■可靠的冠状动脉微血管功能评估至关重要。测量绝对冠状动脉血流量的技术是有希望的,但需要验证。本研究的目的是:第一,验证生理盐水输注在体内产生最大充血的潜力。第二,验证在高(40-50mL/min)输注速度下连续冠状动脉热稀释测量的绝对冠状动脉血流量并评估其安全性。
■14只闭胸绵羊在全身麻醉下以不同剂量增加的盐水输注速度进行了绝对冠状动脉血流量测量。另外7只开胸绵羊用心外膜多普勒血流探头进行了这些测量。冠状动脉闭塞45s后,将冠状动脉流量与反应性充血进行比较。
■20毫升/分钟的生理盐水输注引起的充血冠状动脉流量明显降低(140对191毫升/分钟;P=0.0165),较低的冠状动脉血流储备(1.82对3.21;P≤0.0001),冠状动脉阻力(655比422木单位;P=0.0053)高于冠状动脉闭塞。另一方面,30mL/min的生理盐水输注导致冠状动脉血流充血(196对192mL/min;P=0.8292),冠状动脉血流储备(2.77对3.21;P=0.1107),和冠状动脉阻力(415对422单位;P=0.9181)与冠状动脉闭塞没有差异。5mL/min时,高血冠状动脉流量为40.7%,40.8%,10mL/min,73.1%,20mL/min,102.3%,30mL/min,99.0%,40mL/min,与闭塞后充血流量相比,输注50mL/min的盐水为98.0%。流量高估存在显著偏差(Bland-Altman:偏差±SD,-73.09±30.52;95%的协议限制,-132.9至-13.27)和40至50mL/min的盐水。偶尔,在更高的输注速率下,缺血改变导致心室纤颤(9.5%,50mL/min).
■30mL/min而不是20mL/min的连续盐水输注引起最大充血。用40至50mL/min的盐水输注速度测量的绝对冠状动脉血流量不准确且不安全。
UNASSIGNED: Reliable assessment of coronary microvascular function is essential. Techniques to measure absolute coronary blood flow are promising but need validation. The objectives of this study were: first, to validate the potential of saline infusion to generate maximum hyperemia in vivo. Second, to validate absolute coronary blood flow measured with continuous coronary thermodilution at high (40-50 mL/min) infusion speeds and asses its safety.
UNASSIGNED: Fourteen closed-chest sheep underwent absolute coronary blood flow measurements with increasing saline infusion speeds at different dosages under general anesthesia. An additional 7 open-chest sheep underwent these measurements with epicardial Doppler flow probes. Coronary flows were compared with reactive hyperemia after 45 s of coronary occlusion.
UNASSIGNED: Twenty milliliters per minute of saline infusion induced a significantly lower hyperemic coronary flow (140 versus 191 mL/min; P=0.0165), lower coronary flow reserve (1.82 versus 3.21; P≤0.0001), and higher coronary resistance (655 versus 422 woods units; P=0.0053) than coronary occlusion. On the other hand, 30 mL/min of saline infusion resulted in hyperemic coronary flow (196 versus 192 mL/min; P=0.8292), coronary flow reserve (2.77 versus 3.21; P=0.1107), and coronary resistance (415 versus 422 woods units; P=0.9181) that were not different from coronary occlusion. Hyperemic coronary flow was 40.7% with 5 mL/min, 40.8% with 10 mL/min, 73.1% with 20 mL/min, 102.3% with 30 mL/min, 99.0% with 40 mL/min, and 98.0% with 50 mL/min of saline infusion when compared with postocclusive hyperemic flow. There was a significant bias toward flow overestimation (Bland-Altman: bias±SD, -73.09±30.52; 95% limits of agreement, -132.9 to -13.27) with 40 to 50 mL/min of saline. Occasionally, ischemic changes resulted in ventricular fibrillation (9.5% with 50 mL/min) at higher infusion rates.
UNASSIGNED: Continuous saline infusion of 30 mL/min but not 20 mL/min induced maximal hyperemia. Absolute coronary blood flow measured with saline infusion speeds of 40 to 50 mL/min was not accurate and not safe.