微压传感式毛细血管测压仪

使用自制的微压传感式设备在显微镜下测量甲襞毛细血管压，传感器能精确测出毛细血管血流受阻时的压力，并可自动调零、自动显示和打印。临床使用证明其数据可靠，精确度高且无创，在使用中配以电子半微量天平，保证了仪器的精度、且操作简易，适于临床，优于国外使用的有创性微管插入测压法。     

The biological zero signal in laser doppler fluximetry – origins and practical implications

 This study seeks to identify the origin of the signal, known as biological zero, that is obtained using laser Doppler fluximetry when flow is arrested. It makes specific recommendations on how this signal should be measured and handled when undertaking flow studies. The experiments undertaken using flow models, animal and human tissue, organ preparations and human subjects showed that, although there may be contributions to the no-flow laser Doppler signal from vasomotion, Brownian motion from within the vascular compartment and the effects of cuff compression, the predominant contribution is from Brownian motion arising from the interstitial compartment. The biological zero signal is additive to the flow signal providing conditions within the interstitium remain constant with changes in blood flow. It is thus concluded that the biological zero signal arises from Brownian motion of the macro molecules within the interstitium. This signal should be obtained following 3–5 min of cuff occlusion with inflation applied rapidly with the smallest cuff that is compatible with flow arrest. Biological zero should be measured under each experimental condition and subtracted from the flow signal. Received: 13 August 1998 / Received after revision: 5 November 1998 / Accepted: 9 November 1998     

Major organ function under mechanical support: comparative studies of pulsatile and nonpulsatile circulation

We examined a major organ function during 3 h biventricular assisted circulation after acute myocardial infarction model in the pig. In left ventricular circulation, the outflow cannula was placed in the ascending aorta and an inflow cannula through the mitral valve in the left ventricle. A pump (pulsatile group, Zeon Medical, Inc., Tokyo, Japan and nonpulsatile group, Nikkiso HPM-15, Nikkiso, Inc., Tokyo, Japan) was connected to each cannula. In right ventricular circulation, the outflow cannula was placed in the pulmonary artery and an inflow cannula in the right ventricle. The right ventricular circulation was supported by a nonpulsatile pump (Nikkiso HPM-15). The items measured were the regional blood flows of the cortex and medulla in the kidney, white matter and gray mater in brain, and liver; renal arterial flow; carotid arterial flow; portal vein flow; common hepatic arterial flow; arterial ketone body ratio (AKBR); and lactate/pyrubic acid (L/P). In the pulsatile group, the renal cortical blood flow increased, and the medulla blood flow decreased. On the other hand, in the nonpulsatile group, both regional blood flows decreased. That means that in the pulsatile assisted group intrarenal redistribution improved rather than in the nonpulsatile assisted group. In addition the liver regional blood flow, AKBR, and L/P showed significant differences between the pulsatile and nonpulsatile groups. On the other hand, the white matter and gray matter regional blood flows and carotid arterial flow did not show significant differences between the groups. The results of our study indicated that pulsatile circulation produced superior circulation in the kidney and liver, and microcirculation on the cell level was superior as well in early treatment of acute heart failure.     

Assessment of efficacy of bothropic antivenom therapy on microcirculatory effects induced by Bothrops jararaca snake venom.

Intravenous administration of antibothropic antivenom (BAv) neutralises the systemic effects, but does not efficiently reverse the local symptoms elicited by the Bothrops jararaca venom (BjV). The mechanisms involved in this poor protection have not been clarified. In this work, intravital microscopy studies were carried out to determine the efficacy of different schedules of BAv treatment on local effects evoked by topical application of BjV in the microcirculatory network of the internal spermatic fascia of Wistar rats. Results demonstrated that BAv administration 15 min before, simultaneously with, or 15 min after BjV application did not totally reverse the local symptoms, represented by disturbances of coagulation, development of haemorrhage lesions, vascular permeability increase and increment on leukocyte-endothelium interactions. This lack of effectiveness neither reflects an inadequate amount of specific antibodies in the antivenom against toxins responsible for local effects nor an insufficient dose of circulating BAv during the assays. Administration of fluorescein isothiocyanate (FITC) labelled-BAv showed the dynamics of distribution of the antivenom in the microcirculatory network. Images obtained from prior and simultaneously treated animals showed that the antivenom remains at luminal side of vessels before venom application, and the latency time to antivenom leakage is coincidental to that for local effects evoked by the venom. In addition, images from posterior treatment demonstrated that the intense alterations in the microcirculatory network impair antivenom distribution at the site of injection. Together, our data show that the lack of effectiveness of antivenom therapy is due to impaired and delayed venom and antivenom interaction at the site of injury.     

