AIM: To study the effect of chronic hypoxic hypercapnia on gene expression of thromboxane synthase and prostacyclin synthase in pulmonary arterioles. METHODS: Sprague-Dawley rats were randomly divided into two groups: control group and hypoxic hypercapnic group. TXS mRNA and PGI 2-S mRNA were observed in pulmonary arterioles by in situ hybridization. RESULTS:mPAP, weight ratio of right ventricle (RV) to left ventricle plus septum(LV+S), contents of TXB 2 and 6-keto-PGF1 ? in plasma and lung and TXS mRNA in pulmonary arterioles were much higher in rats of hypoxic hypercapnic group than those of control group. Differences of PGI 2-S mRNA in pulmonary arterioles were not significant in two groups. Light microscopy showed hypertrophy of vessel smooth muscle cells and vessel cavity straitness were found in hypoxic hypercapnic group. CONCLUSION: Changes of gene expressions of thromboxane synthase and prostacyclin synthase and imbalance of TXA 2/PGI 2 may play an important role in hypoxic hypercapnic pulmonary hypertension.

Achievements of the 30-year research work on Pi-Wei Doctrine were summarized. They are: (1) ratio of salivin activity and excretion rate of D-xylose in patients with spleen deficiency are different from those in the normal subjects;(2) the principle of syndrome differentiation and treatment is embodied in the methodology of herbal medicine pharmacology for complex prescription; (3) the above findings are further confirmed by the research in molecular and cellular level which indicates that TCM syndromes and pharmacological mechanisms of herbal medicines have their material basis and the regulatory effect of complex prescription on TCM syndromes is actually the pharmacological mechanism of herbal medicines. It is suggested that the research of herbal medicine should be based on the guidance of traditional Chinese medicinal theory and carried out in clinical practice.

AIM: To investigate the changes of vascular endothelial growth factor (VEGF) in the pulmonary circulation of rats with different hypoxia and hypercapnia duration. METHODS: Forty SD rats were randomly divided into normol control group (N), exposed to hypoxia hypercapnia for 2 weeks group (T), for 4 weeks group (F), for 8 weeks group (E). The levels of VEGF were measured and the ultrastructure of pulmonary arterioles was observed by electron microscopy. RESULTS: Mean pulmonary arterial pressure (mPAP), weight ratio of RV to LV+S, the levels of VEGF in serum and lung tissue, the expression of VEGF and VEGF mRNA in group T, F, E were significantly higher than that in group N. With the prolong duration, base of endothelial cell was narrowed, proliferation of smooth muscle cells and collagenous fibers of pulmonary arterioles in rats were increased gradually. CONCLUSIONS: Hypoxia and hypercapnia increase the expression of VEGF mRNA and synthesis of VEGF. VEGF may play an important role in the pathogenesis of hypoxia pulmonary hypertension and reconstruction of pulmonary artery.

AIM: To study the role and the mechani sm of heme oxygenas/endogenous carbon monoxide on nitric oxide synthase/nitric oxide system in rats with pulmo nary hypertension induced by hypoxic hypercapnia. METHODS: Spr ague-Dawley rats w ere randomly divided into three groups: control group (A group),hypoxic hypercap n ic group (B group), hypoxic hypercapnia+hemin group (C group). Blood CO concentr at ion (COHb%),NO concentration,HO-1 activity, iNOS, cNOS in blood serum and lung h omogenate were measured, respectively. RESULTS: ① mPAP and RV /(LV+S) of B g roup were significantly higher than those of A and C group( P

The action of dl - tetrahydropal-matine(dl-THP) was studied in two preparations in vitro : the isolated rat gastric mucosa and parietal cells, dl-THP was found to inhibit significantly basal acid formation by the gastric mucosa in a dose - response fashion. The effect was reversible, acid secretion returning to control levels 1. 5~2h after the preparation underwent a double wash, dl - THP also produced asignificant and dose - dependent inhibition of histamine - induced secretion in the gastric mucosa and parietal cells, shifted the histamine dose -response cuver to the right and suppressed the maximum acid production, with pD_2~1 values of 4. 72 and 4. 70, respectively.

