Finger blood circulation in forest workers with raynaud phenomena of occupational origin

Summary In one experimental series 52 forest workers sat naked at 11 °C air temperature for 35 min. During the last 15 min the right hand and forearm were exposed to 2 °C air in a cooling-box. Finger skin temperatures were recorded thermoelectrically. Finger pulse volumes were recorded by mercury strain gauges. 10 subjects suffered from traumatic vasospastic disease (TVD) attribuatable to use of chain-saws (Group III). 30 subjects used chain-saws but had no symptoms (Group II). 12 subjects had not been exposed to occupational vibration (Group I). Upon general cold exposure the fingers in Group III cooled to significantly (p< 0.01) lower temperatures than did the fingers in Group I. This difference may reflect an individual predisposition to TVD, or it may be due to an increment of finger cold vasoconstriction caused by occupational vibration and appearing before full-fledged attacks of Raynaud phenomena. Such attacks were not provoked by the present cold exposure.In a second experimental series 26 forest workers with TVD exposed one hand to 5 °C water for 20 min. The occurrence and the magnitude of the cold-induced vasodilatation did not differ between the fingers reportedly affected by TVD and those where symptoms had not been observed.     

The effects of acute and chronic lipopolysaccharide infusion in rats on the efferent function of sensory nerves in the isolated mesenteric arterial bed

Capsaicin-sensitive sensory neurons are stimulated by noxious stimuli, and may be activated in endotoxaemia. The present study investigated the acute and chronic effects of lipopolysaccharide upon the efferent function of these nerves. Conscious rats received infusion (i.v.) of lipopolysaccharide (150 microg kg(-1) h(-1)) or saline for 2 or 24 h. Following infusion, animals were killed and the mesenteric arterial bed isolated and perfused with Krebs' solution. Electrical field stimulation of capsaicin-sensitive sensory nerves was investigated. Postjunctional mechanisms of sensory neurotransmission were examined using calcitonin gene-related peptide, and endothelial and smooth muscle function assessed using acetylcholine and sodium nitroprusside, respectively. All preparations exhibited dose dependency to the agonists, and frequency dependency to electrical field stimulation. No significant differences were observed between the four groups (2-h saline, 24-h saline, 2-h lipopolysaccharide and 24-h lipopolysaccharide) with regard to responses to electrical field stimulation, acetylcholine, sodium nitroprusside or calcitonin gene-related peptide. Thus, the efferent function of capsaicin-sensitive sensory nerves is unaltered in the isolated mesenteric arterial bed prepared ex vivo from rats receiving lipopolysaccharide, either acutely (2 h) or chronically (24 h).     

S-petasin and butterbur lactones dilate vessels through blockage of voltage gated calcium channels and block DNA synthesis

Eremophilanlactones isolated from roots of Petasites hybridus (L.) G.M. et Sch. (Asteraceae) and S-petasin have vasodilatory effects with pD(2) -log (EC(50)) values of 6.01+/-0.08, 5.24+/-0.10, 4.74+/-0.13, and 5.43+/-0.06 for S-petasin, the (Z)-3-methylthioacrylic ester of 2beta-hydroxy-8betaH-7(11)-eremophilene-12,8-olide, the angelic ester of 2beta-hydroxy-8alphaH-7(11)-eremophilene-12,8-olide, and the angelic ester of 2beta-hydroxy-8betaH-7(11)-eremophilene-12,8-olide, respectively, in the mesenteric arteries. The pD(2) values were somewhat lower for all compounds in aortic segments. The vasodilation was caused by a blockage of the voltage gated calcium channels. S-petasin, (Z)-3-methylthioacrylic ester of 2beta-hydroxy-8betaH-7(11)-eremophilene-12,8-olide, and the angelic ester of 2beta-hydroxy-8alphaH-7(11)-eremophilene-12,8-olide displayed similar potencies in inhibiting DNA synthesis in cardiomyocytes and vascular smooth muscle cells.     

