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The effect of naloxone on the electric activity of sympathetic nerve in rabbit SMAO shock

Chinese Journal of Pathophysiology.1986;0(02):-.

This paper shows the influence of naloxone injected into the lateral ventricle of brain on the SMAO (superior mesenteric artery occlusion) shock in rabbits as well as the electric activity of sympathetic nerve in the course of shock.This experiment in 40 rabbits proved that the electric activity of the sympathetic nerve in the naloxone group was more enhanced and the duration was much longer than the control group after loosing the occuiation. From these it is clear that the central activity of the sympathetic nerve is related to the reversal effect of naloxone on shock. However the blood pressure in the group of naloxone could be maintained at a higher level and much longer after the electric activity of the sympathetic nerve had decreased. As a result, it may be inferred that there are still other factors contributing to the blood pressure, beside the regulation by the tonicity of sympathetic nerve. The significant extension of survival time in the naloxone group fully explained that naloxone played an important role in revering SMAO shock. Therefore naloxone is valuable in clinical treatment.

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Somatosensory evoked potentials in patients with diabetes mellitus

Wenbin LI

Chinese Journal of Pathophysiology.1986;0(03):-.

Using the average technique of the electronic computer, we recorded the somatosensory evoked Potentials (SEPs) by electrical stimulation of median nerve (MN) and posterior tibial nerve (PTN) in twenty-three normal subjects and twenty-five diabetic patients. The peak latencies of SEPs components were prolonged, and the afferent conduction velocities of MN and PTN were reduced in most patients. In some patients, the central conduction time (N13-N20 and P40-N80 conduction time) was prolonged. Besides, there was a significant change in the shape of triphasal potentials recorded from Erb's point.and popliteal fossa. These results suggest: there not only was abnormality of conductive function of peripheralnerves, but also, the conductive function of central nervous system might be involved in diabetes mellitus.

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Beneficial effects of droxicainide on ventricular fibrillation and infarct size after coronary occlusion

Anyun SHI

Chinese Journal of Pathophysiology.1986;0(01):-.

The effect of droxicainide was investigated in a rabbit model of myocardial ischemia and reperfusion. The rabbits were randomized to either a saline-treated control group (n=18) or a droxieainide-treated group (n=11). In the control group, the incidence of ventricular fibrillation after coronary ligation was 14/18 (77.7%) and nine died (64.3%). Ventricular fibrillation occurred in eight (72.7%) droxieainide treated rabbits, but all reverted spontaneously (P

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Effects of several factors on ability of amino acid uptake by regenerating rat liver

Ping LIU

Chinese Journal of Pathophysiology.1986;0(02):-.

24hr after partial hepatectomy, the isolated remnant liver of rat was perfused to study the effects of several factors on the ability of amino acid intake. The results were as follows: (1). Twenty-four hours after operation the hepatic uptakes of amino acid increased in the hepatectomized groups. The ability of enhanced amino acid uptake by remnant liver depended on hepatic protein synthesis. In a certain range of hepatectomy there was a positive correlation between the amounts of liver which had been cut off and the amounts of amino acid uptake by remnant liver. (2). The addition of insulin alone to the perfusate could stimulate amino acid uptakes by remnant liver and the addition of glucagon alone had no effect. But, when insulin was added to the perfusate in combination with glucagon the hepatic uptake of amino acid was much higher. (3). The extract from regenerating rat liver rather than that from normal adult rat liver may contain certain factor(s) which can stimulate amino acid uptakes by remnant liver.

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Effect of needling on the endogenous pyrogen fever of rabbit

Chenglong SHI

Chinese Journal of Pathophysiology.1986;0(02):-.

Fever model induced by endogenous pyrogen was used to study the effect of needling "Bai hui" point on fever. 126 rabbits served as experimental animal. The present experiment was divided into three parts: Ⅰ. Ⅱ. (injection of pyrogen)and Ⅲ. (no injection), and each part was redivided into experimental (needling "Bai hui" point or "non-channel point) and control (no needling) groups.The findings were: (1) In febrile rabbits induced by endogenous pyrogen, needling "Bai hui" points had significant febrifugal effect, i.e, inhibiting the rise of body temperature, increasing the amplitude of defervescence and accelerating the febrifugal rate. (2) In febrile rabbits, needling "non-channel points" had no marked febrifugal effect, i. e. showing the rise of body temperature, after that, accelerating the febrifugal rate. (3) On body temperature of healthy rabbits, needling "Bai hui" points hnd no hignificant effect.

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Effect of PP60c-Src on Ang Ⅱ- induced signal transduction in rat vascular smooth muscle cells

Meixiang XIANG ; Dong LIU

Chinese Journal of Pathophysiology.2005;21(4):685-689.

