Effect of cigarette smoking on the gastric mucosal blood volume index and hemoglobin oxygenation in man

The acute effect of cigarette smoking on the gastric mucosal blood volume index and the oxygen saturation of hemoglobin (SO2) in the gastric mucosa was investigated in 12 young male volunteers using reflectance spectrophotometry during endoscopy. Six of these volunteers were habitual smokers who had smoked more than 20 cigarettes a day for more than five years. The others were non-habitual smokers who smoked less than 20 cigarettes a year. The indices of mucosal blood volume and the mucosal blood SO2 level were calculated from the spectra obtained at the lesser curvature of the lower corpus of the stomach before and after cigarette smoking. The indices of mucosal blood volume and mucosal blood SO2 decreased significantly after one to three puffs of cigarette smoking in all subjects as compared to the value before smoking, and the degree of decrease in these parameters was significantly greater in the non-habitual smokers than in the habitual smokers. These results suggest that only one to three puffs of cigarette smoking causes a decrease in the mucosal blood volume and the mucosal blood SO2 which might be related to weakening of mucosal defensive factors.     

Effect of hepatic collateral hemodynamics on gastric mucosal blood flow in patients with liver cirrhosis

The dependence of the gastric mucosal change in liver cirrhosis on the extrahepatic collaterals is still unknown. Therefore we studied the influence of these collateral hemodynamics on gastric mucosal blood flow and gastric mucosal lesions. The subjects were 23 cirrhotic patients and were divided into two groups by the findings of percutaneous transhepatic portography. The first group consisted of 14 cases whose extrahepatic collaterals were via esophageal varices (group I). The second group included 9 cases having collaterals other than esophageal varices (group II). Multiple red spots were observed in 13 of 14 cases in group I, and two of nine cases in group II. Gastric mucosal blood flow was 2.0±0.9 volts (mean±sd) in group I, 4.0±1.2 in group II. A statistically significant difference was observed between groups I and II. Gastric mucosal blood flow was not significantly correlated with portal venous pressure in group I. It is concluded that, in liver cirrhosis, gastric mucosal blood flow is changeable according to the types of the extrahepatic collaterals.     

Seasonal differences in blood cell parameters and the association with cigarette smoking

Summary Seasonal changes in red cell parameters need to be defined in order to properly interpret laboratory results. In this study blood counts were obtained prospectively in 104 healthy men (84 non-smokers and 20 smokers) aged 28–63 years during the summer and winter months. Seasonal changes in plasma volume were also calculated. In healthy non-smokers, their haemoglobin concentration and haematocrit ratio were lower in summer than in winter with a concomitant 5.5% increase in plasma volume. In smokers, there was no change in plasma volume, but haematocrit levels increased in summer. We conclude that both smoking status and seasonal variation should be taken into account in the evaluation of blood count results. Further studies are warranted to determine if our results can be extrapolated to subjects of both sexes and of various ages exposed to different climatic conditions.     

The effects of a prostaglandin E1 analogue, misoprostol, on gastric mucosal blood volume index and haemoglobin oxygenation in humans

A double-blind placebo-controlled parallel design study was conducted in 12 healthy male volunteers to examine the effects of misoprostol, a newly synthesized prostaglandin E₁ analogue, on gastric mucosal haemodynamics in human. The indices of mucosal blood volume (expressed as ΔEr) and mucosal blood haemoglobin oxygenation (Hb-SO₂) were measured at 20 locations in the stomach prior to and after administration of misoprostol or its placebo using reflectance spectrophotometry during endoscopy. It was found that after misoprostol administration, mucosal blood volume was increased by approximately 10–25% throughout the stomach without any significant change in mucosal blood Hb-SO₂. Administration of placebo produced no significant change in these parameters. The results suggest that misoprostol has the potential to accelerate healing of gastric ulcers by increasing the gastric mucosal blood volume and oxygenation in addition to its gastric acid antisecretory activity.     

