Hatton M W, Southward S M, Ross-Ouellet B, DeReske M, Blajchman M A, Richardson M
Department of Pathology, McMaster University Health Sciences Centre, Hamilton, Ontario, Canada.
Arterioscler Thromb Vasc Biol. 1996 Sep;16(9):1147-55. doi: 10.1161/01.atv.16.9.1147.
The ability of the rabbit aorta intima-media (IM) layer to adsorb certain plasma proteins was measured for up to 20 months after a deendothelializing injury in vivo. Purified radioiodinated rabbit fibrinogen, antithrombin, or prothrombin was injected intravenously into either uninjured or sham-injured rabbits (controls) or rabbits at various times (5 minutes to 20 months) after a balloon-catheter injury to the aorta. After a 10-minute circulation time, a blood sample was taken, and the rabbit was exsanguinated rapidly (via a carotid cannula) and the aorta excised. Uptake of each radiolabeled protein was measured as bound radioactivity per square centimeter of platelet- or endothelium-free aorta IM and was compared with the radioactivity (ergo concentration) in blood at exsanguination. Fibrinogen adsorption by the IM was maximal at 5 minutes after injury (10.9 +/- 2.3 pmol/cm2 IM) and declined slowly to 4 to 6 pmol/cm2 at 12 months (controls: 0.8 +/- 0.1 pmol/cm2). Uptake of prothrombin (3.7 +/- 0.5 pmol/cm2 at 5 minutes) decreased to approximately 2 pmol/cm2 at 12 months (controls: 0.3 pmol/cm2). Antithrombin adsorption by the IM (3.3 +/- 0.4 pmol/cm2 at 5 minutes) paralleled that of prothrombin over 12 months (controls: 0.3 to 0.4 pmol/cm2), the molar ratio ranging from 0.8 to 1.2. At 20 months, the ballooned aorta had a significantly thickened intima and was approximately 90% reendothelialized. Injection of horseradish peroxidase (HRP) into rabbits at 1 or 12 months after balloon injury showed clearly that HRP activity was present throughout the entire depth of the deendothelialized, but not the reendothelialized, thickened intima. These results may indicate that an elevated turnover of hemostatic proteins continues within the deendothelialized intima after injury, conceivably until reendothelialization is complete.
在体内进行去内皮损伤后长达20个月的时间里,对兔主动脉内膜-中膜(IM)层吸附某些血浆蛋白的能力进行了测定。将纯化的放射性碘化兔纤维蛋白原、抗凝血酶或凝血酶原静脉注射到未受伤或假受伤的兔子(对照组)或在球囊导管损伤主动脉后的不同时间点(5分钟至20个月)的兔子体内。经过10分钟的循环时间后,采集血样,然后迅速放血(通过颈动脉插管)并切除主动脉。每种放射性标记蛋白的摄取量以每平方厘米无血小板或无内皮的主动脉IM的结合放射性来衡量,并与放血时血液中的放射性(即浓度)进行比较。损伤后5分钟时,IM对纤维蛋白原的吸附量最大(10.9±2.3 pmol/cm² IM),并在12个月时缓慢下降至4至6 pmol/cm²(对照组:0.8±0.1 pmol/cm²)。凝血酶原的摄取量(5分钟时为3.7±0.5 pmol/cm²)在12个月时降至约2 pmol/cm²(对照组:0.3 pmol/cm²)。IM对抗凝血酶的吸附量(5分钟时为3.3±0.4 pmol/cm²)在12个月内与凝血酶原的吸附量平行(对照组:0.3至0.4 pmol/cm²),摩尔比在0.8至1.2之间。在20个月时,球囊损伤的主动脉内膜明显增厚,且约90%重新内皮化。在球囊损伤后1个月或12个月向兔子注射辣根过氧化物酶(HRP),结果清楚显示,在去内皮但未重新内皮化的增厚内膜的整个深度均存在HRP活性。这些结果可能表明,损伤后去内皮的内膜中止血蛋白的更新率升高,推测这种情况会持续到重新内皮化完成。