ObjectiveTo investigate the influence of norepinephrine on pulmonary vessel pressure in animal model of septic shock. MethodsTwelve health mongrel dogs were randomly divided into a control group (n=5, intravenously injected with normal saline 1 mL/kg) and an endotoxin group(n=7, intravenously injected with lipopolysaccharide 1 mg/kg). When the systemic blood pressure decreased by more than 40% of baseline before administration, the dogs in two groups were intravenously injected with NE 0.5, 1.0, 2.0, 5.0μg·kg-1·min-1. The interval of each dose was more than 10 minutes. The changes of the pulmonary arterial pressure (PAP), pulmonary venous pressure (PVP), and systemic arterial rressure (SAP) were recorded and compared between two groups. ResultsIn the control group, PAP didn't change significantly after administration (P < 0.05), however, PVP increased obviously after NE administration in dose of 2.0 and 5.0μg·kg-1·min-1 (P < 0.05), and SAP increased obviously after NE administration in dose of 1.0, 2.0 and 5.0μg·kg-1·min-1 (P < 0.01). In the endotoxin group, PAP increased obviously after NE administration in dose of 2.0 and 5.0μg·kg-1·min-1 (P < 0.05), while PVP didn't change significantly (P > 0.05), and SAP increased obviously after NE administration in dose of 1.0, 2.0 and 5.0μg·kg-1·min-1 (P < 0.05). There were significant differences in SAP (P < 0.05), not in PAP and PVP (P > 0.05), between two groups after NE administration at dose of 1.0, 2.0 and 5.0μg·kg-1·min-1. The PVP/SAP and PAP/SAP values didn't change significantly after administration in the control group (P > 0.05). In the endotoxin group, the PVP/SAP and PAP/SAP values increased significantly after LPS administration, and decreased slightly after NE administration in dose of 2.0 and 5.0μg·kg-1·min-1 (P < 0.05). ConclusionsNE administration in septic shock can not increase the angiotasis of the pulmonary vein. NE administration in dose of 2.0 and 5.0μg·kg-1·min-1 can cause the increase of PAP and SAP, but the increase of PAP is lower than the increase of SAP.
ObjectiveTo investigate the regulatory roles and changes of M3 receptor subtype in lipopolysaccharide (LPS)-preincubated rabbit pulmonary arteries, and assess the mechanism of altered vascular reactivity in septic shock. MethodsPulmonary arteries with intact endothelium were isolated from 26 male New ealand white rabbits weighing 2.0 to 2.5kg. he isolated pulmonary arteries were randomized into two grouops, including a normal group with normal saline and darifenacin adminstration, and an endotoxin group with LPS-preincubation and darifenacin adminstration.he response of arteries to phenylephrine (100μmol/L) and acetylcholine(ACH)(1μmol/L, 10μmol/L, 100μmol/L)were measured in normal and darifenacin-preincubated circumstances. ResultsThe percentages of ralaxation to ACH (1μmol/L, 10μmol/L, 100μmol/L) were (0.095±0.034)%, (0.150±0.036)%, and (0.445±0.090)% in the normal group, and (0.044±0.016)%, (0.093±0.029)%, (0.311±0.028)% in the endotoxin (LPS 4μg/mL, 4h) group. After pretreatment with M3 receptor antagonist darifenacin on different concentrations, the EC50 values responding to ACH (1μmol/L, 10μmol/L, 100μmol/L) were 1.483, 2.757, 2.958 in the normal group, and 6.015, 6.242, 6.411 in the endotoxin group. After pretreatment with M3 receptor antagonist darifenacin on different concentrations, the inherent activity of a value to ACH (1μmol/L, 10μmol/L, 100μmol/L) were 0.0146, 0.0323, 0.0825 in the normal group, and 0.0124, 0.0245, 0.0556 in the endotoxin group. ConclusionsLPS pre-incubation can reduce the relaxation response to ACH, and M3 receptor subtypes mediated this relaxation response. LPS also reduce the M3 receptor subtype intrinsic activity, which may be one of the mechanisms of decreased relaxation response to ACH in pulmonary arteris after LPS pretreatment, and also one of the mechanisms of pulmonary hypertension in septic shock.
