缺氧条件下冻伤对大鼠微循环血液灌流量的影响

本文采用体重２００±２０ｇ健康雄性Ｗｉｓｔａｒ大鼠,随机分为平原冻伤（ＦＮ）组、急性缺氧冻伤（ＦＡＨ）组和缺氧习服缺氧冻伤（ＦＨＡＣ）组,实验观察了大鼠右后肢重度冻伤前后各组大鼠双后肢皮肤微循环灌流量的改变。结果表明,平原冻伤使大鼠双后肢微循环灌流量明显减少,提示局部重度冻伤对微循环的影响不只局限于冻区也涉及到对侧肢体。冷冻前ＦＡＨ组大鼠微循环灌流量已明显低于ＦＮ组,表明急性缺氧时血容量进行代偿性的再分配,使微循环灌流量减少;ＦＡＨ组大鼠冻后双后肢微循环灌流量的改变结果提示急性缺氧可加重其冻伤对微循环的损伤程度。ＦＨＡＣ组大鼠冻前微循环灌流量非常明显地低于正常对照,也明显低于急性缺氧对照,表明缺氧习服可造成微循环障碍;ＦＨＡＣ组大鼠冻肢微循环灌流量非常明显地低于ＦＮ组,提示缺氧习服加重高原冻伤引起的微循环障碍。     

急性缺氧和缺氧习服对鼠足冻伤组织存活面积的影响

本工作观察了急性缺氧和缺氧习服对Ｗｉｓｔａｒ大鼠左后足冻伤组织存活面积的影响。急性缺氧冻伤组和平原冻伤组大鼠冻足ＴＳＡ分别为５７．６８％、６０．２５％和６７．７７％、６６．８８％,损伤程度基本相同,表明大鼠模拟６０００ｍ高度急性缺氧８ｈ不加重冻伤引起的组织损伤。大鼠模拟６０００ｍ高度减压缺氧习服１４ｄ或２８ｄ后再作－１５℃或－２０℃冻伤,冻足ＴＳＡ仅为１４、８４％－２３．９１％,明显少于急性缺氧冻     

缺氧习服对冻伤大鼠骨骼肌耗氧量的影响

目的与方法使用生物组织氧耗测量系统测定了常氧冻伤(FN)、急性缺氧冻伤(FAH)和缺氧习服缺氧冻伤(FHAC)大鼠后肢重度冻伤前后腓肠肌耗氧量的变化,以探讨缺氧习服加重冻伤组织损伤的机理.结果冻前,FHAC组腓肠肌耗氧量降低26.2%.冻后1d,FN、FAH和FHAC组腓肠肌耗氧量为5.93±0.66,4.74±1.87和0.76±0.39[kPa/(g*min)],分别较各自冻前水平降低76.3%,77.9%和95.9%,FHAC组明显低于其余两组;冻后5d三组的耗氧量分别恢复至各自冻前水平的62.8%、44.9%和28.8%,FHAC组仍明显低于其余两组,提示缺氧习服冻伤后骨骼肌代谢率降低更明显,恢复更缓慢.结论缺氧习服和冻伤均使腓肠肌耗氧量明显减少,二者的叠加使缺氧习服大鼠冻后腓肠肌耗氧量进一步降低,表明组织代谢的变化是影响冻伤组织损伤及修复的主要因素之一.     

缺氧对家兔脑表面微血管直径和血流速度的影响

已有实验对急性缺氧和低氧适应时全脑和局部脑血流的改变进行了较为系统的研究,表明脑血流的改变与急性高山病的发生和严重程度以及低氧适应性有密切关系,但尚未从微循环角度进一步探讨。Kontos等和Ivanov等都报道了缺氧时脑表面微血管扩张,但未进行连续观察。为从微循环角度探讨低氧适应机理和急性高山病的发生机理,我们对急性缺氧和经低氧适应后缺氧时家兔脑表面微循环进行了连续观察。     

缺氧条件下建立SD大鼠牙周炎动物模型的研究

目的:在模拟高原缺氧条件下建立稳定的缺氧SD大鼠牙周炎动物模型。方法:40只SD大鼠,雌雄各半,采用随机数字表法分为4组:常氧对照组(A组),常氧牙周炎组(B组),缺氧对照组(C组),缺氧牙周炎组(D组),每组10只。B、D组大鼠结扎牙颈部、高糖饮食、口腔涂菌及注射激素,A、C组不作任何处理,正常饮食。C、D组喂养的同时进入模拟海拔5000 m的低压氧舱。8 w后检测牙龈指数GI、菌斑指数PLI、牙周袋深度PD、牙槽骨吸收度ABL及组织病理学观察,对模型进行评估。结果:GI、PD及ABL指数在B组与A组,D组与C组,C组与A组,D组与B组比较均有统计学差异(P0.05)。PLI指数在B组与A组,D组与C组比较有统计学差异(P0.05),在C组与A组,D组与B组比较无统计学差异(P0.05)。HE染色见A、C组无明显改变,B、D组牙龈糜烂,结合上皮向根方增殖迁移,牙周膜间隙增宽。结论:将采用结扎牙颈部、高糖饮食、口腔涂菌及注射激素综合方法作用的SD大鼠放入模拟海拔5000 m的低压氧舱,建立模拟高原缺氧大鼠牙周炎模型具有可行性,为高原牙周病的防治奠基了实验基础。     

