Falk A, Myrvold H E, Haglund U
Circ Shock. 1982;9(4):419-32.
The purpose of the present investigation was to explore a possible relationship between cardiopulmonary function and small intestinal mucosal lesions in experimental septic shock. The filling pressure of the left ventricle of the heart (LVEDP) and the maximal pressure change during systole (max dP/dt) were monitored continuously by a tip-transducer catheter. The pulmonary and femoral arterial pressures and pressure changes in the trachea were recorded. The aortic blood flow was measured electromagnetically. Stroke volume, external cardiac work, and the pulmonary vascular resistance could be calculated. Twenty-two cats were made septic by i.v. infusion of live E. coli bacteria. Controls received saline i.v. After 2 hours of bacteremia, preload was increased by a rapid infusion of dextran to unmask cardiac dysfunction. Small intestinal specimens were taken for microscopical examination. The occurrence and the degree of mucosal damage was established. Thirteen cats had virtually normal mucosal appearances, whereas nine disclosed severe lesions. The loading procedure revealed a more pronounced cardiac dysfunction in cats with severe mucosal damage, compared to those without. Pulmonary vasoconstriction, bronchoconstriction, and impaired ventilation-perfusion ratio were also demonstrated, but these signs of pulmonary dysfunction did not differ when comparing animals with and without mucosal damage. A correlation between impaired cardiac function on one hand and hypotension--intestinal mucosal lesions on the other, suggests cardiotoxic material released from the damaged intestine as one contributing mechanism.
本研究的目的是探讨实验性脓毒症休克时心肺功能与小肠黏膜病变之间可能存在的关系。通过顶端换能器导管连续监测心脏左心室充盈压(LVEDP)和收缩期最大压力变化(最大dP/dt)。记录肺动脉和股动脉压力以及气管内的压力变化。用电磁法测量主动脉血流量。可计算出每搏输出量、心脏外部做功和肺血管阻力。通过静脉输注活大肠杆菌使22只猫发生脓毒症。对照组静脉输注生理盐水。菌血症2小时后,通过快速输注右旋糖酐增加前负荷以揭示心脏功能障碍。取小肠标本进行显微镜检查,确定黏膜损伤的发生情况和程度。13只猫的黏膜外观基本正常,而9只猫出现严重病变。与无严重黏膜损伤的猫相比,负荷试验显示有严重黏膜损伤的猫心脏功能障碍更为明显。还证实存在肺血管收缩、支气管收缩和通气/灌注比受损,但比较有和无黏膜损伤的动物时,这些肺功能障碍的体征并无差异。一方面心脏功能受损,另一方面存在低血压和肠道黏膜病变,二者之间的相关性表明,受损肠道释放的心脏毒性物质是其中一个促成机制。