McDonough K H, Causey K M
Department of Physiology, Louisiana State University Medical Center, New Orleans 70112, USA.
Shock. 1994 Jun;1(6):432-7. doi: 10.1097/00024382-199406000-00007.
Gram-negative sepsis as well as administration of agents that simulate or occur naturally subsequent to a septic challenge, can present as an oxidant stress to the myocardium. These stresses may then induce the development of protection of the heart from future stresses. This protection of the heart may occur in spite of the fact that sepsis itself induces myocardial dysfunction. In the present study we determined if sepsis is protective of a 50 min ischemic episode, one in which some degree of irreversible damage may occur. In addition we determined if sepsis-induced protection was still present when this ischemic challenge was imposed upon the heart of the alcoholic septic animal in which the chronic alcoholic state can lead to a potentiation of sepsis induced cardiac depression. Thus animals were fed an ethanol containing diet or a control diet for 8-10 weeks and were then made septic by the administration of Escherichia coli into the dorsal subcutaneous space. Control animals received sterile saline. The following day, hearts were studied in the isovolumic beating preparation and, after basal function was assessed, hearts were made globally ischemic for 50 min and reperfused for 30 min. Left ventricular pressure was continuously monitored and coronary flow was measured at specific intervals. After ischemia and reperfusion, hearts from control- and alcohol-fed animals that were nonseptic showed significantly decreased left ventricular performance. Ventricular pressure development of hearts from septic and alcoholic septic rats was not significantly decreased after ischemia and reperfusion compared to preischemia although preischemic function was significantly lower in the sepsis groups compared to their nonseptic control groups.(ABSTRACT TRUNCATED AT 250 WORDS)
革兰氏阴性菌败血症以及在败血症激发后模拟或自然产生的物质的给药，可表现为对心肌的氧化应激。这些应激随后可能诱导心脏对未来应激产生保护作用。尽管败血症本身会诱发心肌功能障碍，但心脏的这种保护作用仍可能发生。在本研究中，我们确定败血症是否对50分钟的缺血发作具有保护作用，在这种缺血发作中可能会发生一定程度的不可逆损伤。此外，当这种缺血刺激施加于酒精性败血症动物的心脏时，我们确定败血症诱导的保护作用是否仍然存在，在这种动物中，慢性酒精状态可导致败血症诱导的心脏抑制作用增强。因此，给动物喂食含乙醇的饮食或对照饮食8 - 10周，然后通过将大肠杆菌注入背部皮下空间使其发生败血症。对照动物接受无菌盐水。第二天，在等容搏动制备中研究心脏，在评估基础功能后，使心脏整体缺血50分钟并再灌注30分钟。连续监测左心室压力，并在特定间隔测量冠状动脉血流量。缺血和再灌注后，未发生败血症的对照动物和喂食酒精的动物的心脏左心室功能显著下降。与缺血前相比，败血症大鼠和酒精性败血症大鼠的心脏在缺血和再灌注后的心室压力发展没有显著降低，尽管败血症组的缺血前功能与其未发生败血症的对照组相比显著更低。（摘要截断于250字）
