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INSTRUCTIONS FOR AUTHORS

ＣｈｉｎｅｓｅＭｅｄｉｃａｌＪｏｕｒｎａｌ（ＣＭＪ）ａｎｄｔｈｅＪｏｕｒｎａｌｏｎＣＤＲＯＭａｒｅｐｕｂｌｉｓｈｅｄｍｏｎｔｈｌｙｂｙｔｈｅＣｈｉｎｅｓｅＭｅｄｉｃａｌＡｓｓｏｃｉａｔｉｏｎａｎｄｄｉｓｔｒｉｂｕｔｅｄｗｏｒｌｄｗｉｄｅ．ＭａｎｕｓｃｒｉｐｔｓａｒｅｗｅｌｃｏｍｅｆｒｏｍａｎｙｐａｒｔｏｆｔｈｅｗｏｒｌｄａｎｄｓｈｏｕｌｄｂｅｓｅｎｔｔｏｔｈｅＥｄｉｔｏｒｉａｌＯｆｆｉｃｅ，ＣｈｉｎｅｓｅＭｅｄｉｃａｌＪｏｕｒｎａｌ，ＣｈｉｎｅｓｅＭｅｄｉｃａｌＡｓｓｏｃｉａｔｉｏｎ，４２Ｄｏ…     

A Study of the Best Probes to Detect HLA-DPB1, DQB1 Allele Genes

ＡＳｔｕｄｙｏｆｔｈｅＢｅｓｔＰｒｏｂｅｓｔｏＤｅｔｅｃｔＨＬＡ－ＤＰＢ１，ＤＱＢ１ＡｌｌｅｌｅＧｅｎｅｓＫｅＢｉｎｇｓｈｅｎ（克丙申）ａｎｄＳｕｎＸｉａｏｍｉｎｇ（孙晓明）（ＤｅｐａｒｔｍｅｎｔｏｆＩｍｍｕｎｏｌｏｇｙ，ＪｉｎａｎＭｉｌｉｔａｒｙＧ...     

General Introduction of China Academy of Traditional Chinese Medicine

ＧｅｎｅｒａｌＩｎｔｒｏｄｕｃｔｉｏｎｏｆＣｈｉｎａＡｃａｄｅｍｙｏｆＴｒａｄｉｔｉｏｎａｌＣｈｉｎｅｓｅＭｅｄｉｃｉｎｅＣｈｉｎａＡｃａｄｅｍｙｏｆＴｒａｄｉｔｉｏｎａｌＣｈｉｎｅｓｅＭｅｄｉｃｉｎｅ（ＣＡＴＣＭ），ｉｎａｕｇｕｒａｔｅｄｏｎＤｅｃ...     

Assessment of Right Coronary Artery Fistula by Multiplane Transesophageal Echocardiography

ＡｓｓｅｓｓｍｅｎｔｏｆＲｉｇｈｔＣｏｒｏｎａｒｙＡｒｔｅｒｙＦｉｓｔｕｌａｂｙ　ＭｕｌｔｉｐｌａｎｅＴｒａｎｓｅｓｏｐｈａｇｅａｌＥｃｈｏｃａｒｄｉｏｇｒａｐｈｙＹＡＮＧＹａ（杨娅）；ＷＡＮＧＸｉｎｆａｎｇ（王新房）；ＬＩＺｈｉａｎ（李治安）（Ｄｅ...     

Use of Different Doses and Administrative Patterns of Vecuronium for Rapid Intubation and Pharmacodyamic Study

ＵｓｅｏｆＤｉｆｆｅｒｅｎｔＤｏｓｅｓａｎｄＡｄｍｉｎｉｓｔｒａｔｉｖｅＰａｔｔｅｒｎｓｏｆＶｅｃｕｒｏｎｉｕｍｆｏｒＲａｐｉｄＩｎｔｕｂａｔｉｏｎａｎｄＰｈａｒｍａｃｏｄｙａｍｉｃ　ＳｔｕｄｙＧｕｏＸｉａｎｇｙａｎｇ；（郭向阳）ＬｕｏＡｉｌｕｎ；（...     