糖皮质激素诱导性股骨头坏死模型的血管改变

目的　探讨在糖皮质激素诱导股骨头坏死过程中血管形态的改变与髓腔内脂肪填塞的关系。　方法　 12～ 18个月龄的健康日本大耳白兔 5 2只 ,按 2 5mg·kg-1·d-1注射地塞米松建立股骨头坏死模型 ,通过血管铸型扫描电镜观察、墨汁灌注切片光镜观察及图像分析等方法观察用药中和停药后股骨头病理和血管形态的变化。　结果　用药 2周出现股骨头髓腔内脂肪填塞 ,窦状隙血管因脂肪细胞压迫变细 ,血管铸型、墨汁灌注切片显示了血管表面压迹。病变随用药时间的延长而加重 ,窦状隙血管逐渐失去其结构特征。图像分析示股骨头内血管面积进行性下降 ,8周约为对照组的1/ 4。停药 6周负重区髓腔内仍存在明显脂肪化 ,血管纤细、稀少。实验 4周 ,股骨头内出现典型骨坏死灶。随时间的延长 ,坏死灶增大、股骨头坏死程度加重。　结论　髓腔内脂肪填塞是导致糖皮质激素诱导性股骨头坏死中缺血损害的重要病理因素之一 ,尤其在股骨头坏死的早期起着非常重要的作用     

前列康宝的药理学研究

实验结果表明，前列康宝具有明显的抗前列腺增生，抗炎及改善微循环作用。     

动脉化静脉皮瓣成活机制的实验研究

目的 直视下观测动脉化静脉皮瓣的血液循环途径,探讨其成活机制。方法 选用15只中国大白兔30只耳朵,设计动脉化静脉皮瓣模型,应用微循环显微镜在不同时间观察皮瓣微循环的血液途径(1h、2h、4h、8h)。结果 皮瓣全部成活。皮瓣组织内毛细管管网是一个“立体”的网状结构;静脉皮瓣早期可见毛细血管床关闭,动脉血在微静脉间快速流动;随毛细血管逐渐开放,动脉血逆流进入微循环,完成循环重建。结论在引流静脉保持通畅的前提下,静脉皮瓣可借助静脉系统重建有效血液循环并保持成活。     

大鼠子宫壁及子宫系膜微循环的观察方法

目的 建立大鼠子宫壁及子宫系膜微循环的观察方法.方法 30只SD雌性大鼠,给予体积分数2％戊巴比妥钠腹腔注射（30 mg/kg体质量）麻醉.常规消毒腹部,大鼠仰卧位固定,两侧下肢尽量外展.于腹部正中线外约0.5 cm处做一纵行长约1.5 ～2 cm的切口,钝性分离皮下组织,拉出一侧子宫及其韧带,置于透明有机玻璃槽的微循环恒温箱中（水控温度37.5℃）,固定摊平在箱内有机玻璃小台柱（直径约为20 mm,高度约15 mm）上,用37℃的林格氏液湿润子宫表面及其韧带,用冷光源为外射光,观察子宫壁及子宫系膜微循环,固定视野内观察微血管各参数值.随机选取15只大鼠尾静脉注射缩宫素2 IU,30 min后观察子宫微循环的变化.结果 子宫系膜的微动脉管径约为8～ 15 μm,微静脉管径约为25 ～ 45 μm;大鼠子宫壁微动脉管径约为6～ 12 μm,微静脉管径约为15 ～ 30 μm.注射缩宫素后,子宫系膜和子宫壁的微动脉血管管径分别收缩了38.24％和25.14％,和正常组比较有统计学差异（P＜0.05,P＜0.05）.结论 大鼠子宫系膜的微血管解剖位置明显,分离操作方便,其微循环动静脉血管清晰,血流丰富,有利于进行动物及人类疾病的防治和药物研究.     

Involvement of endothelin/ nitric oxide balance in hepatic ischemia/ reperfusion injury

Introduction: Endothelin (ET) and nitric oxide (NO) act as opponents in the regulation of the hepatic microcirculation. During ischemia/reperfusion (I/R) ET levels are increased, whereas no rise in NO levels is observed. This imbalance may be responsible for microcirculatory disturbances. The aim of this study was to restore the delicate ET/NO balance to maintain the integrity of the hepatic microcirculation and to reduce I/R injury. Methods: Ischemia was induced by crossclamping of the hepatoduodenal ligament for 30 min with portal decompression using a splenocaval shunt (56 Wistar rats, 200–250 g). Sham operation, ischemia and treatment groups with the endothelin receptor antagonist (ERA) bosentan (1 mg/kg body weight i.v.) and the NO donor l-arginine (400 mg/kg body weight i.v.) were performed. For assessment of the microcirculation, sinusoidal perfusion rate, diameters of sinusoids and postsinusoidal venules, leukocyte endothelium interactions and velocity of free-flowing leukocytes were investigated by means of in vivo microscopy 30–90 min after reperfusion. Local hepatic tissue pO₂ was measured prior to ischemia, 30 min and 60 min after reperfusion and aspartate aminotransferase (AST)/alanine aminotransferase (ALT) levels were investigated 2 h and 6 h after reperfusion. Results: After ischemia, sinusoidal and venular diameters were reduced to 76% and 85%, respectively, of sham operation group values (P<0.05), but were maintained at baseline in ERA (98/102%) and NO (102/105%) groups (P<0.05). Increased postischemic leukocyte sticking in sinusoids (144%) and venules (435%) was reduced by therapy to 110/253% (ERA) and 111/ 324% (NO), respectively (P<0.05). Perfusion rate was increased to 93% and 94% compared with 82% in the ischemia group (P<0.05). Concomitant with the improved microcirculation in therapy groups, local hepatic tissue pO₂ was improved 30 min after reperfusion in the ERA (11.0 mmHg) and the l-arginine group (11.5 mmHg) relative to the ischemic group (6.9 mmHg) (P<0.05). In addition, postischemic AST/ALT increase was reduced by therapy. Conclusion: Our results indicate that maintenance of ET/NO balance by blocking ET receptors, as well as providing a NO donor, protects the liver microcirculation and reduces hepatic I/R injury. Received: 14 August 1998 Accepted: 13 October 1998