AIM: The aim of the present study was to clarify the mechanism of intracellular signal transduction in Ang Ⅱ- induced proliferation of vascular smooth muscular cells (VSMC) by observing the effect of c- Src on Ang Ⅱ- mediated mitogen- activated protein kinase (MAPK) activation and c- Fos protein expression in cultured VSMC of rats. METHODS: Cultured aortic VSMCs from SD rats were transfected with anti-sense c-Src oligodeoxynucleotides (ODNs) wrapt with lipofectin to inhibit c- Src activity and protein production. Untransfected VSMCs were used as control. We observed the role of Ang Ⅱ stimulation in MAPK activation and c- Fos protein expression. c- Src kinase activity was measured by protein immunoprecipitation and kinase autophosphorylation. The phosphorylation rate of the substrate myelin basic protein (MBP) was employed to assess MAPK activity.Western immunoblot was used to detect protein expression of c- Src and c-Fos. RESULTS: c-Src protein expression in VSMC transfected with different concentrations of anti- sense ODNs significantly decreased in a negative dose- effect manner. c- Src kinase activity was also markedly inhibited. Following the stimulation of Ang Ⅱ on transfected VSMCs with anti-sense ODNs, the increase rate of c- Src activity was 8.7% of that in control, the activity of MAPK was 1.6% compared with control and c- Fos protein expression was as 30.0% as that of control. CONCLUSION: Ang Ⅱ induces c- Src activation. MAPK activation and c - Fos protein expression by Ang Ⅱ is dependent on c- Src activation. These findings indicate that c- Src is an important signal factor in Ang Ⅱ-induced VSMC proliferation.

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Growth-inhibitory effects of selective cyclooxygenase-2 inhibitor on colon cancer cells and its possible mechanisms

Xiaoqing JIA ; Lihui HAN ; Ning ZHONG ; Fanli MENG ; Ming YAN ; Wenjie LI ; Yanqing LI ; Shangzhong ZHANG

Chinese Journal of Pathophysiology.2005;21(5):985-989.

AIM: To evaluate the growth-inhibitory effects of NS-398, a selective cyclooxygenase-2 inhibitor, in human colon cancer HT-29 cells and its possible mechanisms. METHODS: MTT assay was applied to detect the cell proliferation. Flow cytometry was performed to detect apoptosis rate and cell cycle. RT-PCR was used to detect the expression of bcl-2 mRNA and bax mRNA. Alteration of cytoskeleton component F-actin was observed by confocal laser scanning microscope. RESULTS: NS-398 could inhibit growth of HT-29 cells in dose-and time-dependent manners. Flow cytometry revealed that NS-398 could induce apoptosis and cause G0/G1 arrest of HT-29 cells in a dose-dependent manner. After 72 h incubation with NS-398 at different concentrations, the expression level of bcl-2 mRNA was lowered and the ratio of bcl-2 to bax was decreased in HT-29 cells. F-actin was mainly distributed around nuclei forming annular structure in HT-29 cells. After exposure to NS-398, the annular structure around nuclei disappeared and fluorescence intensity of F-actin decreased obviously. CONCLUSION: NS-398 can inhibit the growth effectively and induce apoptosis in HT-29 cells in vitro, which is associated with the down-regulation of bcl-2 to bax ratio and the disruption of cytoskeleton.

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Pulmonary function in patients with type 2 diabetes mellitus

Shanping JIANG ; Liwen HUANG ; Yiqun LI ; Guojuan LAO ; Helin DING ; Yan LI ; Li YAN

Chinese Journal of Pathophysiology.2005;21(3):574-579.

AIM: To evaluate the pulmonary function in patients with type 2 diabetes mellitus in order to identify whether the lung is a target organ of chronic pathologic changes in diabetes mellitus. METHODS: Pulmonary ventilation function and diffusion capacity were studied in 107 patients with type 2 diabetes mellitus and 61 healthy subjects matched for age and sex. Glycosylated hemoglobin (HbA1c), urine albumin excretion rate (AER), fundus examination and nerve conduction velocity were included as parameters of glycemic control and diabetic microangiopathies. RESULTS: Pulmonary ventilation function was similar in type 2 diabetic group and the control. Compared with the control, carbon monoxide diffusion capacity (DLCO) and DLCO corrected by alveolar volume (DLCO/VA) were significantly lower in type 2 diabetic group (P<0.05). DLCO and DLCO/VA were inversely correlated with microangiopathy score (r: -0.291, -0.324, respectively, P<0.01). Furthermore, DLCO/VA was negatively correlated with age and duration of diabetes mellitus (r: -0.269, -0.236, respectively, P<0.05). CONCLUSIONS: Pulmonary ventilation function is normal in patients with type 2 diabetes mellitus, but their diffusion capacity is impaired. It suggests that the lung may also be the target organ of the chronic pathologic changes of diabetes mellitus.