Doppler ultrasound evaluation of acute effects of cigarette smoking on portal blood flow in man

The acute systemic haemodynamic effects of cigarette smoking are well known, but there are no studies dealing with the possible smoke-related acute changes of splanchnic circulation in man. In the present study we evaluated the acute effects of cigarette smoking on portal blood flow (PBF) in normal subjects by the use of Doppler ultrasound. Twenty-three normal volunteers were asked to smoke two cigarettes with a known total nicotine content (1.1 mg each) in a supine position. Each cigarette was smoked during a 5 min period and a 5 min interval between the two cigarettes was allowed. Both mean PBF velocity and volume were evaluated at time 0 (basal values) and 8, 15, 30, 45 and 60 min after the first inhalation of the first cigarette. The basal mean PBF velocity (22 cm/s; 95% CI 20.9–24.2) was significantly decreased at 8 min (19 cm/s; 95% CI 17.9–20.8; P< 0.0007) and 15 min (20 cm/s; 95% CI 17.8–21.3; P< 0.005). Similarly, the PBF volumes at 8 min (710 mL/min; 95% CI 660–876; P< 0.002) and 15 min (750 mL/min; 95% CI 650–862; P< 0.005) were significantly lower than those measured at time 0 (850 mL/min; 95% CI 766–987). Both mean PBF velocity and volume measured at successive times did not differ significantly from basal values. The present study shows that cigarette smoking causes acute and transient reduction of PBF velocity and volume in normal subjects.     

Acute effects of Helicobacter pylori extracts on gastric mucosal blood flow in the mouse

AIM： To investigate the mechanisms underlying the reduction in gastric blood flow induced by a luminal water extract of Hellcobacter pylori （HPE）. METHODS： The stomachs of isoflurane-anesthetized mice were exteriorized, and the mucosal surface exposed. Blood flow was measured with the laserDoppler technique, and systemic arterial blood pressure monitored. C57BL/6 mice were exposed to water extract produced from Hpylori strain 88-23. To investigate the role of a nerveor iNOS-mediated pathway, we used intraluminal lidocaine and iNOS-/- mice. Blood flow response to the endogenous nitric oxide synthase inhibitor asymmetric dimethyl arginine （ADMA） was also assessed. RESULTS： In wild-type mice, HPE decreased mucosal blood flow by approximately 30%. This reduction was abolished in iNOS-deficient mice, and by pre-treatment with lidocaine. Luminally applied ADMA resulted in reduction in blood flow similar to that observed in wildtype mice exposed to HPE. CONCLUSION： A H py/ori water extract reduces gastric mucosal blood flow acutely through iNOS- and nerve-mediated pathways.     

Somatostatin reduces gastric mucosal blood flow in patients with portal hypertensive gastropathy

Agents which decrease gastric mucosal blood flow (GMBF) are postulated to have beneficial effects in arresting gastrointestinal bleeding in cirrhotic patients with portal hypertension. Our objective was to test the hypothesis that in a dose that significantly lowers wedged hepatic venous pressure (WHVP), a bolus injection of somatostatin will significantly decrease GMBF in patients with portal hypertensive gastropathy (PHG). In this placebo-controlled, double-blind, crossover study, 20 cirrhotic patients with PHG were randomly assigned to receive either somatostatin followed by placebo (Group A) or placebo followed by somatostatin (Group B). Wedged hepatic venous pressure was monitored. GMBF in the antrum and corpus was assessed by reflectance spectrophotometry. Indices of hemoglobin concentration (IHb) and indices of oxygen content (ISO₂) were recorded. Nine patients were assigned to Group A, and 11 to Group B. Mild PHG was seen in 16 patients, and severe PHG in 4 patients. Baseline WHVP, IHb, and ISO₂ were similar in both treatment groups. Wedged hepatic venous pressure (WHVP) was significantly lowered [median, 17.6%; interquartile range (–27.0, –12.6%); P=0.0008] after a 250-µg bolus injection of somatostatin. This dose of somatostatin significantly reduced IHb both in the antrum [–10.2% (–23.4, 0.4%)] and in the corpus [–5.8% (–16.6, 5.6%)] compared to placebo (P=0.02 and 0.04, respectively). Intravenous bolus injection of 250 µg somatostatin significantly reduces WHVP and GMBF in patients with PHG. Whether this ability to decrease the GMBF in PHG makes somatostatin an effective treatment in acute gastrointestinal bleeding in PHG deserves to be studied.     

