高脂血症兔球结膜微循环的改变

本实验用胆固醇粉喂家兔,造成实验性高脂血症,活体观察球结膜微循环的形态、流态及血管周围状态等１５项指标,并用球结膜微循环综合定量评价方法计算了综合积分值。处死后取球结膜进行组织学检查。结果表明：高脂血症家兔球结膜微循环有明显改变,主要为微血管形态异常、血流减慢、红细胞聚集、白微栓、静脉壁上有白色斑块等改变。球结膜微循环综合积分值明显增加,高于实验前。球结膜组织学检查发现上皮层下有泡沫细胞、血管壁增厚、有空泡、静脉内有血栓。虹膜睫状体内除有多数泡沫细胞外,还有胆固醇的菱形结晶。上述改变表明,高脂血症兔球结膜微循环有明显改变。血液有高凝、高聚倾向。黑茶中的茶色素有抗凝、抑制血小板聚集、促进纤溶等作用,口服黑茶可改善高脂血症兔球结膜微循环障碍。     

肾上腺髓质素对大鼠肠系膜微血管和微淋巴管的作用

应用活体显微电视录象技术,观察上腺髓质素对大鼠肠系膜微血管微淋巴管的作用及其对去甲肾上腺素,内皮素作用的是结果表明,ＡＤＭ直接扩张肠系膜各级微血管和向一淋巴管,拮抗ＮＥ和ＥＴ引起的微血效及微循环血流液态的异常改变。ＡＤＭ的上述作用可被一氧化氮生成抑制剂Ｎ＾９－ｎｉｔｒｏ－Ｌ－ａｒｇｉｎｉｎｅ（Ｌ－ＮＮＡ）显著抑制。     

微生态制剂益康口服液对微循环和血栓形成的影响

目的：观察益康口服液(双歧杆菌、乳酸链球菌、人参、茯苓、黄芪等)对微动脉(A)、微静脉(V)及微静脉血流速度(v)的作用和大鼠血栓形成的影响。方法：体微循环实验观察微生态制剂益康口服液对正常小鼠耳廓微循环的影响;利用大鼠体外颈总动脉-颈外静脉血流旁路法形成血小板血栓,观察益康口服液对大鼠血栓形成的影响。结果：益康口服液能明显扩张微动脉、微静脉,明显加快微静脉血流速度;提示其具有较好的改善微循环作用。结论：益康口服液能够抑制大鼠血栓的形成,提示其具有抗血小板粘附聚集作用。     

小鼠急性低氧暴露时脑微循环障碍的研究

本研究旨在通过急性减压缺氧状态下脑微循环改变的观察进一步探讨急性高原病的发生机理。实验采用鼠尾静脉注射吖啶橙荧光素作标记,落射荧光显微镜观察分析。结果表明,急性低氧状态下脑血管普遍扩张,但脑表面微血管的扩张大于脑深部微血管的扩张,微动脉的扩张大于微静脉的扩张;脑表面及深部的毛细血管开放数目增多、密度增加、间距缩小;脑血流随缺氧加重而变慢并有淤积;微血管周围有渗出及出血;神经细胞肿胀,胞浆内有空泡水肿。提示急性高原缺氧状态下脑微循环有明显障碍。     

基于显微图像的牛蛙肠系膜微循环观察

在动物活体上进行微循环观察是微循环研究的主要手段,肠系膜是脏器微循环的良好观察部位。通过医学图像分析系统可直接观察、录像、测量并记录正常状态下牛蛙肠系膜微血管的口径及开放数量、血流流态与流速、血流量等指标,并可观察滴加药物后上述指标发生的变化,探讨微循环的功能状态及药物等因素对微循环的影响。     