缺氧对大鼠海马脑片诱发电位的影响

在脑缺氧损伤的研究中,离体海马切片既可排除血脑屏障,又保持原有神经环路,所得实验结果接近在体实验,是研究脑缺氧的理想模型。近几年来国外已有人报道了缺氧时海马脑片诱发电位的变化;但同时用两个脑片比较不同程度的低氧对脑片诱发电位的影响,却少有报道。本实验采用自行设计的双孔脑片电生理实验系统,用不同浓度的低氧混合气造成不同程度的缺氧环境,以探明不同缺氧程度影响脑片电反应的时间曲线,寻求海马脑片缺氧损伤的特征性反应与不可逆损伤发生的临界值。     

缺氧和低氧适应对家兔脑深部微血管某些参数的影响

本文系用QTM-970图像分析系统，对急性缺氧，慢性缺氧和低氧适应时家兔的脑灰质，白质和延脑微血管的某些参数进行了定量分析，结果表明，急性缺氧时，大脑灰质的毛细血管面积密度明显增加（P<0.01)，毛细血管间距减小；延脑毛细血管面积密度减小（P<0.01)，毛细血管间距增加（P<0.05)。慢性缺氧和低氧适应时，大脑白质毛细血管面积密度明显减小（P<0.05)。本实验结果提示，大脑不同部位的微血管对缺氧的反应不同，且不同部位的微血管对急，慢性缺氧的反应亦不同。     

人尾加压素Ⅱ对大鼠脑微循环的影响

目的:探讨尾加压素Ⅱ(UII)对于大鼠软脑膜微循环的影响.方法:健康成年SD大鼠随机分为对照组、生理盐水(NS)、UII(10-7mol/L)、去甲肾上腺素(NA,10-6mol/L)、UII(10-7mol/L) NA(10-6mol/L)等五组,采用活体微循环观测技术观察大鼠软脑膜微血管内径、血流速度等微循环参数,采用激光多普勒血流量仪测定软脑膜血流量的变化.结果:正常对照组软脑膜细动脉和细静脉血管内径分别为(35.4±3.6)μm和(40.6±8.5)μm,UII组于滴加UII(10-7mol/L)后即刻细动脉和细静脉出现收缩,1 min时细动脉和细静脉收缩达到高峰,血管内径分别为(25.6±3.4)μm和(23.4±3.3)μm (与正常对照组比较,P均<0.05);细动、静脉内血流速度无明显变化(与正常对照组比较P均>0.05);软脑膜血流量于滴加UII(10-7mol/L)后1 min开始升高,5 min达到高峰(3.5±0.4 )PU 值,正常对照组(2.3±0.6)PU值(P<0.05).结论:UII可以使大鼠软脑膜微血管收缩,血流量增加.     

缺氧对冻伤兔足皮肤温度和肌糖元含量的影响

采用测定冻伤兔足皮肤温度和肌糖元含量的方法,间接观察在缺氧条件下兔足重度冻伤血液循环和肌肉能量代谢的改变。实验结果表明：平原冻伤组、急性缺氧冻伤组、缺氧两周冻伤组冻足皮肤温度和肌糖元含量均明显降低。经４０℃０．１％的洗必泰液多次温浸治疗冻伤兔足,平原冻伤组和急性缺氧冻伤组的治疗足皮肤温度和肌糖元含量均高于未治疗足,无明显差异,提示在此种条件下冻足的血液循环障碍可能更加严重。     

Vascular casts demonstrate microcirculatory insufficiency in acute frostbite

The use of vascular microcorrosion casts (vascular replicas) has made it possible to demonstrate the degree of damage to the microcirculation in experimentally induced frostbite. This approach provides a direct method for demonstrating vascular patency. Four groups of animals were used in this investigation. The left hind limbs of anesthetized rats were cooled to -10 degrees C in groups one and three and to -20 degrees C in groups two and four, as measured by needle thermocouples placed under the gastrocnemius muscles. Thermocouples were also placed in the left hind footpads of groups three and four. The sheathed limbs were cooled in an alcohol bath at approximately 1.1 degree C per minute. All limbs exposed to the cold bath were rewarmed to 37 degrees C in a 40 degree C water bath. The right hind limbs served as uninjured controls. The footpad temperatures recorded in groups three and four were used in conjunction with the temperatures recorded under the gastrocnemius muscles to characterize the footpad temperatures in groups one and two. Vascular microcorrosion casts were made from the left and right hind paws of groups one and two using Batson's modified methyl methacrylate. Scanning electron microscopic examination of the casts demonstrated dramatic differences between the vascular integrity of control paws and that of frozen paws. Exposure to the cold temperatures destroyed most of the microcirculation. In addition, the weights of the casts from the control paws were significantly different from the weights of the casts from the frozen paws. It was concluded that this model for evaluating frostbite injury accurately demonstrates the extent of microvascular damage and has significant potential as a method for evaluating therapeutic drug regimens.     