垂体后叶素对门脉高压性胃病胃粘膜灌注的影响

目的 探讨垂体后叶素对门脉高压性胃病（ＰＨＧ）大鼠胃粘膜血流量（ＧＭＢＦ）和血浆胰高粘素的影响。方法 部分结扎大鼠门脉主干２ｗｋ后,采用激光多普勒血流计（ＬＤＦ）测定大鼠ＧＭＢＦ,观察了垂体后叶素输注前和输注后３０ｍｉｎ ＧＭＢＦ,门脉压力（ＰＶＰ）的变化;测定了输注垂体后叶素３０ｍｉｎ后血浆胰高糖素的含量。结果 输注垂体后叶素１０ｍｉｎ ＰＨＧ大鼠的ＧＭＢＦ开始降低（Ｐ〈０．０５）,１５ｍｉｎ显     

胃黏膜保护剂的作用及其机制的研究

目的 比较枸橼酸铋钾－1、枸橼酸铋钾－2及蔗糖硫酸酯碱式铝盐（硫糖铝）对胃黏膜的保护作用并研究作用机制。方法 采用乙醇、应激、阿司匹林及盐酸诱发大鼠胃黏膜急性损伤，用50％醋酸接触胃浆膜面产生慢性胃溃疡。枸橼酸铋钾－1、2和硫糖铝的急性损伤药物剂量分别为37.5,40和335mg/kg。给药3d，每天2次；慢性溃疡给药的剂量同急性损伤剂量，但给药11d，每天2次。检查损伤指数及溃疡面积。结果 （1）枸橼酸铋钾－1、枸橼酸铋钾－2和硫糖铝有低抗乙醇、应激、阿司匹林和盐酸诱发的胃黏膜损伤作用，并促进醋酸溃疡的愈合。（2）这种保护黏膜、促进溃疡愈合的作用机制与增加胃黏膜血流量、增加胃黏膜的醌还原酶、谷胱甘肽S－转移酶（GST）和谷胱甘肽还原酶（GR）的 活性及增加碱性成纤维生成因子（bFGF)mRNA和诱导型一氧化氮合酶（iNOS)mRNA的表达有关。结论 保护黏膜药枸橼酸铋钾－1、枸橼酸铋钾－2及硫糖铝有抵抗损伤，促进溃疡愈合的作用，其作用机制是增加胃黏膜血流量，减少氧自由基，增加bFGF及NOS。     

左旋精氨酸甲酯及左旋精氨酸对应激状态下胃黏膜耐受性细胞保护作用的影响

目的：探讨内源性一氧化氮（NO）在应激状态下胃黏膜耐受性细胞保护中的作用及其可能的机制。方法：以重复浸水束缚应激（WRS）制作动物模型,以左旋精氨酸甲酯（L－NAME）或左旋精氨酸（L－Arg）抑制或促进内源性NO的合成,动态检测胃黏膜血流量（GMBF）、溃疡指数（UI）、黏膜一化氮含量的变化。结果：重复应激后,实验对照组大鼠UI明显下降,同时GMBF上升,黏膜内NO含量增高;L－NAME使WWRS引起的胃黏膜损伤加重,消除了GMBF的递增趋势,黏膜NO含量下降;而L－Arg可减轻WRS造成的黏膜损伤,GMBF、黏膜NO含量增相应增加;GMBF、UI、黏膜NO含量变化之间有相关关系。结论：内源性NO通过调节GMBF而介导耐受性细胞保护作用,L－NAME抑制其合成,延缓这一作用,L－Arg增加其合成,促进该作用。     

Review of the role of cigarette smoking in diabetic foot

Diabetic foot ulceration has been a serious issue over the past decades in Asia, causing economic and social problems. Therefore, it is important to identify and reduce the risk factors of diabetic foot. Cigarette smoking has been reported to be associated with diabetes and its macrovascular complications, but the relationship between smoking and diabetic foot ulcers is still unclear. In the present review, we summarize the effects of cigarette smoking on diabetic foot ulcers with respect to peripheral neuropathy, vascular alterations and wound healing. One underlying mechanism of these impacts might be the smoking‐induced oxidative stress inside the cells. At the end of this review, the current mainstream therapies for smoking cessation are also outlined. We believe that it is urgent for all diabetic patients to quit smoking so as to reduce their chances of developing foot ulcers and to improve the prognosis of diabetic foot ulcers.     

