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.

This experiment, using cultured bovine pulmonary artery endothelial cells (BPAEC), was undertaken to investigate roles of endogenous ONOO- in lipopolysaccharide (LPS)-caused injury to endothelial cells. The fluorescent intensity of nitrotyrosine (NT), a marker of ONOO- generation, in BPAEC represented content of endogenous ONOO- generation. The fluorescent intensity of NT and number of NT positive cells were detected with flow cytometry, and the percentage of NT positive cells was calculated. Results were as follows. (1) LPS (1 mg/L, 5 mg/L and 10 mg/L) caused marked increase in fluorescent intensity of NT in a dose dependent manner. The number and percentage of NT positive cells were markedly increased (P＜0.05). Aminoguanidine (AG), a selective inhibitor of inducible nitric oxide synthase, inhibited the increase in fluorescent intensity of NT in BPAEC induced by LPS. However, the number and percentage of NT positive cells had tendency to reduce. (2) LPS caused the enhancement of MDA content and activity of LDH in cultured supernatant (P＜0.01). AG reversed the enhancement of MDA content induced by LPS (P＜0.01). In contrast, AG had marginal effect on activity of LDH. (3) LPS induced the increase in apoptotic rate in BPAEC in a dose dependent manner. Some BPAEC stained with fluorescent probe ethidium bromide showed morphological features of apoptosis with chromatin condensation and nuclear fragmentation. AG reduced the apoptotic rate and number of apoptotic cells, both of which were still higher than those of vehicle group (P＜0.05). (4) LPS inhibited mitochondrial respiration. Effect of LPS on mitochondrial membrane potential (ΔΨ) depended on the doses of LPS. 1 mg/L LPS led to a little increase in ΔΨ, while 5 mg/L and 10 mg/L LPS significantly reduced ΔΨ. In conclusion, LPS caused injury to cultured BPAEC and increased production of ONOO-. Cytotoxicity of LPS may be mediated by endogenous ONOO-.

Abstract The variation of functional protein C (PC), the activities of total plas. minogen activator and antithrombin Ⅲ (ATⅢ) were observed in canine SMAO shock. The results indicated that under normal conditions, compared with into-pulmonary blood (IPB), in out-pulmonary blood (OPB) the functional PC increased and ATⅢ activity decreased significantly (P

The concentrations of CuZn-SOD and malondialdehyde (MDA) in in-flowingand out-going pulmonary blood(IPB, OPB) were observed dynamically during intestinal ischemic-reperfusion in rabbits. The results showed that in normal subjects the content of SOD of OPB was higher than IPB, P

In this study we found: 1\, There was endogenous ONOO- formation in lungs in the early stage of endotoxic shock. Exogenous ONOO- led to increase in microvascular permeability, severe lung pathological changes and enhanced MDA content. 2\, It was, for the first time, found that responses of isolated pulmonary artery preincubated with ONOO- showed abnormal manifestations. (1) Low dose of ONOO- let to the inhibition of endothelial dependent relaxation, but enhacement of contractile response, both of which were similar to changes of reactivity in isolated pulmonary artery induced by LPS. (2) High dose of ONOO- reduced contractile response to PE and relaxation to SNP. 3\, ONOO- had direct effect for relaxation of precontracted isolated pulmonary artery. The relaxing action of ONOO- was weak and was negtively regulated by endothelial cells, supporting the notion that ONOO- may be involved in pulmonary hypertension in the early stage of endotoxic shock. 4\, It was, for the first time, found that LPS-induced increase in endogenous ONOO- generation in BPAEC and that endogenous ONOO- mediated injury to BPAEC induced by LPS, which may be a novel mechanism for endotoxin-elicited damage to endothelial cells. 5\, Exposure of pulmonary artery to LPS led to reduction in endothelial dependent relaxation but enhancement in contractile response, both of which were reversed by concomitant exposure to CCK and LPS. 6\, CCK protected cultured BPAEC against the detrimental effects of LPS such as lipoperoxide damages and cellular apoptosis as well as LPS-induced endogenous ONOO- formation. The underlying mechanism of CCK for cytoprotection may be mediated by its receptors and related to its reduced ability of endothelia to generate ONOO- induced by LPS.

