULTSArterial blood gas analysis showed that PaO(2) (mmHg) decreased more significantly in IHPH (73.85 +/- 6.51) rats than in PHPH (97.39 +/- 1.33), PCS (95.23 +/- 2.22) and SO rats (99.05 +/- 0.75). Alveolar-arterial oxygen gradient (A-aG) (mmHg) increased more significantly in IHPH rats (32.99 +/- 6.57) than in PHPH (4.98 +/- 1.69), PCS (6.51 +/- 2.04) and SO rats (3.23 +/- 0.81). Changes of vascular active substance in plasma and lung indicated that the level of lung NO of IHPH (19.78 +/- 5.33) was increased significantly more than that of PHPH (13.21 +/- 3.99) and PCS (13.89 +/- 3.16). These levels in lung homogenate increased more significantly than those SO (8.71 +/- 1.68). The levels of ET-1 in IHPH rats (195.1 +/- 36.2) was significantly lower than in PHPH (234.8 +/- 71.0), PCS (240.4 +/- 66.5) and SO rats (271.8 +/- 40.6). ET-1 mRNA in situ hybridization showed that there was no significant difference in positive expression of ET-1 mRNA in alveolar arteries and small bronchi. The expression of ET-1 mRNA was significantly lower in alveolar capillary endothelia (5.12 +/- 1.27) than in PHPH (7.43 +/- 0.83), PCS (7.07 +/- 0.86) and SO (7.81 +/- 1.98) rats.

CONCLUSIONThe low expressions of ET-1 mRNA in HPS rat alveolar capillary endothelia accompanied by decreased ET-1 levels in lung may play an important role in the mechanism of HPS.

Animals ; Disease Models, Animal ; Endothelin-1 ; biosynthesis ; genetics ; Hepatopulmonary Syndrome ; metabolism ; pathology ; Image Processing, Computer-Assisted ; In Situ Hybridization ; Lung ; metabolism ; pathology ; Male ; Nitrates ; metabolism ; Nitrites ; metabolism ; RNA, Messenger ; biosynthesis ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo evaluate the role of endogenous vasoactive substances in hyperdynamic circulation after orthotopic liver transplantation (OLT) in cirrhotic rats.

METHODSMale SD rats were randomly divided into 4 groups: normal controls (NL, n = 10), rats with intrahepatic portal hypertension (IHPH, n = 10), normal rats with OLT (NL-OLT, n = 9), and IHPH rats with OLT (IHPH-OLT, n = 16). IHPH-OLT rats were divided into 2 subgroups: Group A (3 days after OLT, n = 9) and Group B (7 days after OLT, n = 7). IHPH was induced by injection of CCI(4) and OLT was performed using cuffs for the anastomosis of suprahepatic inferior vena cava, infrahepatic vena cava and portal vein. Radioactive microsphere method was used for hemodynamic study. The concentrations of plasma glucagon (Glu), nitric oxide (NO), prostaglandin (PGI(2)), thromboxaneA(2) (TXA(2)) and endothelin (ET) were measured by radioimmunoassay.

RESULTSNo significant difference in hemodynamic changes was observed between NL-OLT and NL rats, except for mean arterial blood pressure. No significant changes in NO and PGI(2) were seen between NL-OLT and NL rats. Glu, ET and TXA(2) were significantly elevated in NL-OLT rats compared with NL rats (P < 0.05). Characteristics of systemic and splanchnic hyperdynamic circulatory states were observed in IHPH, IHPH-OLT A, IHPH-OLT B rats. Both the magnitude of hyperhemodynamics and increasing concentrations of Glu and NO occurred in the order of IHPH > IHPH-OLT A > IHPH-OLT B rats. The level of plasma PGI(2) in IHPH rats was significantly elevated compared with NL rats, while PGI(2) in IHPH-OLT A and B rats was found to be lower than in IHPH rats (P < 0.05). There was no obvious difference in PGI(2) between IHPH-OLT B and NL rats. Vasoconstrictors including ET and TXA(2) were found elevated in IHPH-OLT rats.

CONCLUSIONSOLT does not induce postoperative hyperhemodynamics per se. Vasodilators including NO and Glu, especially NO, play an important role in the hyperhemodynamics of IHPH and IHPH-OLT rats. The results of the present study demonstrate that the persistence of systemic and splanchnic hyperkinetic circulation in the early stages after OLT may result from those non-eliminated factors that caused hyperhemodynamics in liver cirrhosis patients with portal hypertension before OLT.

Animals ; Endothelins ; blood ; physiology ; Epoprostenol ; blood ; physiology ; Glucagon ; blood ; physiology ; Hemodynamics ; Liver Cirrhosis, Experimental ; physiopathology ; Liver Transplantation ; Male ; Nitric Oxide ; blood ; physiology ; Rats ; Rats, Sprague-Dawley ; Thromboxane A2 ; blood ; physiology