埃索美拉唑对胃黏膜的保护作用及其机制

目的:探讨埃索美拉唑对大鼠胃黏膜保护的作用及其机制.方法:在乙醇诱导大鼠胃黏膜损伤前,预先给予埃索美拉唑(20 mg/kg)灌胃,L-硝基-精氨酸甲酯(L-NAME,4 mg/kg)和L-精氨酸(250 mg/kg)iv.采用激光多普勒血流计(LDF)测定胃黏膜血流量(GMBF),镉粒还原和比色法测定胃黏膜和血浆NO-2/NO-3含量,并观察胃黏膜损伤指数(ulcer index,UI)、溃疡坏死组织和中性粒细胞浸润严重程度的变化.结果:与模型损伤组比,埃索美拉唑组大鼠UI明显降低(5.6±2.2 vs 25.3±2.4,P＜0.01),溃疡坏死组织和中性粒细胞浸润程度明显减轻(P＜0.01).预先用L-NAME处理后,埃索美拉唑保护胃黏膜损伤作用明显减弱;L-NAME抑制作用可被L-精氨酸拮抗.向胃内灌注埃索美拉唑,可增加GMBF、胃黏膜和血浆NO-2/NO-3,L-NAME可逆转这种作用,但对埃索美拉唑抑制酸分泌作用无明显影响.结论:埃索美拉唑通过NO介导对大鼠胃黏膜损伤有重要的保护作用,而与埃索美拉唑抑制酸分泌作用无关.     

Reg基因在胃黏膜损伤与癌变中的作用

近10年来,关于Reg基因在肿瘤特别是消化系统肿瘤中的研究进展很快,其作用主要包括:急性期反应物、凝集素以及胰岛细胞、神经细胞和消化系统上皮细胞的抗凋亡因子或者生长因子。此文重点阐述Reg家族成员在胃黏膜损伤修复和癌变中的作用。     

Influence of Helicobacter pylori on the gastric mucosal barrier

AIM: To study the influence of Helicobacter pylori (Hp) on the gastric mucosal barrier (GMB) by the measurement of the potential difference (PD). METHODS: Fifty seven chronic gastritis cases were diagnosed endoscopically and confirmed by forceps mucosal biopsy. PD was measured by the Takeuchi method, and Hp was detected by both culture (modified Skirrow method) and press printing method with the Giemsa stain. Patients were divided randomly into three groups (De-Nol, WeiTong-Ling, and Placebo) for a course of 6 wk therapy. RESULTS: PD across the mucosa of antrum was significantly lower in Hp (+) patients than in Hp (-) patients (16.44 ± 2.36 vs 19.58 ± 2.44, P < 0.0001). In Hp (+) patients, PD in the antrum increased markedly (16.88 ± 2.56 vs 20.03 ± 2.21, P < 0.0001) after Hp was cleared up by the De-Nol treatment. CONCLUSION: Our data strongly indicated that Hp infection might cause a gastric mucosal barrier to be impaired markedly while the clearance of Hp by De-Nol recovered the integrity of the gastric mucosal barrier significantly.     

吸烟对血清总胆红素浓度的影响及其在致冠心病中的作用

目的：探讨吸烟对血清总胆红素浓度的影响及其在致冠心病（ Ｃ Ｈ Ｄ）中的作用。方法：对符合条件的１４８例患者作选择性冠状动脉造影检查,同时调查其吸烟史,分成吸烟组（５４例）、戒烟组（２８例）及非吸烟组（６６例）。采清晨空腹静脉血测定血清总胆红素浓度并进行比较。结果：吸烟组血清总胆红素浓度显著低于戒烟组（ Ｐ ＜ ０．０５）及非吸烟组（ Ｐ ＜ ０．０１）,而戒烟组与非吸烟组间血清总胆红素浓度无显著性差异。血清总胆红素浓度与 Ｃ Ｈ Ｄ 发病率间有明显负相关（ Ｐ ＜ ０．０１）。血清胆红素水平越低者,患 Ｃ Ｈ Ｄ 的相对危险度越高。结论：吸烟显著降低血清总胆红素浓度并可能以此作为其增加 Ｃ Ｈ Ｄ 危险性的途径之一。     