内皮功能异常在X综合征患者中的发病学意义

目的 研究内皮功能异常在Ｘ综合征患者中的发病学意义。方法 测定了１５例Ｘ综合征患者胸痛发作前后血中循环内皮细胞数（ＣＥＣ）和内皮素（ＥＴ）－１含量,并采用高分辨超声技术检测其血管内皮依赖性舒张功能的变化,与２０例正常人进行对照。结果 （１）Ｘ综合征患者ＣＥＣ数及ＥＴ－１水平明显高于正常对照组（Ｐ值均〈０．０１）。ＥＴ－１含量与ＣＥＣ数变化呈显著的正相关（ｒ＝０．６７,Ｐ〈０．０１）。（２）Ｘ综合征     

Identification of a Ca<Superscript>2+</Superscript>-Sensing Receptor in Rat Trigeminal Ganglia,Sensory Axons,and Tooth Dental Pulp

Extracellular Ca²⁺ regulates dentin formation, but little information is available on this regulatory mechanism. We have previously reported that sensory denervation reduces dentin formation, suggesting a role for sensory nerves in tooth mineralization. The G protein-coupled Ca²⁺-sensing receptor (CaR) is expressed in dorsal root ganglia and perivascular sensory nerves in mesenteric arterioles, and activation of these receptors by Ca²⁺ has been shown to induce vascular relaxation. The present study determined CaR expression in tooth dental pulp (DP), sensory axons, and trigeminal ganglion (TG) as well as the effect of increased [Ca²⁺]_e or a calcimimetic on tooth blood flow. The distribution of CaR, studied by immunochemistry, RT-PCR, and Western blot, indicates abundant expression of CaR in sensory axons in the jaws, TG, and DP. Restriction analysis of PCR products with specific endonucleases showed the presence of CaR message in TG and DP, and Western blotting indicates the expression of mature and immature forms of the receptor in these tissues. Pulpal blood flow, measured by laser-Doppler flowmetry, increased by 67% ± 6% (n = 12) following receptor stimulation with 5 mM Ca²⁺, which was completely inhibited by 5 μM IBTx, a high-conductance K_Ca channel blocker indicating a mechanism involving hyperpolarization. NPS R-467 (10 μM) increased blood flow by 85% ± 18% (n = 6), suggesting regulation through the CaR. Our results suggest that the CaR is present in sensory nerves, DP, and TG and that an increase in Ca²⁺ in the DP causes vasodilatation, which may contribute to accumulation of Ca²⁺ during dentin mineralization.     

Possible Involvement of Ca2+ Activated K+ Channels, SK Channel, in the Quercetin-Induced Vasodilatation

Effects of quercetin, a kind of flavonoids, on the vasodilating actions were investigated. Among the mechanisms for quercetin-induced vasodilatation in rat aorta, the involvement with the Ca²⁺ activated K⁺ (K_Ca) channel was examined. Pretreatment with NE (5 µM) or KCl (60 mM) was carried out and then, the modulation by quercetin of the constriction was examined using rat aorta ring strips (3 mm) at 36.5℃. Quercetin (0.1 to 100 µM) relaxed the NE-induced vasoconstrictions in a concentration-dependent manner. NO synthesis (NOS) inhibitor, NG-monomethyl-L-arginine acetate (L-NMMA), at 100 µM reduced the quercetin (100 µM)-induced vasodilatation from 97.8±3.7% (n=10) to 78.0±11.6% (n=5, p<0.05). Another NOS inhibitor, L-NG-nitro arginine methyl ester (L-NAME), at 100 µM also had the similar effect. In the presence of both 100 µM L-NMMA and 10 µM indomethacin, the quercetin-induced vasodilatation was further attenuated by 100 µM tetraethylammonium (TEA, a K_Ca channel inhibitor). Also TEA decreased the quercetin-induced vasodilatation in endothelium-denuded rat aorta. Used other K_Ca channel inhibitors, the quercetin-induced vasodilatation was attenuated by 0.3 µM apamin (a SK channel inhibitor), but not by 30 nM charybdotoxin (a BK and IK channel inhibitor). Quercetin caused a concentration-dependent vasodilatation, due to the endothelium-dependent and -independent actions. Also quercetin contributes to the vasodilatation selectively with SK channel on smooth muscle.     