用荧光血管造影对大鼠肺表面微循环的活体观察

本实验采用人工胸膜再造及荧光素钠血管内造影的方法观察了大鼠活体肺表面的微循环及其运动反应并同时进行连续摄像录像分析。这种肺微循环的观察方法能清楚地判断肺血流方向,区分肺微动、静脉,而且各级血管显影清晰、边界明确,能准确地测量微血管的真实口径变化及其对刺激的反应与动态改变。血管紧张素Ⅱ收缩管径40μm以上的肺微动脉,去甲肾上腺素既收缩肺微动脉,又收缩微静脉,而血小板激活因子则轻度扩张肺微动脉,急性肺泡缺氧亦可致肺微动脉及微静脉收缩。这些结果提示:肺微血管对循环中的活性物质及肺泡缺氧有明显的反应,这种反应可能在通气/血流比值调节方面起重要作用。该实验模型可用于肺微循环的调节及某些药物和致病因素作用的研究。     

蝮蛇抗栓酶对实验性矽肺治疗作用的研究

本文报告了蝮蛇抗栓酶对大鼠实验性矽肺的治疗有很好的疗效。其治疗机理为：通过染尘大鼠肺干重及全肺胶原蛋白测定其Ｔ／Ｃ值分别为０．６８和０．７１,其病理切片以１级为主。提示蝮蛇抗栓酶有抑制肺纤维化的作用,延缓矽肺的进展;通过用ＴＢＡ反应萤光比色法测定肺组织中丙二醛（ＭＤＡ）含量,结果表明：蝮蛇抗栓酶能显著地降低肺组织中ＭＤＡ含量（Ｐ＜０．０１）。提示蝮蛇抗栓酶具有体内抗氧化作用,提高体内ＳＯＤ水平,促进体内抗脂质过氧化的作用。抑制和减慢了肺组织原纤维化过程,从而起到抗胶原反应的作用。同时对抗了矽尘对肺组织损伤作用;通过测定染尘大鼠血液流变学中全血高切和低切粘度比,血浆粘度比、红细胞聚集指数和血沉等指标,均高于正常对照组,说明矽肺存在高粘滞血症,用蝮蛇抗栓酶治疗后其五项指标与矽肺对照组比较有显著性差异（Ｐ＜０．０５）提示蝮蛇抗栓酶有效地改变血液中的高粘滞状态,改善微循环,使矽肺病情得以缓解。     

蝮蛇抗栓酶对微循环作用的实验与临床研究

对实验性失血性休克的４０只大鼠和１５只家兔静注不同剂量的抗栓酶,用激光多普勒微循环血流计测定肾表面固定部位的微循环血流量,发现用药后血流量显著增加且与尿量相一致;阻断６０只沙鼠颈动脉造成脑缺血模型,在颅顶开窗用微循环显微镜观察用药后软脑膜微循环的变化,发现微循环血流速度加快并显示一定的冲击力,且能减少白细胞数及贴壁滚动;用２０只家兔做成ＤＩＣ模型,给抗栓酶后观察肠系膜微循环,发现毛细血管开放数增多,微循环流态改善。观察３３例脑血栓形成期病人用抗栓酶治疗前后甲襞微循环的变化,发现治疗后微循环总积分值改善,流态改善更明显     

肝素钠对肢体缺血/再灌注损伤大鼠肠系膜微循环的保护作用

目的:通过观察肝素钠对肢体缺血/再灌注(LI/R)过程中肠系膜微循环的动态变化和血液流变性的影响,探讨肝素减轻LI/R损伤的可能机制,为LI/R损伤的防治提供理论依据。方法:实验采用本室常规方法复制大鼠LI/R模型,正常雄性Wistar大鼠20只,随机分为2组(n=10):肝素组(H组)和单纯缺血/再灌注组(I/R组),两组动物均于再灌注损伤后2h时动态观察肠系膜微血管管径、血流速度、白细胞黏附、白微栓及微血管壁的完整性(管周出血)等情况,同时测定各组动物血液流变学指标和血清中P-选择素和细胞间粘附分子1(ICAM-1)的值。结果:肠系膜微动、静脉管径扩张,血流速度减慢,微血管中大量白细胞贴壁、粘附,白微栓形成增多,与I/R组比较,H组大鼠肠系膜微动脉血流速度(AFV)和微静脉血流速度(VFV)显著下降(P0.01);血浆黏度(ηp)、全血低切还原黏度(Lηre)、全血高切还原黏度(Hηre)、红细胞压积(Hct)、红细胞聚集指数(EAI)、血沉方程K值(ESRK)、红细胞刚性指数(TK)均显著下降(P0.01);红细胞变形指数(EDI)显著升高(P0.01);血清中P-选择素、ICAM-1水平均显著下降(P0.01)。结论:肝素可能通过降低血清中P-选择素和ICAM-1的水平而改善肢体缺血/再灌注损伤大鼠的全身微循环状态。     