西沙比利对大鼠胃粘膜血流影响的实验研究

目的本文研究了西沙比利对大鼠胃粘膜血流的影响,并进而探讨其可能的作用机制.方法32只Wistar大鼠随机分为对照组,西沙比利0.5mg/kg组,1mg/kg组和2mg/kg组,采用中性红分泌法和grees-reactin方法检测胃粘膜血流及一氧化氮含量.结果西沙比利1mg/kg组大鼠胃粘膜血流量为(0.7±0.13mL/min),显著高于空白对照组(0.45±0.18mL/min)和西沙比利0.5mg/kg组(0.4±0.24mL/min)(P＜0.50),且西沙比利1mg/kg组胃粘膜一氧化氮含量亦显著高于空白对照组(23.32±7.40μmol/L/mg vs16.93±3.87μmol/l/mg)和西沙比利0.5mg/kg组(16.76±1.06μmol/L/mg)(P＜0.05).西沙比利2mg/kg组胃粘膜血流量为(0.3±0.17mL/min),显著低于空白对照组(0.45±0.18mL/min)(P＜0.05),其一氧化氮含量(4.35±1.52μmol/L/mg)亦显著低于空白对照组(P＜0.05).结论西沙比利通过影响胃粘膜内一氧化氮含量从而改变胃粘膜血流,西沙比利1mg/kg对大鼠胃粘膜具有保护作用.     

一氧化氮和前列腺素在门静脉高压性胃病大鼠胃粘膜灌注中的作用

目的 探讨一氧化氮（NO）和前列腺素在门静脉高压性胃病（PHG）大鼠胃粘膜灌注中的作用。方法 部分结扎大鼠门静脉主干2周后,采用中性红清除率法测定大鼠胃粘膜血流量（GMBF）,同时观察门静脉压力（PVP）的变化。结果 PHG组大鼠GMBF和PVP显著高于假手术组（t=3.431、3．312,P＜0．01）。低剂量的NO合成酶抑制剂L－硝基－精氨酸甲酯（L－NAME）呈剂量依赖性降低PHG大鼠GMBF,而对假手术组GMBF无明显影响;高剂量的L－NAME（12mg/kg)能非常显著降低PHG和假手术组大鼠GMBF。前列腺素环氧合酶抑制剂消炎痛能明显降低PHG组大鼠GMBF,而对假手术组GMBF无明显影响;预先给消炎痛处理后在假手术组大鼠中,静脉注射低剂量L－NAME（4mg/kg)前后GMBF无明显变化,高剂量L－NAME（12mg/kg)降低大鼠的GMBF与未用消炎痛处理组比无明显变化;预先给消炎痛处理后在PHG组大鼠中,L－NAME剂量（4mg/kg、12mg/kg)依赖性降低大鼠的GMBF与未用消炎痛处理组比无明显改变。结论 NO、前列腺素在调节PHG大鼠的GMBF起重要作用,但两者无协同作用。     

内镜下黏膜切除术治疗胃肠道息肉样病变的70例临床分析

目的 探讨内镜下黏膜切除术（ endoscopic mucosal resection,EMR） 在切除胃肠道息肉中的应用价值.方法 回顾性分析70例（82枚息肉）行EMR治疗胃肠道息肉的临床资料.结果 30例患者40枚胃息肉及40例患者42枚结肠息肉经EMR 治疗后,病变均完整切除,无出血、感染和穿孔等并发症发生.结论 EMR是临床上治疗胃肠道息肉的一种安全有效的内镜治疗手段,值得临床推广.     

Epalrestat prevents the decrease in gastric mucosal blood flow and protects the gastric mucosa in streptozotocin diabetic rats

We have recently reported that steady-state gastric mucosal blood flow (GMBF) is decreased in streptozotocin (STZ) diabetic rats, and that their GMBF response to burn-stress is impaired, probably via a nitric oxide (NO)-mediated mechanism. Accordingly, this study was designed to investigate the relation of aldose reductase (AR) and NO synthase to the regulation of GMBF during chronic hyperglycemia. STZ rats were treated with or without chronic oral administration of an AR inhibitor, epalrestat (EPA) and/or an NO synthase inhibitor, N-nitro-L-arginine methyl ester (L-NAME). GMBF was measured by laser-Doppler velocimetry (LDV). In the STZ rats, GMBF after a 24-h fasting period was decreased significantly 4 weeks after the onset of diabetes and this was accompanied by an increase in the gastric ulcer index (UI) (a measure of the length of gastric erosions and ulcers). Chronic oral administration of EPA to the STZ rats dose-dependently inhibited the increased UI and the decreased GMBF after the fasting stress, whereas chronic oral administration of L-NAME further increased the UI and further decreased the GMBF. EPA administered in combination with L-NAME to the STZ rats reduced the effects of L-NAME, but the effects did not reach significance. These results suggest that EPA protects the gastric mucosa of diabetic rats, by preventing the decrease in GMBF that is, at least in part, caused by NO-related mechanisms. (Received Mar. 3, 1998; accepted Aug. 28, 1998)