Effects of prostaglandins and leukotrienes on hypoxic pulmonary vasoconstriction in rats

Alveolar hypoxia can induce pulmonary vaso-constriction,but the mechanism of hypoxic pul-monary vasoconstriction remains unknown. It mightrelate to arachidonic acid released from endotheliumor to the vasoactive substances released from othercells in lung tissue during hypoxia.Furthermore,theextra- pulmonary reflex and the directive effectof hy-poxia on pulmonary vascular smooth muscles mightalso be involved.In this study,we conducted in vivorats experiment and employed in vitro perfused lungex…     

Sympathetic innervation of pulmonary circulation and its role in hypoxic pulmonary vasoconstriction

The purposes of this study were to localize the position of spinal center of sympathetic nerve which controls the pulmonary circulation, and to evaluate the role of pulmonary sympathetic nerve in hypoxic pulmonary vasoconstriction (HPV) in pithed rat model. The sympathetic preganglionic fibers arising from C₇–T₁₀ segments were stimulated electrically in succession. During stimulation the pulmonary vascular resistance (PVR) was increased in all segments tested, most significantly in C₇-T₄ (about 28 % above control value), obviously higher than that in T₅-T₁₀. The higher the stimulated spinal segments, the larger the ratio of ΔPVR/ΔSVR. Alveolar hypoxia (12%O₂–88% N₂) could induce HPV in pithed rat. In the presence of hypoxia, stimulation of T₁–T₃ segments caused a double increment in PVR and -P_p, as compared with those during normoxia (P<0.05). The data show that 1) the spinal center of sympathetic nerve regulating the vasomotion of pulmonary circulation is located in the C₇-T₄ segments; 2) the excitation of sympathetic nervous system during hypoxia could enhance HPV.     

Relation of TXA2 and PGI2 to the difference in hypoxic pulmonary vasoconstriction between different strains of rats

TXB₂ and 6-keto-PGF₁ α levels in arterial and venous plasma of Wistar and Hilltop rats during hypoxia were measured to investigate the roles of TXA₂ and PGI₂ in hypoxic pulmonary vasoconstriction (HPV) and responsiveness difference of pulmonary vessels to hypoxia between different strains of rats. The results showed that PGI₂ might play an important role in maintaining the low resistance in pulmonary circulation of these two strains of rats. Increased TXA₂ during hypoxia may partially mediate HPV in Wistar rats, while augmented PGI₂ during hypoxia may modulate HPV in Wistar rats. This might be the important mechanism responsible for more intensive responsiveness of pulmonary vessels to hypoxia in Hilltop rats than in Wistar rats.     

Effects of cigarette smoking,hypoxia and vasoactive mediators on the production of PGI2 and TXA2 in cultured pulmonary artery endothelial cells

Summary Effects of cigarette smoke extract (CSE) and some vasoactive mediators on the production of PGI₂ and TXA₂ in normoxic and hypoxic pulmonary artery endothelial cells (PAECs) in culture were studied. The production of PGI₂ in PAECs was inhibited by hypoxia or verapamil, but promoted by angiotensin II (A II), noradrenaline (NE) or platelet activating factor (PAF), while that of TXA₂ slightly increased except when treated with PAF. The effect of A II, NE, PAF and verapamil, however, was not influenced by hypoxia. CSE inhibited the production of PGI₂ in normoxic PAECs but did not further reduce 6-keto-PGF_1α in hypoxic PAECs medium. The results suggested that a) the production of PGI₂ during hypoxia might be stimulated by vasoactive mediators produced during hypoxia, not by hypoxia directly; b) the production and release of PGI, were related to intracellular calcium, c) the augmented production of PGI₂ might be one of the mechanisms in the pulmonary vasodilating role of PAF: and d) prostaglandin production might be associated with the alteration of hypoxic pulmonary vasoreactivity after cigarette smoking.     

一氧化氮对急、慢性缺氧大鼠血流动力学及缺氧性肺血管收缩反应的影响

观察了吸入０．００４％的一氧化氮（ＮＯ）对急、慢性缺氧大鼠血流动力学、缺氧性肺血管收缩反应（ＨＰＶ）、血气及高铁血红蛋白（ＭｅｔＨｂ）的影响。结果表明：（１）常氧吸入ＮＯ时能明显降低慢性缺氧大鼠肺动脉平均压（Ｐｐａ）和肺血管阻力（ＰＶＲ），但对正常大鼠的Ｐｐａ和ＰＶＲ无明显影响；（２）慢性缺氧大鼠急性缺氧时ＨＰＶ较正常大鼠弱，吸入ＮＯ不但降低两者的急性缺氧肺动脉高压，且完全逆转两者的ＨＰＶ；（３）吸入ＮＯ对急、慢性缺氧大鼠体循环血流动力学、血气及ＭｅｔＨｂ含量无明显影响。提示吸入ＮＯ能选择性降低，急、慢性缺氧性肺动脉高血压，且逆转ＨＰＶ。     

Wirkung der Lipoxygenase- und Cyclooxygenase-Metaboliten auf die akute hypoxische pulmonale Vasokonstriktion beim Schweinchen