家兔Bezold—Jarisch反射的血流动力学效应

在40只麻醉兔,观察经冠脉内注射尼古丁诱发Bezold-Jarisch反射时的血流动力学变化。反射效应表现为心率减慢、动脉血压和左心室收缩压降低以及左心室内压微分值减小。切断两侧窦神经和减压神经后,上述效应增强;两侧迷走神经切断后,多数动物反射效应消失。 冠脉内注射尼古丁后,心输出量和总外周阻力均下降。人工起搏心脏以防止心率减慢时,对上述效应无明显影响。动物阿托品化并切除两侧星状神经节后,心率减慢基本消失,但动脉血压降低的程度并无明显变化。结果提示,Bezold-Jarisch反射时所表现的动脉血压降低,可归因于心输出量减少和总外周阻力降低,而以后者为主。     

ADDITIONAL MECHANISMS FOR THE ORIGIN OF BUBBLES IN ANIMALS DECOMPRESSED TO SIMULATED ALTITUDES

1. A heavy ingestion of frothy emulsified fat by rats and bullfrogs does not increase susceptibility to bubble formation when the animals are decompressed 2 to 72 hours later. This indicates that gaseous films (bubble nuclei) initially present do not pass across the intestinal wall with the digested fat, and also that high fat content per se in the lymph and blood does not increase susceptibility to bubble formation. 2. Liquid caprylic acid injected into veins of bullfrogs crystallizes when the frogs are cooled. The crystallization causes bubbles to form without muscular activity on subsequent decompression. Cooling normal bullfrogs to 1–2°C. fails, however, to crystallize any substances occurring naturally in the animals that might act in a similar manner. 3. When bullfrogs are cooled (e.g. to –5° to –10°C.) until ice forms in the blood vessels, and are then warmed and decompressed, bubbles form in the absence of exercise. Crystallization of water in the body thus forms nuclei or even small bubbles that persist. If only one foot is frozen, bubbles originate in the frozen foot. In some cases visible bubbles were observed in thawed feet at sea level (i.e. without decompression). When frog''s blood is partly frozen in test tubes or in tied off sections of veins, bubbles will appear on decompression in the absence of mechanical agitation. The practical relation of this phenomenon to flight at high altitude should not be overlooked. 4. Fracturing a leg bone (tibia or femur) in a frog induces bubble formation on subsequent decompression. Bubble nuclei, which persist for ½ to 1 hour, are probably formed as a result of the intense mechanical disturbance when the bone snaps. Fracturing of bone is considerably more effective than crushing muscles for producing bubbles in frogs.     

内耳减压病豚鼠听力和耳蜗组织的病理变化

研究探讨了内耳减压病豚鼠皮层听觉诱发电位阈值、耳蜗火棉胶切片、酶组织化学和透射电镜观察的变化。结果表明,豚鼠内耳减压病导致听力损失,耳蜗广泛的病理损害.毛细胞琥珀酸脱氢酶活性降低。提出了加压治疗内耳减压病时配合改善微循环、增加能量供应等见解。     

Compositional Discrimination of Decompression and Decomposition Gas Bubbles in Bycaught Seals and Dolphins

Gas bubbles in marine mammals entangled and drowned in gillnets have been previously described by computed tomography, gross examination and histopathology. The absence of bacteria or autolytic changes in the tissues of those animals suggested that the gas was produced peri- or post-mortem by a fast decompression, probably by quickly hauling animals entangled in the net at depth to the surface. Gas composition analysis and gas scoring are two new diagnostic tools available to distinguish gas embolisms from putrefaction gases. With this goal, these methods have been successfully applied to pathological studies of marine mammals. In this study, we characterized the flux and composition of the gas bubbles from bycaught marine mammals in anchored sink gillnets and bottom otter trawls. We compared these data with marine mammals stranded on Cape Cod, MA, USA. Fresh animals or with moderate decomposition (decomposition scores of 2 and 3) were prioritized. Results showed that bycaught animals presented with significantly higher gas scores than stranded animals. Gas composition analyses indicate that gas was formed by decompression, confirming the decompression hypothesis.     

