MYOCARDIAL METABOLISM IN A CANINE MODEL OF HUMAN BACTERIAL SEPSIS

败血症和感染性休克是重症监护室死亡的主要原因。 在美国的护理病房。美国国立卫生研究院重症监护医学部有 开发了一种人类细菌性败血症的犬模型。这是人类的模型 感染性休克近距离。使用磷-31磁体技术 资源光谱学(31 PMR)我们已经开发了一种研究 感染性休克心肌抑制的机制。目的 培育的比格犬被植入感染或无菌的腹膜内 纤维蛋白凝块。两天后，当心肌抑制被证明是 最大限度，在氟烷麻醉下进行开胸手术。外科手术 用来放置冠状静脉窦和颈动脉导管，左 脑室MRS表面线圈。31 PMRS，心肌耗氧量(MUO2) 葡萄糖和乳酸的提取在光谱过程中被连续测定 考虑到细胞内的测量而获得的 磷酸肌酸和三磷酸腺苷。总而言之，在犬科期间 感染性休克这一方案允许心脏之间的相关性 在不同工作负荷下的功能和新陈代谢。

Septicemia and septic shock are the leading causes of death in intensive care units in the United States. The NIH Critical Care Medicine Dept. has developed a canine model of human bacterial sepsis. This models human septic shock closely. Using the techniques of phosphorus-31 Magnetic Resource Spectroscopy (31 PMRs) we have developed a method of studying the mechanisms underlying the myocardial depression of septic shock. Purpose bred beagles are intraperitoneally implanted with infected or sterile fibrin clots. Two days later, when myocardial depression has been shown to be maximal, a thoracotomy is performed under Halothane anesthesia. Surgery is used to place a coronary sinus and carotid artery catheters, and a left ventricle MRS Surface Coil. 31 PMRS, myocardial oxygen consumption (MUO2) glucose, and lactate extraction are serially determined during a spectra having been obtained allowing for measurements of intracellular phosphocreative and adenosine triphosphate. In summary, during canine septic shock this protocol allows for correlations between cardiac function and metabolism at varying workloads.