BACKGROUND: The onset of vascular dementia (VD) is closely related to brain ischemic-hypoxia. Previous research has proved that behavioral disturbance can be obviously attenuated by xingnao qizhi capsule in VD rats; however, it remains unclear whether the improvement of VD is due to the protection on ischemic cells.OBJECTIVE: Pheochromocytoma PC12 cells were cultured in vitro and exposed to Na2S2O4 to induce hypoxia injury. Then serum pharmacological technique was used to investigate the protection of xingnao qizhi drug serum on hypoxia-injured PC12 cells.DESIGN: Randomized controlled study.SETTING: School of Traditional Chinese Medicine of Hebei Medical College.PARTICIPANTS: This study was conduced at the Experimental Animal Laboratory and Cell Culture Laboratory, School of Traditional Chinese Medicine of Hebei Medical College, between June and December 2003.Forty SD rats were randomized into 5 groups, namely serum control group (n=12) and xingnao qizhi serum 25.42, 12.71, 6.35 and 3.18 g/kg groups (n=7). PC12 cell line was purchased form the Cell Center of Chinese Academy of Medical Sciences.serum 25.42, 12.71, 6.35 and 3.18 g/kg groups were exposed through gastric lavage to xingnao qizhi of corresponding dosages (composed of wolfberwhile normal saline was given by gastric lavage to rats in control group in dosage of 10 mL/kg, twice a day at an interval of 12 hours for 3 consecutive days. One hour after the last administration, femoral blood samples were collected when rats were deeply anaesthetized and serum was sepainto 6 groups. Cells in control group were cultured with control serum while in experimental model groups cells were exposed to Na2S2O4 to induce hypoxia injury 1 hour later. Cells in Xingnao Qizhi 25.42, 12.71,6.35 and 3.18 g/kg groups were cultured in 5% drug serum with corresponding dosage of xingnao qizhi drug for 1 hour before being exposed to changes of PC12 cells in the six groups were observed under reversal microscope after exposure to Na2S2O4 for 16 hours; the inhibition rate of lactate dehydrogenase production and PC12 cell injury (MTT method) was calculated for assessing cell activity.nase production and PC12 cell injury.of xingnao qizhi displayed better refraction, with fewer cell fragments that tion: It was 81.6%, 69.6%, 54.4% and 27.8% in xingnao qizhi 25.42,PC12 cell injury: It was 82.9%, 75.6%, 65.9% and 53.7% in Xingnao Qizhi 25.42, 12.71, 6.35 and 3.18 g/kg groups, respectively.CONCLUSION: xingnao qizhi drug serum can markedly attenuate hypoxia injury of PC12 cells in dose-dependant manner, which is presented by strengthened cell activity and decreased lactate dehydrogenase activity.

AIM: To explore the roles of vascular endothelial growth factor (VEGF) in hypoxia pulmonary hypertension and effects of SHENYI Capsule. METHODS: Thirty SD rats were randomly divided into normal control group (N), hypoxia hypercapnia group (F), and hypoxia hypercapnia+SHENYI Capsule group (S). The levels of VEGF in serum and lung tissue are measured by ELISA, the ultrastructure of pulmonary arterioles was observed by electron microscopy, and the expression of VEGFmRNA was observed by in situ hybirdization. RESULTS: Mean pulmonary arterial pressure (mPAP), weight ratio of RV to LV+S, the levels of VEGF in serum, and lung tissue of group F were significantly higher than those of group N and group S (P

ObjectiveTo explore the clinical diagnostic value of ambulatory EEG (AEEG) in epilepsy and atypical epilepsy.MethodsThe monitoring of 24-hour AEEG were performed in 67 epileptic and 53 atypical epileptic.Results65.7% of epileptic cases presented abnormality, and 34.0% of atypical epilepsy. The 85.5% of epileptic form discharges were found in the stage of sleep, especially in the Ⅰor Ⅱstage of NREM. The main epileptic form discharges was sharp waves.ConclusionThe monitoring of 24-hour AEEG may play important role in the diagnosis of epilepsy or atypical epilepsy, but can do little in the classification and detecting the focus of epilepsy.

AIM: To study the effect of ligustrazine on pulmonary hypertensive rats induced by hypoxic hy- percapnia. METHODS: Thirty rats were randomly divided into three groups: control group(A), hypoxic hypercapnic group (B), hypoxic hypercapnia+ligustrazine (lig. ) group(C). RESULTS: (1) Mean pulmonary axterial pressure (mPAP)of group B was significantly higher than that of group A and mPAP of group C was significantly lower than that of group B(P0.05); (2)Electron microscopy and immunohistochemistry showed ligustrazing could inhibit the diposition of col- lagenous fiber(collagen type Ⅰ )in pulmonary arterioles induced by hypoxic hypercapnia; (3) Plasma endothelin level of group C was significantly lower than that of group B (P

In order to investigate the levels of stem cell factor (SCF) and its receptor c-kit protein and mRNA in pediatric aplastic anemia (AA) and their relevance to the pathogenesis, immunocytochemical and in situ hybridization were utilized to detect the expression of SCF and its receptor c-kit gene protein and mRNA, respectively in 59 children with AA and 51 normal controls. The relationship between SCF and c-kit and the pathogenesis of AA was analyzed subsequently. The results showed that the positive rate of SCF protein and mRNA expression in children with AA was significantly lower than that in healthy controls (P < 0.05). However, there was no significant difference in the positive rate of c-kit protein and mRNA expression between children with AA and control group (P > 0.05). It was concluded that the expression of SCF is significantly decreased in children with AA, which may be closely associated with the pathogenesis of the AA. c-kit may be unrelated to the development of pediatric AA. Therefore, AA in children may have abnormalities at SCF/c-kit signal transduction levels.
Anemia, Aplastic/etiology ; Anemia, Aplastic/*metabolism ; RNA, Messenger/biosynthesis ; RNA, Messenger/genetics ; Receptors, Colony-Stimulating Factor/*biosynthesis ; Receptors, Colony-Stimulating Factor/genetics ; Stem Cell Factor/*biosynthesis ; Stem Cell Factor/genetics