The role of lipoxygenase and cyclooxygeriase metabolites in acute hypoxic pulmonary vasoconstriction (HPV) was studied in piglets, it has been found that acute alveolar hypoxia induced remarkable pulmonary vasoconstrion, associated with an increase in cardiac output. The hypoxic pulmonary vasoconstriction response was insignificantly attenuated after infusion of DEC. indomethacin potentiated mar kedly the increase in pulmonary artery pressure and pulmonary vascular resistance and thus augmented HPV. It is inferred that hypoxic pulmonary vsaoconstriction in piglet may be mediated by other important mediators in addition to leukotrienes, but modulated by prostaglandins to prevent an excessive rise in pulmonary artery pressure.     

ET－1和NO对肺动脉平滑肌细胞DNA合成的作用及缺氧对其调制的研究

观察内皮素－１（ＥＴ－１）和一氧化氮（ＮＯ）在缺氧性肺血管结构重组中的作用，发现ＥＴ－１可促进肺动脉平滑肌细胞（ＰＡＳＭＣ）ＤＮＡ合成，其促进作用呈剂量依赖性；ＮＯ供应剂ＳＮＰ则起抑制作用，ＮＯ的抑制增殖作用主要由ｃＧＭＰ介导。在此基础上观察到缺氧可促进ＰＡＳＭＣ对ＥＴ－１的增殖反应，同时可抑制ＰＡＳＭＣ胞浆内可溶性鸟苷酸环化酶活性而降低ＰＡＳＭＣ对ＮＯ等舒血管药物的反应性。提示ＥＴ－１和ＮＯ及缺氧在缺氧性肺血管结构重组中具有重要的作用。     

Role of sympathetic nerve and adrenal gland in the potentiation of hypoxic pulmonary vasoconstriction during cigarette smoking

Summary The aim of this study was to investigate the role of sympathetic nerve and adrenal gland in the changes in hemodynamics and hypoxic pulmonary vasoconstriction (HPV) induced by cigarette smoking in Wistar rats. Data showed that an increment of pulmonary vascular resistance (PVR) induced by alveolar hypoxia was partially prevented by prazosin (α₁-receptor blocker) and prazosin combined with propranolol (β-receptor blocker), but not significantly affected by propranolol or adrenalectomy. Cigarette smoking tould increase PVR and potentiate HPV, whereas the potentiation of HPV was partially inhibited by prazosin and strengthened by propranolol, but not affected by adrenalectomy. It is suggested that the sympathetic nerve excitation caused by cigarette smoking may play a role in the strengthening of HPV.     

Strain difference in pulmonary vascular responsiveness to hypoxia in rats

The difference in pulmonary vascular response to hypoxia between Hilltop Sprague-Dawley (HT) rats and Wistar (W) rats was studied. Effects of inhibitor of leukotriene (LT) synthesis or prostaglandin (PG) synthesis on hypoxic pulmonary vasoconstriction (HPV) and chronic pulmonary hypertension were observed, and variations in plasma TXB₂ and 6-keto-PGF_1a during hypoxia were determined. The results showed that in rats of both strains LTs are the major mediator of HPV, which is also mediated by vasoconstrictive PGs in HT rats, while modulated by vasodilative PGs in W rats. This might be the crucial mechanism responsible for the higher pulmonary vascular responsiveness in HT rats. Differences in the modulating effect of histamine and in the structural feature of pulmonary arteriole might be contributing factors as well.     

A study of endothelium-dependent proliferation of pulmonary smooth muscle cells in vitro

Summary The direct effect of hypoxia and the effect of hypoxic endothelial cells conditioned medium on cultured pulmonary arterial smooth muscle cells in vitro were studied with phase contrast microscopy,³H-thymidine labelled technique and flow cytometric measurements. The results showed that direct hypoxia inhibited proliferation of pulmonary arterial smooth muscle cells, retained pulmonary arterial smooth muscle cells in the Go/G₁ phase and decreased³H-thymidine incorporation into pulmonary arterial smooth muscle cells and that hypoxic endothelial cells conditioned medium stimulated proliferation of pulmonary arterial smooth muscle cells, promoted pulmonary arterial smooth muscle cells from G₀/G₁ phase to S phase and increased³H-thymidine incorporation into pulmonary arterial smooth muscle cells. It was reasonable to believe that hypoxia might enable pulmonary arterial endothelial cells to secrete some growth factors which could stimulate proliferation of pulmonary arterial smooth muscle cells, thereby playing an important role in structural remodeling of the pulmonary arteries and in the development of hypoxic pulmonary hypertension.