Effect of alveolar hypoxia on regional pulmonary perfusion

We examined the effects of varying levels of alveolar hypoxia on regional distribution of pulmonary blood flow (QL) in control-ventilated sheep. Regional distribution of QL was measured using 15-micron-diam labeled microspheres during the base-line period and at two levels of hypoxemia (arterial O2 partial pressure 44 and 20 Torr). During the base-line period, regional distribution of QL in the prone position was uniform [14 +/- 4% (SE) of QL/g bloodless dry lung wt in the upper lung and 16 +/- 2% of QL/g in the dependent lung]. During hypoxemia, however, the regional distribution of QL increased in the upper lung (20 +/- 3% of QL/g) while it decreased in the dependent lung (10 +/- 2% of QL/g). The degree of flow distribution was proportional to the severity of hypoxemia. The flow distribution was not associated with significant increases in pulmonary blood flow (2.0 +/- 0.4----2.4 +/- 0.5----2.6 +/- 0.1 l/min) but was associated with increases in mean pulmonary arterial pressure (17.8 +/- 1.3----21.7 +/- 1.1----29.0 +/- 3.8 Torr). Therefore alveolar hypoxia results in a relative increase in regional pulmonary perfusion to the upper lung, which depends on the level of pulmonary hypertension. The increased upper lung perfusion may be due to recruitment in the upper lung or to vasodilation in this region.     

Effect of acute hypoxia on microcirculatory and tissue oxygen levels in rat cremaster muscle.

Repeated exposure to brief periods of hypoxia leads to pathophysiological changes in experimental animals similar to those seen in sleep apnea. To determine the effects of such exposure on oxygen levels in vivo, we used an optical method to measure PO2 in microcirculatory vessels and tissue of the rat cremaster muscle during a 1-min step reduction of inspired oxygen fraction from 0.21 to 0.07. Under control conditions, PO2 was 98.1 +/- 1.9 Torr in arterial blood, 52.2 +/- 2.8 Torr in 29.0 +/- 2.7-microm arterioles, 26.8 +/- 1.7 Torr in the tissue interstitium near venous capillaries, and 35.1 +/- 2.6 Torr in 29.7 +/- 1.9-microm venules. The initial fall in PO2 during hypoxia was significantly greater in arterial blood, being 93% complete in the first 10 s, whereas it was 68% complete in arterioles, 47% at the tissue sites, and 38% in venules. In the 10- to 30-s period, the fall in normalized tissue and venular PO2 was significantly greater than in arterial PO2. At the end of hypoxic exposure, PO2 at all measurement sites had fallen very nearly in proportion to that in the inspired gas, but tissue oxygen levels did not reach critical PO2. Significant differences in oxyhemoglobin desaturation rate were also observed between arterial and microcirculatory vessels during hypoxia. In conclusion, the fall in microcirculatory and tissue oxygen levels in resting skeletal muscle is significantly slower than in arterial blood during a step reduction to an inspired oxygen fraction of 0.07, and tissue PO2 does not reach anaerobic levels.     

Effect of hypoxia on the concentration of nicotinamide coenzymes in the tissues of newborn rats]

The content of nicotinamide coenzymes (NAD, NAD-H, NADP, NADP-H) was studied in the brain, heart and liver tissue of the newborn rats kept in hypoxic gaseous medium with a 4% oxygen content for 2 1/2 hours. There was a marked reduction of NAD content, an accumulation of NAD-H and a more than two-fold fall of the NAD/NAD-H ratio particularly marked in the brain and heart. A reduction of the NADP-H values chiefly in the liver and of the general pool of NAD-phosphates in the tissues of the newborn rats under study occurred under the same conditions. The data obtained led to the conclusion that oxygen deficiency had a significant influence on the concentration and the ratio of the nicotinamide coenzymes in the tissues of newborn rats, that in its turn led to the changes in the level and the direction of the redox processes under the conditions of hypoxia.     

Effect of hypobaric hypoxia on immune function in albino rats

 The effect of exposure to hypoxia on macrophage activity, lymphocyte function and oxidative stress was investigated. Hypoxia enhanced peritoneal macrophage activity as revealed by enhanced phagocytosis and free radical production. There was no significant change in antibody titres to sheep red blood cells in either serum or spleen during hypoxia. However, there was a considerable reduction in the delayed-type hypersensitivity response to sheep red blood cells, indicating the impairment of T-cell activity. Hypoxia decreased the blood glutathione (reduced) level and increased plasma malondialdehyde by a factor of about 2. It is therefore speculated that hypoxia imposes an oxidative stress leading to decreased T-cell acivity. Received: 1 September 1997 / Accepted: 22 May 1998