Vascular responses of isolated mesenteric resistance and basilar arteries from short- and long-term diabetic rats

Vascular dysfunctions, e.g. alterations in the reactivity of blood vessels to neurotransmitters and hormones, are a well-established complication of diabetes mellitus. Whether these impairments are a consequence of direct postsynaptic deficits and/or indirect presynaptic deficits remains to be determined. To this end, we investigated the influence of the duration of diabetes on relaxation and contraction responses of isolated mesenteric resistance and equally-sized basilar arteries to postsynaptic activation by various vasoactive agents, using streptozotocin-induced diabetic rats and age-matched controls. Relaxation responses to vasodilator agents were studied in KCl-precontracted arteries. The duration of diabetes (4 or 40 weeks) did not affect the vasodilator responses to sodium nitroprusside or salbutamol in either artery. In mesenteric resistance vessels from short-term (4 weeks) and long-term (40 weeks) diabetic rats the vasoconstrictor responses to KCl, serotonin and vasopressin were the same as those in non-diabetic rats; however, the sensitivity (EC₅₀) to noradrenaline was slightly but significantly enhanced after the long-term diabetic state. In contrast to the mesenteric arteries, noradrenaline did not cause contraction in basilar arteries taken from diabetic and control rats. Thus, there appear to be important differences in the reactivity to noradrenaline of the peripheral and cerebral vasculature. The basilar artery from short-term and long-term diabetic rats did not show different responsiveness to vasopressin whereas to serotonin a significant enhanced and decreased sensitivity (EC₁₀ and EC₅₀) was demonstrated in short-term and long-term diabetes, respectively. Our findings indicate that postsynaptic impairments do not play a major role in the alterations of vasoreactivity to vasodilators, noradrenaline or vasopressin seen in experimental diabetes. However, the duration of the diabetic state may have serious consequences for vasoreactivity of basilar arteries to serotonin and, therefore, warrants further investigations. Received: 17 June 1998 / Accepted: 3 August 1998     

The action of ATP on the hepatic arterial and portal venous vascular networks of the rabbit liver: the role of adenosine

ATP is released from blood vessels during periods of hypoxia and may be responsible for hepatic arterial vasodilatation during instances of reduced hepatic portal venous flow. The role of adenosine in ATP-induced vasodilator and vasoconstrictor responses of the hepatic arterial and portal venous vascular networks respectively was studied in the isolated dual-perfused rabbit liver in vitro to ascertain whether ATP could be catabolised to adenosine during transit through the hepatic parenchyma. Intra-arterial and intra-portal injections of ATP (−10 to −4 log mol/100 g liver) resulted in dose-dependent vasodilatation in the hepatic artery and vasoconstriction in the portal vein. Addition of 8-phenyltheophylline (10 μM), a non-selective P₁-purinoceptor antagonist, to the hepatic arterial and portal venous perfusate significantly inhibited the hepatic arterial ED₅₀ for responses to intra-arterial injected ATP from −8.70±0.22 to −7.63±0.28 log mol/100 g liver (P<0.001); it also inhibited hepatic arterial responses to, mid-range, portal venous injections of ATP. The data suggest that the hepatic arterial vasodilatation to ATP is partly mediated via catabolism to adenosine and may be an important mechanism during periods of relative hepatic hypoxia associated with portal flow reduction.     

门静脉压升高是胆盐诱发急性胰腺炎微循环障碍的始动环节

有报道,在胆盐诱发的急性胰腺炎早期,胰腺动脉收缩导致了胰腺微循环障碍。本实验的目的就是验证上述发现是否正确。胆胰管内注射牛黄脱氧胆酸钠诱发大鼠和犬胰腺炎;使用活体显微镜观察大鼠胰腺微动脉管径的变化;记录犬胰腺小动脉压的变化;计数机能毛细血管并乘以胰腺湿重校正;用激光多普勒测量胰腺灌流量。我们发现,在诱发胰腺炎后20min内大鼠胰腺微动脉扩张;犬胰腺动脉压从104.5±4.8mmHg降到54.6±5.6mmHg;5min时下腔静脉血的血细胞压积显著低于门静脉血;校正了的胰腺机能毛细血管密度增加。胰腺微循环障碍与门静脉压升高(最多升高9.18±0.78mmHg)同时发生。将门静脉压降低至基础水平可使胰腺灌流量增加约2.4倍。实验显示,在胆盐诱发急性胰腺炎的早期,胰腺动脉发生了扩张而不是收缩;这时门静脉压升高;门静脉压升高大大减小了胰腺血管压差,并导致血浆丢失和局部血液浓缩,导致胰腺微循环障碍。