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Conjugated agent insulin-antisense-c-myb-PS-ODN enhances the inhibitory effect on proliferation of rat aortic artery smooth muscle cells

Guanghui YI ; Shangzhi XIAO ; Yongzong YANG

Chinese Journal of Pathophysiology.2001;17(8):772-773.

AIM:Vascular smooth muscle cell (SMC) proliferation and migration from the arterial wall media into the intima are believed to play a critical role in the pathogenesis of restenosis. Several studies have demonstrated that phosphothioate (PS) oligodeoxynucleotides targeted against genes involved in SMC proliferation inhibits in vitro SMC proliferation and migration. However, the therapeutic effect of antisense ODN on the individual who receives the treatment of delivery of the agent depends on the efficacy of this agent in great degree. We investigated the inhibition effect of a novel agent, insulin-antisense-c-myb-PS-ODN on SMC proliferation in vitro.　METHODS：The rat aortic artery SMCs were cultured in Dulbecco's modified Eagel's medium. The passage 8 to 13 were used as the experiment. Cell surface receptor binding assay was quantified through counting gamma particles emitted from 125　　　　I labeled insulin. SMC rapid proliferation was brought by stimulation of high concentration of fetal bovine serum (FBS). The novel agent of insulin conjugated to the antisense-c-myb-PS-ODN was obtained via incubation of both in condition of certain reagents, pH, temperature, and ion concentration. The characterization and purification of the agent was performed through HPLC. Inhibition of SMC proliferation was reflected by incorporation rate of trillium labeled thymidine deoxyribonucleotide.RESULTS：The binding efficacy of insulin to the receptor was remarkably increased in SMC cultured in supplement of 20% FBS. The inhibition effect of conjugator insulin-c-myb-antisense-PS-ODN was stronger than that of the simple c-myb-antisense-PS-ODN. The inhibition rate of conjugator and simple form on SMC proliferation were 48.34% and 29.54%, respectively. CONCLUSION：The binding efficacy and specificity of c-myb-antisense-PS-ODN to SMC may be enhanced by the insulin receptor mediation through the insulin-insulin receptor interaction. The insulin-receptor targeted method may be a potential and specific therapeutic pathway for restenosis.

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Effect of cholecystokinin-octapeptide on changes in rabbit pulmonary artery reactivity induced by tumor necrosis factor-alpha in vitro and the preliminary study of its mechanisms

Aihong MENG ; Yiling LING ; Dianhua WANG ; Zhenyong GU ; Shujin LI ; Tienian ZHU

Chinese Journal of Pathophysiology.2001;17(8):771-772.

AIM：The mechanism of tumor necrosis factor-alpha (TNF-α) induced pulmonary artery hypertension(PAH) in endotoxic shock (ES) is not clear. Cholecystokinin-octapeptide (CCK-8) had anti-ES and anti-PAH effects. The impact of CCK-8 on changes in vascular reactivity and endothelial ultrastructure induced by TNF-α was studied. The role of nitric oxide (NO) was preliminarily studied. METHODS：Rabbit pulmonary artery rings were divided into four groups: TNF-α, TNF-α+CCK-8, CCK-8 and Vehicle. The rings were incubated for 2 h, 7 h or 14 h. Relaxative responses to ACh(10-8-10-5 mol/L)， SNP (10-9-10-6 mol/L) and contractile responses to PE(10-8-10-5 mol/L) were generated seperately. The NOS activity of rings was detected and the ultrastructure of endothelium was observed in the groups that incubated for 7 h.RESULTS:The relaxative responses to ACh were not affected by TNF-α and CCK-8 after incubation for 2 h. TNF-α(7 h,14 h) significantly reduced ACh-induced endothelium-dependent relaxation response of pulmonary artery. CCK-8 reversed the effect. CCK-8 itself had no effect on responses of normal pulmonary artery. Contraction to PE and relaxation to SNP were unaffected by TNF-α, CCK-8. The NOS activity increased in the TNF-α and the TNF-α+CCK-8 groups. While no significant difference was obseved between the Vehicle and the CCK-8 groups. Endothelial injury in TNF-α group and alleviated changes in TNF-α+CCK-8 group were observed. CONCLUSION:TNF-α significantly inhibits endothelium-dependent relaxation, which be one of the mechanisms of PAH induced by TNF-α during ES. It was found for the first time that CCK-8 reversed TNF-α induced impairment of endothelium-dependent relaxation and alleviated structural injury of endothelium, which might be one of the mechanisms of anti-PAH effect by CCK-8 during ES. The effects of TNF-α and CCK-8 might be related to NO.

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