Raper R F, Sibbald W J, Hobson J, Neal A, Cheung H
A.C. Burton Vascular Biology Laboratory, Victoria Hospital Research Institute, London, ON, Canada.
Crit Care Med. 1993 Aug;21(8):1192-9. doi: 10.1097/00003246-199308000-00020.
To determine whether hyperdynamic sepsis is associated with dysregulation in the control of myocardial blood flow rates unrelated to hypotension or the use of anesthetic agents.
Prospective, nonrandomized, controlled trial.
Experimental laboratory.
Fifteen mature male sheep (34 to 61 kg).
Data were recorded in study subjects before and after the induction of sepsis following cecal ligation and perforation. Data were then recorded during: a) an infusion of prostaglandin E1 (PGE1), which decreased mean arterial perfusing pressure; and b) an infusion of zymosan-activated plasma, which increased mean pulmonary arterial pressures.
Myocardial blood flow rates were measured by the radiolabeled microsphere technique and cardiac index was measured by the thermodilution technique. Cardiac index (change delta) postcecal ligation and perforation minus baseline (+2.3 +/- 1.0 L/min/m2; p < .01) was increased in the septic study. Blood flow rate to the left ventricle was simultaneously increased, and was not further affected when the PGE1 infusion decreased the mean arterial perfusing pressures (-19 +/- 4%). During the infusion of zymosan-activated plasma, mean pulmonary arterial pressures increased (50 +/- 30%) and right ventricular blood flow was increased (zymosan minus postcecal ligation and perforation study: delta 17.8 +/- 50 mL/100 g/min; p < .01).
In this model of hyperdynamic sepsis, increases in blood flow to both the left and right ventricles were positively coupled to changes in respective ventricular work. From the interventional PGE1 and zymosan-activated plasma infusion studies, we found no evidence to support previous suggestions that the regulation of myocardial blood flow rates according to changes in perfusing pressure and/or metabolic oxygen need is significantly altered during hyperdynamic sepsis.
确定高动力型脓毒症是否与心肌血流速率控制失调相关，这种失调与低血压或麻醉剂的使用无关。
前瞻性、非随机对照试验。
实验实验室。
15只成年雄性绵羊（34至61千克）。
在盲肠结扎并穿孔诱导脓毒症前后记录研究对象的数据。然后在以下过程中记录数据：a）输注前列腺素E1（PGE1），这会降低平均动脉灌注压；b）输注酵母聚糖激活血浆，这会升高平均肺动脉压。
采用放射性微球技术测量心肌血流速率，采用热稀释技术测量心脏指数。脓毒症研究中，盲肠结扎并穿孔后心脏指数（变化量δ）减去基线值（+2.3±1.0升/分钟/平方米；p<0.01）升高。左心室血流速率同时增加，当输注PGE1使平均动脉灌注压降低（-19±4%）时，左心室血流速率未进一步受影响。在输注酵母聚糖激活血浆期间，平均肺动脉压升高（50±30%），右心室血流增加（酵母聚糖减去盲肠结扎并穿孔研究：δ为17.8±50毫升/100克/分钟；p<0.01）。
在这个高动力型脓毒症模型中，左、右心室血流的增加与各自心室做功的变化呈正相关。从干预性PGE1和酵母聚糖激活血浆输注研究中，我们没有发现证据支持之前的观点，即在高动力型脓毒症期间，根据灌注压和/或代谢需氧量的变化对心肌血流速率的调节会发生显著改变。
