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。 美国的护理单位。美国国立卫生研究院重症监护医学部具有 开发了一个人类细菌性败血症的犬模型。这个模型是人类的 感染性休克利用磷-31磁性技术 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潜在机制。目的 将感染的或不育的 纤维蛋白凝块两天后，当心肌抑制被证明 最大程度上，在氟烷麻醉下进行胸廓切开术。手术 用于放置冠状窦和颈动脉导管，以及左 心室MRS表面线圈。31例PMRS，心肌耗氧量（MUO 2） 葡萄糖和乳酸盐提取在光谱期间连续测定 已经获得允许测量细胞内的 磷酸化和三磷酸腺苷。总之，在犬 脓毒性休克该方案考虑到心脏 功能和代谢的变化。

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.