Our previous experiments confirmed that endothelial derived ONOO- mediated injury to cultured BPAEC induced by LPS, and that CCK protected endothelial functions against the detrimental effect of LPS in vitro. In the present study, using cultured BPAEC, we investigated effect of CCK on LPS-induced generation of ONOO- in BPAEC and on injury to BPAEC induced by LPS. Results were as follows.(1)CCK inhibited increase in endothelial generation of ONOO- induced by LPS, for fluorescent intensity of NT in BPAEC reduced from (6.55±0.30) AU of LPS group to (4.37±0.08) AU (P＜0.01), the latter being still higher than (3.27±0.15) AU of vehicle group (P＜0.01). In contrast, the number and percentage of NT positive cells reduced a little. Proglumide, a nonspecific inhibitor of CCK receptors, might in part reverse the effect of CCK. (2)CCK markedly reduced MDA content in supernatant in LPS group (P＜0.01), which was completely reversed by proglumide(P＜0.01). Activities of LDH in supernatant in LPS, LPS+CCK group were (85.30±8.66) U/L and (71.33±4.07) U/L, respectively. Proglumide elicited increase in activity of LDH ［(81.00±6.35) U/L］. However, effect of CCK or proglumide was not significant in the alterations of activity of LDH. (3)CCK significantly inhibited increase in apoptotic rate in BPAEC induced by LPS, from 13.50%±0.60% of LPS group to 5.35%±0.25%(P＜0.001), the latter being completely reversed by proglumide with apoptotic rate of 11.45%±0.65%(P＜0.05).These results further confirmed that CCK afforded the cyoprotection for the mitigation lipoperoxide damage and inhibition of apoptosis in BPAEC induced by LPS. The cytoprotection of CCK may be mediated by CCK receptors and related to the reductive ability of endothelia to generate ONOO- induced by LPS.

Objective To explore the relationship between total bile acid(TBA)concentration and fetal pulmonary surfactant in intrahepatic cholestasis of pregnancy(ICP).Methods Fifry five patients with ICP(ICP group)who received cesarean section from April 2008 to February 2010 in Second Xiangya Hospital,Central South University,were recruited.The general conditions of the neonates within 7 days after birth in ICP group were recorded.Those with fetal distress,neonatal asphyxia,or neonatal respiratory distress syndrome were referred as pathological neonates, others were referred as normal neonates. Over the same period, 23 healthy gravidas were recruited as control group. Enzymatic method was used to detect the TBA concentrations in maternal blood, cord blood and amniotic fluid. ELISA was employed to measure the urfactant protein A (SP-A) concentration in cord blood. High performance liquid chromatography system was used to detect the concentrations of phesphatidylcholine (PC),phosphatidylinositol (PI),lysophosphatidylcholine ( LPC), and sphingomyelin(SM) in amniotic fluid. Results ( 1 ) The concentrations of TBA in maternal blood, cord blood and amniotic fluid were ( 30. 1 ± 7.9 ), (9. 3± 3. 3 ) and (4. 4 ± 1.5 ) mmol/L in ICP group, (4. 8 ± 2. 2), (4. 9 ± 0. 9) and ( 1.4 v 1.1 ) mmol/L in control group, respectively. The differences between the two groups were significant ( P ＜ 0. 05 ). ( 2 ) The SP-A concentration in cord blood in ICP group was ( 29. 5 ± 6. 4 ) μg/L, significantly higher than that in control group, which was ( 22. 6 ± 7. 4 )μg/L ( P＜ 0. 05 ). ( 3 ) There were 20 pathological neonates and 35 normal neonates in ICP group. In pathological neonates, the concentrations of TBA and SP-A in cord blood were (10.9 ± 2.2) mmol/L,(37.0 ± 5.9 ) μg/L, respectively; and were ( 8.0 ± 2. 8 ) mmol/L, ( 26. 7 ± 4. 8 ) μg/L in normal neonates. The differences were significant (P＜ 0. 05 ). (4) There was a positive correlation between TBA concentration in cord blood and in maternal blood ( r1 = 0. 706, P＜0. 05 ). The TBA concentration in cord blood was positively correlated with SP-A concentration as well ( r3 = 0. 494,P ＜ 0. 05 ). (5) The PC and PI concentrations in amniotic fluid were (65.4 ± 7.2) mg/L and ( 3. 8 ± 0. 6 ) mg/L in ICP group, ( 69. 7 ±3.7) mg/L and (4. 3 ± 0. 7 ) mg/L in control group, respectively. The differences were significant (P ＜0. 05 ). The concentration of LPC in amniotic fluid in ICP group was (4. 8 ±0. 9) mg/L, significantly higher than that in control group (P＜0. 05), which was (4. 2 ±0. 6) mg/L. The concentration of SM in amniotic fluid was (3.5±0. 8) mg/L in ICP group, (4. 0 ± 0. 5 ) mg/L in control group, with no significant difference ( P＞0. 05 ). (6) The ratio of PC/LPC in ICP group ( 14. 2± 3. 2 ) was significantly lower than that in control group ( 16. 9 ± 2. 5 ) ( P＜ 0. 05 ). ( 7 ) The TBA concentration in cord blood was negatively correlated with PC and PI concentrations (r1 = -0. 561, r2 = -0. 407, P ＜ 0. 05 ), and had no correlation with LPC concentration (r3 = 0. 260, P＞ 0. 05). Conclusions ( 1 ) The fetal TBA concentrations in both cord blood and amniotic fluid of patients with ICP was higher than those of healthy gravidas, they were also positively correlated with maternal TBA concentration. (2) ICP resulted in the change of fetal pulmonary surfactant and this change was associated with TBA concentrations in both cord blood and amniotic fluid.