Objective To compare the vasoactive effects of norepinephrine( NE) and dopamine of different doses on isolated rabbit pulmonary and systemic arteries in septic shock. Methods Six paired pulmonary and systemic arterial rings were prepared fromsix rabbits, and matched randomly assigned into a normal group and a LPS group. The assigned groups were intervened by different doses of NE. Another six paired pulmonary and systemic arterial rings were prepared from another six rabbits. They were assigned to different groups as above and intervened by different doses of dopamine. The LPS groups were pre-incubated in RPMI mediumsupplemented with4 μg/mL LPS to simulate septic shock. The tension of arterial rings was measured and its response to NE and dopamine were studied. Results ( 1) In the normal groups, the contraction of the systemic arteries was ber than the pulmonary arteries in response to low,middle dose of NE, and high dose of dopamine ( all P lt; 0. 05) , and which was weaker in response to middle dose of dopamine and similar in response to high dose of NE( P gt;0. 05) . Both the pulmonary and systemic arteriesrelaxed in response to low dose of dopamine. ( 2) After LPS pre-incubation, the contraction of the systemic arteries was weaker than the pulmonary arteries in response to low dose of dopamine ( P lt;0. 05) , and which was similar in response to low,middle and high dose of NE, and middle, high dose of dopamine. ( 3) Comparing the LPS groups with the normal groups, the contraction in response to middle dose of dopamine increased in the systemic arteries and dreased in the pulmonary arteries ( P lt;0. 05) . Conclusions In septic shock, the vasoactive effect of different doses of NE is not different between pulmonary and systemic arteries. But middle dose of dopamine can increase the contraction of systemic arteries and decrease the contraction of pulmonary arteries.
ObjectiveTo systematically review the effectiveness and safety of bupropion for smoking cessation in smokers with cardiovascular disease. MethodsDatabases including The Cochrane Library, PubMed, EMbase, Web of Science, CBM, CNKI, WanFang Data and VIP databases were electronically searched from inception to February 23rd, 2013. Randomized controlled trials (RCTs) on bupropion versus placebo for smoking cessation in smokers with cardiovascular disease were included. Two reviewers independently screened literature according to the inclusion and exclusion criteria, extracted the data, and assessed the methodological quality of included studies. Meta-analysis was performed by using RevMan 5.1 software. ResultsIn total, 4 studies involving 1 415 patients were finally included. The results of metaanalyses indicated that, compared with placebo, bupropion significantly increased the point prevalence abstinence rate at 3 months (RR=1.79, 95%CI 1.14 to 2.83, P=0.01). However, the point prevalence abstinence rates at 6 months (RR=1.81, 95%CI 0.77 to 4.24, P=0.18) and 12 months (RR=1.46, 95%CI 0.94 to 2.27, P=0.10), and the continuous abstinence rates at 3 months (RR=1.48, 95%CI 0.89 to 2.47, P=0.13), 6 months (RR=1.41, 95%CI 0.79 to 2.51, P=0.25), and 12 months (RR=1.43, 95%CI 0.93 to 2.17, P=0.10) were similar in the two groups. The use of bupropion did not increase all-cause mortality (RR=1.13, 95%CI 0.49 to 2.56, P=0.78) and the incidence of cardiovascular events (RR=1.25, 95%CI 0.95 to 1.64, P=0.11). ConclusionBupropion is safe to use in smokers with cardiovascular disease. Although bupropion could increase the point prevalence abstinence rate at 3 months, it is not effective for long-term smoking cessation. Due to the limited quantity and quality of the included studies, more large-scale high-quality RCTs are required to verify the aforementioned conclusion.
ObjectiveTo observe the relationship of serum tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), and C-reactive protein (CRP) with obstructive sleep apnea hypopnea syndrome (OSAHS) associated pulmonary hypertension (OSAHS-PH). MethodsFrom September 2013 to October 2014, 38 OSAHS patients, 32 OSAHS-PH patients and 35 healthy subjects were enrolled from the General Hospital of Ningxia Medical University. OSAHS was diagnosed by polysomnography. The pulmonary artery systolic pressure (PASP) was measured by echocardiograph, and the diagnose criteria for pulmonary hypertension was PASP≥40 mm Hg. Serum TNF-α, IL-6, CRP and endothelin 1 (ET-1) were detected by enzyme-linked immunosorbent assay. The correlation between TNF-α, IL-6, CRP, ET-1 and PASP was analyzed. ResultsThe serum levels of TNF-α, IL-6, CRP and ET-1 were remarkably different among three groups (F=55.34, 25.05, 23.85, 34.06 respectively; all P < 0.05). The levels of TNF-α, IL-6, CRP and ET-1 in the OSAHS group were higher than those in the healthy group, and lower than those in the OSAHS-PH group (all P < 0.05). The PASP was positively correlated with the levels of the four factors (r=0.755, 0.762, 0.747, 0.759 respectively; all P < 0.01). ConclusionThe levels of serum TNF-α, IL-6 and CRP are correlated with pulmonary hypertension and they may be involved in the process of OSAHS-PH.