Formation of gas bubbles in biological tissues in decompression (a mathematical model)

A mathematical model simulating transport of gases between a bubble resulted from decompression and tissue around is presented. With the help of the model the influence of gas mixture and density of the bubble forming centres upon the growth rate was studied. An important part of CO2 in the bubble forming was found out. The bubbles with He have been shown to grow faster than those with N2. At a 5-10-fold decrease of the outer pressure during 1-2 seconds the bubbles can reach sizes which violate hemodynamics in the system of microcirculation.     

Hyperbaric oxygen may reduce gas bubbles in decompressed prawns by eliminating gas nuclei.

It is accepted that gas bubbles grow from preexisting gas nuclei in tissue. The possibility of eliminating gas nuclei may be of benefit in preventing decompression sickness. In the present study, we examined the hypothesis that hyperbaric oxygen may replace the resident gas in the nuclei with oxygen and, because of its metabolic role, eliminate the nuclei themselves. After pretreatment with oxygen, prawns were 98% saturated with nitrogen before explosive decompression at 30 m/min. Ten transparent prawns were exposed to four experimental profiles in a crossover design: 1) 10-min compression to 203 kPa with air; 2) 10-min compression with oxygen; 3) 10-min compression with oxygen to 203 kPa followed by 12 min air at 203 kPa; and 4) 10 min in normobaric oxygen followed by compression to 203 kPa with air. Bubbles were measured after explosive decompression. We found that pretreatment with hyperbaric oxygen (profile C) significantly reduces the number of bubbles and bubble volume. We suggest that hyperbaric oxygen eliminates bubble nuclei in the prawn.     

Circadian rhythm of ketone bodies in the blood of fasting rats

SPF male Wistar rats were kept under standard conditions with a light: dark schedule of 12:12 h. The total ketone body concentration was determined in the blood, and the non-esterified fatty acid level in the serum, of fed rats and of animals which had fasted 24 and 48 h. The amount of ketone bodies in fed rats rose in the second half of the light period and fell with the onset of the dark period. After a 24 h fast, the amount of ketone bodies in the blood rose, but the basic characteristics of the curve and the rhythm remained the same as in fed animals. After a 48 h fast, the mean ketone body concentration was decoupled, a significant phase shift occurred and the rhythm was lost. No relationship between the oscillations of the total ketone body concentration in the blood and the oscillations of the serum non-esterified fatty acid level was found.     

Pulmonary vascular changes following air embolism in the dog.

The effect of an intravenous injection of air in a dose of 1 ml/kg body weight was determined in 15 healthy mongrel dogs. In 4 control dogs the mean pulmonary artery pressure rose to 2-3 times the resting values at 30 seconds, and carbon monoxide diffusing capacity and pulmonary capillary blood volume decreased by half. In the animals pretreated either with heparin or with methysergide (antiserotonin group) the results were the same as in the control animals. In the vagotomized dogs, the rise in pulmonary artery pressure was not significant, and the decrease in pulmonary capillary blood volume was of lesser magnitude and shorter duration than in the control and the antiserotonin dogs. It is concluded that the intravenous injection of air in supine dogs causes a transient obstruction of small pulmonary arteries. Evidence is presented to implicate a vagal mechanism in both main aspects of the response, namely the pulmonary artery pressure rise, and the partial obstruction of the pulmonary capillary bed. These studies offer additional explanation of the symptoms of respiratory distress observed in rapid decompression.     

Effect of hypobaric air, oxygen, heliox (50:50), or heliox (80:20) breathing on air bubbles in adipose tissue.