OBJECTIVETo observe the effects of bloodletting pricking, cupping and surrounding acupuncture on blood inflammation-related indices in patients with acute herpes zoster (HZ), and to explore the mechanism of pain control and treatment.

METHODSA total of 60 patients were randomly divided into an observation group and a control group, 30 cases in each one. In the observation group, the patients were treated with bloodletting pricking at herpes, followed by cupping treatment; also the surrounding acupuncture was performed at injured skin. The treatment was given once a day and once every other day after the first 3 days; totally one-week treatment was given. In the control group, the patients were treated with intravenous drip of acyclovir and oral administration of vitamin B1 and B12, once a day for total one week. The visual analogue scale (VAS) and percentages of neutrophil, lymphocyte in peripheral and local blood were observed before and after treatment in the two groups.

RESULTSAfter treatment, the score of VAS was significantly reduced in both groups (both P < 0.05); compared with the control group, the score of VAS and the time of pain relieve were significantly improved in the observation group (P < 0.01, P < 0.05). Compared before treatment, the percentages of lymphocyte in peripheral and local blood were reduced after treatment (both P < 0.05) and the percentages of neutrophil in local blood were increased (both P < 0.05). The lymphocyte in local blood was also reduced after treatment in the control group (P < 0.05); compared with peripheral blood in the observation group and local blood in the control group, the percentages of lymphocyte in local blood were reduced (both P < 0.05).

CONCLUSIONThe efficacy of bloodletting pricking, cupping and surrounding acupuncture on acute herpes zoster is positive, and it can significantly lower the number of lymphocytes in the local blood and increase the number of neutrophil, which is likely to be one of the anti-virus mechanisms.

Acupuncture Therapy ; Adolescent ; Adult ; Aged ; Bloodletting ; Combined Modality Therapy ; Female ; Herpes Zoster ; blood ; immunology ; therapy ; Humans ; Male ; Middle Aged ; Neutrophils ; immunology ; Pain Management ; Young Adult

Objective To study the expression of activator protein-1(AP-1)and connexin 43(Cx43)in uterine smooth muscle of term pregnancy and its relationship with preterm delivery.Methods Immuno-histochemistry was applied for 15 uterine smooth muscle samples of term pregnancy without labor(Group Ⅰ),15 of term pregnancy in labor(group Ⅱ)and 10 of preterm delivery in labor(group Ⅲ)to investigate the expression of two subunits of AP-1(c-Jun and c-Fos)and Cx 43. Results (1)The expression of Cx43 in group Ⅰ and Ⅱ(4.33±0.51 and 4.20±0.42)were significantly higher than that in group Ⅲ(3.15±0.41,P<0.01).Lable index of c-Jun protein in group Ⅲ,Ⅱ and Ⅰ was(52.34±4.18)%,(45.25±5.24)%and(34.14±4.26)%,respectively (P<0.01),and the lable index of c-Fos protein was(53.48±4.36)%,(43.32±6.21)%and(31.29±3.34)%,respectively(P<0.01).Positive correlation was found between the expression of Cx43and c-Jun,c-Fos in pregnancy uterine smooth muscle(r=0.65,0.63,P<0.01). ConclusionsThe Cx43 plays an important role in the onset of labor.The expressions of Cx43 is positively related with the expression of AP-1 in pregnancy uterine smooth muscle.

Recent studies show that cholecystokinin, a brain-gut peptide, also locates in lung tissues in many animals. Cholecystokinin in lung tissues participates in the modulation of the tone of the tracheae and the pulmonary vessels. It also regulates the breathing pattern as a nerve transmitter in the respiratory center. This paper discusses the location and the biological role of cholecystokinin in lung tissues and focuses on its part during lung diseases.