Fretschner R, Klöss T, Guggenberger H, Deusch H, Schmid H J
Klinik für Anaesthesiologie und Transfusionsmedizin, Universitaet Tuebingen, Germany.
Crit Care Med. 1993 May;21(5):747-52. doi: 10.1097/00003246-199305000-00019.
To determine how isoflurance affects the longitudinal distribution of pulmonary vascular resistance and pulmonary gas exchange during Escherichia coli bacteremia.
Prospective, controlled study with open-label assignment of animals to two groups.
Laboratory.
Goehingen minipigs.
Induction of acute respiratory failure by a 4-hr infusion of live E. coli bacteria in 12 animals; six animals anesthetized with methohexital/piritramide; six animals anesthetized with isoflurane. The control group consisted of four animals that received the same surgical procedure, but no E. coli infusion. Two animals were anesthetized with methohexital/piritramide and two with isoflurane, respectively.
Cardiac output and pressures were measured by means of an arterial catheter, Swan-Ganz catheter, and a left atrial catheter. Effective pulmonary capillary pressure was evaluated graphically from a pulmonary artery occlusion pressure decay. Arterial-alveolar PO2 ratio was calculated to evaluate pulmonary function. Measurements were performed before and after 1, 2, and 3.5 hrs of E. coli infusion. Statistical significance was tested with analysis of variance (ANOVA). E. coli infusion caused hypodynamic shock, an increase in pre- and postcapillary pulmonary vascular resistance and respiratory failure. Postcapillary pressure gradient and effective pulmonary capillary pressure were lower in the isoflurane-group. Methohexital-anesthetized animals developed pulmonary dysfunction after 1 hr of bacteremia, whereas isoflurane-anesthetized animals developed pulmonary dysfunction after 3.5 hrs of E. coli infusion (significantly different, ANOVA, p < .05). There were no significant changes in the sham group.
Isoflurane is a pulmonary venodilator. During lethal E. coli infusion, it ameliorates the increase in pulmonary capillary pressure and preserves pulmonary function until vascular permeability increases.
确定异氟烷在大肠杆菌菌血症期间如何影响肺血管阻力的纵向分布和肺气体交换。
前瞻性对照研究，将动物开放标签分配到两组。
实验室。
哥廷根小型猪。
对12只动物进行4小时的活大肠杆菌输注以诱导急性呼吸衰竭；6只动物用美索比妥/匹拉米洞麻醉；6只动物用异氟烷麻醉。对照组由4只接受相同手术操作但未进行大肠杆菌输注的动物组成。分别有2只动物用美索比妥/匹拉米洞麻醉，2只动物用异氟烷麻醉。
通过动脉导管、 Swan-Ganz导管和左心房导管测量心输出量和压力。从肺动脉闭塞压衰减曲线以图形方式评估有效肺毛细血管压。计算动脉-肺泡氧分压比值以评估肺功能。在大肠杆菌输注1、2和3.5小时之前和之后进行测量。采用方差分析（ANOVA）检验统计学意义。大肠杆菌输注导致低动力性休克、毛细血管前和毛细血管后肺血管阻力增加以及呼吸衰竭。异氟烷组的毛细血管后压力梯度和有效肺毛细血管压较低。美索比妥麻醉的动物在菌血症1小时后出现肺功能障碍，而异氟烷麻醉的动物在大肠杆菌输注3.5小时后出现肺功能障碍（方差分析，差异有统计学意义，p < 0.05）。假手术组无显著变化。
异氟烷是一种肺血管扩张剂。在致死性大肠杆菌输注期间，它可改善肺毛细血管压的升高并在血管通透性增加之前维持肺功能。