The fate of bubbles formed in tissues during decompression to altitude after diving or due to accidental loss of cabin pressure during flight has only been indirectly inferred from theoretical modeling and clinical observations with noninvasive bubble-measuring techniques of intravascular bubbles. In this report we visually followed the in vivo resolution of micro-air bubbles injected into adipose tissue of anesthetized rats decompressed from 101.3 kPa to and held at 71 kPa corresponding to approximately 2.750 m above sea level, while the rats breathed air, oxygen, heliox (50:50), or heliox (80:20). During air breathing, bubbles initially grew for 30-80 min, after which they remained stable or began to shrink slowly. Oxygen breathing caused an initial growth of all bubbles for 15-85 min, after which they shrank until they disappeared from view. Bubble growth was significantly greater during breathing of oxygen compared with air and heliox breathing mixtures. During heliox (50:50) breathing, bubbles initially grew for 5-30 min, from which point they shrank until they disappeared from view. After a shift to heliox (80:20) breathing, some bubbles grew slightly for 20-30 min, then shrank until they disappeared from view. Bubble disappearance was significantly faster during breathing of oxygen and heliox mixtures compared with air. In conclusion, the present results show that oxygen breathing at 71 kPa promotes bubble growth in lipid tissue, and it is possible that breathing of heliox may be beneficial in treating decompression sickness during flight.     

Effect of combined recompression and air, oxygen, or heliox breathing on air bubbles in rat tissues.

The fate of bubbles formed in tissues during the ascent from a real or simulated air dive and subjected to therapeutic recompression has only been indirectly inferred from theoretical modeling and clinical observations. We visually followed the resolution of micro air bubbles injected into adipose tissue, spinal white matter, muscle, and tendon of anesthetized rats recompressed to and held at 284 kPa while rats breathed air, oxygen, heliox 80:20, or heliox 50:50. The rats underwent a prolonged hyperbaric air exposure before bubble injection and recompression. In all tissues, bubbles disappeared faster during breathing of oxygen or heliox mixtures than during air breathing. In some of the experiments, oxygen breathing caused a transient growth of the bubbles. In spinal white matter, heliox 50:50 or oxygen breathing resulted in significantly faster bubble resolution than did heliox 80:20 breathing. In conclusion, air bubbles in lipid and aqueous tissues shrink and disappear faster during recompression during breathing of heliox mixtures or oxygen compared with air breathing. The clinical implication of these findings might be that heliox 50:50 is the mixture of choice for the treatment of decompression sickness.     

Ascent rate, age, maximal oxygen uptake, adiposity, and circulating venous bubbles after diving.

Decompression sickness in diving is recognized as a multifactorial phenomenon, depending on several factors, such as decompression rate and individual susceptibility. The Doppler ultrasonic detection of circulating venous bubbles after diving is considered a useful index for the safety of decompression because of the relationship between bubbles and decompression sickness risk. The aim of this study was to assess the effects of ascent rate, age, maximal oxygen uptake (VO(2 max)), and percent body fat on the production of bubbles after diving. Fifty male recreational divers performed two dives at 35 m during 25 min and then ascended in one case at 9 m/min and in the other case at 17 m/min. They performed the same decompression stops in the two cases. Twenty-eight divers were Doppler monitored at 10-min intervals, until 60 min after surfacing, and the data were analyzed by Wilcoxon signed-rank test to compare the effect of ascent rate on the kinetics of bubbles. Twenty-two divers were monitored 60 min after surfacing. The effect on bubble production 60 min after surfacing of the four variables was studied in 47 divers. The data were analyzed by multinomial log-linear model. The analysis showed that the 17 m/min ascent produced more elevated grades of bubbles than the 9 m/min ascent (P < 0.05), except at the 40-min interval, and showed relationships between grades of bubbles and ascent rate and age and interaction terms between VO(2 max) and age, as well as VO(2 max) and percent body fat. Younger, slimmer, or aerobically fitter divers produced fewer bubbles compared with older, fatter, or poorly physically fit divers. These findings and the conclusions of previous studies performed on animals and humans led us to support that ascent rate, age, aerobic fitness, and adiposity are factors of susceptibility for bubble formation after diving.