INFLAMMATORY CHANGES IN PERMEABILITY AND ULTRASTRUCTURE OF SINGLE VESSELS IN THE FROG MESENTERIC MICROCIRCULATION
INFLAMMATORY CHANGES IN PERMEABILITY AND ULTRASTRUCTURE OF SINGLE VESSELS IN THE FROG MESENTERIC MICROCIRCULATION
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DOI：
10.1113/jphysiol.1988.sp016910
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发表时间：
1988-01-01
影响因子：
5.5
通讯作者：
PHILLIPS, ME
中科院分区：
文献类型：
--
作者：
CLOUGH, G;MICHEL, CC;PHILLIPS, ME
1.在15个实验中，单微血管中暴露的脊髓青蛙肠系膜灌注含有牛血清白蛋白（40毫克毫升-1）的林格氏溶液。对于每个容器，其壁的水力渗透性（Lp）和施加在它们两端的有效渗透压（ρ）是相同的。在组织温度从大约15 ℃突然升高之前和之后的预定时间，通过在两个毛细管压力下测量流体过滤速率（Michel，Mason，咖喱，Tooke和Hunter，1974）来确定Δ II）。C至30 - 35 ℃。C.温度超过30度。C似乎会损害适应5 - 10 ℃温度的青蛙的组织。C. 2.在15个实验中的14个中，当温度升高到30 - 35 ℃时，Lp升高。C.在这些实验中的12个中，Lp的增加大于水粘度随温度下降的预期，并且是渐进的。在组织温度升高后1-2分钟进行测量的5根血管中，Lp从初始平均值（±）增加。S.E.M.）3.76（.+-.）0.54）×10-3μ m s-1 cmH2O-1至8.72（±. 1.68）×10-3μ m s-1 cmH2O-1。在组织温度升高后10分钟进行测量的9根血管中，Lp从初始平均值4.03 ± 0.05增加到初始平均值4.03 ± 0.05。0.72）×10-3μ m s-1 cmH2O-1至16.9（±. 3.5). times. 10-3μ m s-1 cmH2O-1。在15和20分钟时观察到Lp的进一步增加。反滤有效渗透压ρ的变化三角洲II，变化很大。在组织加热时显示Lp大变化的12条血管中，有4条显示ρ没有降低。10分钟后Δ II，但ρ.在这些血管中的三个中，Δ II在15分钟时下降。随着Lp的上升，Δ II下降。本文中发展的定量理论允许ρ的变化。根据穿过渗透性增加的血管壁区域的组分（ρ H Δ IIH）和穿过Lp未改变的区域的组分来分析Δ II。在6支血管中，ρ H Δ IIH接近于零;在2支血管中，ρ H Δ IIH为6.2和4.5 cmH 2 O。4.在对五个血管的对照实验中，初始组的Lp和ρ的估计值是：随后在另外20分钟的时间内重复测量Δ II，组织保持在15 °。C.没有观察到Lp的趋势，并且Lp和ρ的重复估计值均为0。Δ II同意它们的初始值。5.暴露于30 - 35 ℃的温度下的血管的超微结构。与24 ℃保温5或15分钟的血管比较。在暴露于30 - 35 ℃的所有容器中，C在每个圆周轮廓中打开一个或两个内皮细胞间连接以形成0.2 μ m或更大的间隙。这些间隙被钌红染色材料覆盖或填充，这些材料似乎与内皮管腔表面的细胞被膜连续。在某些制剂中，细胞表面被膜似乎与对照血管相似，而在其他制剂中，细胞表面被膜似乎大大扩展。6.这表明，增加的渗透性发炎毛细血管和微静脉是发展的结果之间的差距内皮细胞。最初，这些间隙被材料覆盖，该材料看起来与细胞表面涂层连续并且对血清白蛋白具有高反射系数。该表面涂层材料的结构随后发生改变，并且这些改变降低了ρ。并可能进一步增加Lp。
1. In fifteen experiments, single microvessels in the exposed mesenteries of pithed frogs were perfused with Ringer solutions containing bovine serum albumin (40 mg ml-1). For each vessel, the hydraulic permeability of its walls (Lp) and effective osmotic pressure exerted across them (.rho..DELTA.II) were determined from measurements of fluid filtration rates at two capillary pressures (Michel, Mason, Curry, Tooke and Hunter, 1974) before and at predetermined times after the tissue temperature had been raised abruptly from approximately 15.degree. C to 30-35.degree. C. Temperatures greater than 30.degree. C appear to damage the tissues of frogs acclimatized to temperatures of 5-10.degree. C. 2. In fourteen out of fifteen experiments Lp rose when the temperature was raised to 30-35.degree. C. In twelve of these experiments the increase in Lp was greater than expected from the fall in water viscosity with temperature, and was progressive. In five vessels where measurements were made 1-2 min after tissue temperature was raised, Lp increased from an initial mean value (.+-. S.E.M.) of 3.76 (.+-. 0.54) .times. 10-3 .mu.m s-1 cmH2O-1 to one of 8.72 (.+-. 1.68) .times. 10-3 .mu.m s-1 cmH2O-1. In nine vessels where measurements were made at 10 min after tissue temperature was raised, Lp increased from an initial mean value of 4.03 (.+-. 0.72) .times. 10-3 .mu.m s-1 cmH2O-1 to one of 16.9 (.+-. 3.5) .times. 10-3 .mu.m s-1 cmH2O-1. further increases in Lp were seen at 15 and 20 min. 3. The changes in the effective osmotic pressure opposing filtration, .rho..DELTA.II, were very variable. Out of the twelve vessels which showed large changes in Lp with tissue heating, four showed no reduction in .rho..DELTA.II after 10 min, though .rho..DELTA.II fell in three of these vessels at 15 min. In the other eight vessels, .rho..DELTA.II fell as Lp rose. A quantitative theory developed in this paper allowed the changes in .rho..DELTA.II to be analyzed in terms of a component across the regions of vessel wall of increased permeability (.rho.H.DELTA.IIH) and a component across regions where Lp was unchanged. In six vessels .rho.H.DELTA.IIH approximated to zero; in two vessels .rho.H.DELTA.IIH was 6.2 and 4.5 cmH2O. 4. In control experiments on five vessels, an initial group of estimates of Lp and .rho..DELTA.II was followed by repeated measurements over a further 20 min period with the tissue maintained at 15.degree. C. No trends in Lp were observed and the repeated estimates of both Lp and .rho..DELTA.II agreed with their initial values. 5. The ultrastructure of vessels exposed to temperatures of 30-35.degree. C for 5 or 15 min was compared with that of vessels kept at 24.degree. C or less. In all vessels exposed to 30-35.degree. C one or two interendothelial cell junctions were opened in each circumferential profile to form gaps of 0.2 .mu.m or more. These gaps were covered or filled with ruthenium red-staining material which appeared to be continuous with the cell coat of the luminal surface of the endothelium. In some preparations the cell surface coat appeared similar to that of control vessels whereas in others it appeared greatly expanded. 6. It is suggested that the increased permeability of inflamed capillaries and venules is the consequence of the development of gaps between the endothelial cells. Initially these gaps are covered with material which appears to be continuous with the cell surface coat and has a high reflection coefficient to serum albumin. Alterations in the structure of this surface coat material subsequently occur and these reduce .rho. to macromolecules and may further increase Lp.