Lindner J R, Ismail S, Spotnitz W D, Skyba D M, Jayaweera A R, Kaul S
Cardiovascular Division and the Division of Thoracic and Cardiovascular Surgery, University of Virginia School of Medicine, Charlottesville, VA, USA.
Circulation. 1998 Nov 17;98(20):2187-94. doi: 10.1161/01.cir.98.20.2187.
We hypothesized that the persistence of albumin microbubbles within the myocardium during crystalloid cardioplegia (CP) infusion and ischemia-reperfusion (I-R) occurs because of endothelial injury.
The myocardial transit rate of albumin microbubbles was measured in 18 dogs perfused with different CP solutions and in 12 dogs undergoing I-R. Electron microscopy with cationized ferritin labeling of the glycocalyx was performed in 9 additional dogs after CP perfusion and in 3 additional dogs undergoing I-R. Microbubble transit was markedly prolonged during crystalloid CP perfusion. The addition of whole blood to the CP solution accelerated the transit rate in a dose-dependent fashion (P<0.05), which was greater with venous than with arterial blood (P<0.05). The addition of plasma or red blood cells to CP solutions was less effective in improving transit rate than addition of whole blood (P<0.05). Microbubble transit rate was independent of the temperature, K+ content, pH, PO2, osmolality, viscosity, and flow rate of the perfusate. Similarly, a proportion of microbubbles persisted in the myocardium after I-R, which was related to the duration of ischemia (P<0.01) but not of reflow. Crystalloid CP perfusion and I-R resulted in extensive loss of the endothelial glycocalyx without other ultrastructural changes. This effect was partially reversed in the case of crystalloid CP when it was followed by blood CP.
Sonicated albumin microbubbles persist within the myocardium in situations in which the endothelial glycocalyx is damaged. The measurement of the myocardial transit rate of albumin microbubbles may provide an in vivo assessment of endothelial glycocalyx damage.
我们推测，在晶体停搏液（CP）灌注及缺血再灌注（I-R）期间，白蛋白微泡在心肌内持续存在是由于内皮损伤所致。
在18只灌注不同CP溶液的犬及12只接受I-R的犬中测量白蛋白微泡的心肌通过速率。另外，对9只CP灌注后的犬及3只接受I-R的犬进行了用阳离子铁蛋白标记糖萼的电子显微镜检查。在晶体CP灌注期间，微泡通过明显延长。向CP溶液中添加全血可使通过速率呈剂量依赖性加快（P<0.05），静脉血比动脉血的作用更明显（P<0.05）。向CP溶液中添加血浆或红细胞在改善通过速率方面不如添加全血有效（P<0.05）。微泡通过速率与灌注液的温度、钾含量、pH值、氧分压、渗透压、粘度和流速无关。同样，一部分微泡在I-R后仍持续存在于心肌中，这与缺血持续时间有关（P<0.01），但与再灌注时间无关。晶体CP灌注和I-R导致内皮糖萼广泛丢失，而无其他超微结构改变。在晶体CP后接着进行血液CP时，这种效应可部分逆转。
在内皮糖萼受损的情况下，超声处理的白蛋白微泡会持续存在于心肌内。测量白蛋白微泡的心肌通过速率可对内皮糖萼损伤进行体内评估。
