Hellyer P W
Department of Anatomy, Physiological Sciences, and Radiology, College of Veterinary Medicine, North Carolina State University, Raleigh 27606.
Am J Vet Res. 1994 Apr;55(4):458-64.
Effects of endotoxemia on left ventricular contractility and systemic hemodynamics were determined in pentobarbital-anesthetized swine. A multielectrode conductance (volume) catheter and a high-fidelity pressure transducer catheter were passed retrograde into the left ventricle to continuously measure pressure and volume. End-systolic pressure-volume relationships were determined during transient (8 to 10 s) caudal vena caval balloon occlusion. Lactated Ringer's solution was administered at a rate sufficient to maintain left ventricular end-diastolic pressure > or = 6 mm of Hg. Following baseline measurements, Escherichia coli endotoxin (O55-B5) was infused IV at 2.5 micrograms/kg of body weight/h for 3 hours. Left ventricular end-systolic elastance (Ees), the slope of the end-systolic pressure-volume relationship; end-systolic elastance normalized for left ventricular end-diastolic volume (Ees norm); the rate of increase of left ventricular pressure (dP/dt max); and preload recruitable stroke work (PRSW, stroke work-to-end-diastolic volume relationship) did not change in endotoxemic swine, compared with baseline measurements or with values from control (physiologic saline solution-treated) swine. Left ventricular pressures and volumes had marked pig-to-pig variability in the control and endotoxin-treated groups. Determination of Ees, Ees norm, and PRSW was further confounded by development of frequent premature ventricular contractions during caudal vena caval balloon occlusion. Endotoxin significantly (P < 0.05) decreased left ventricular end-diastolic pressure, compared with that in control swine, and significantly (P < 0.01) decreased left ventricular end-diastolic volume, compared with baseline. Endotoxin decreased cardiac index and arterial blood pressure, whereas heart rate, central venous pressure, and mean pulmonary arterial pressure increased.(ABSTRACT TRUNCATED AT 250 WORDS)
在内巴比妥麻醉的猪身上测定内毒素血症对左心室收缩力和全身血流动力学的影响。将多电极电导（容积）导管和高保真压力换能器导管逆行插入左心室，以连续测量压力和容积。在短暂（8至10秒）的尾腔静脉球囊闭塞期间测定收缩末期压力-容积关系。以足以维持左心室舒张末期压力≥6 mmHg的速率输注乳酸林格液。在进行基线测量后，以2.5微克/千克体重/小时的速率静脉输注大肠杆菌内毒素（O55-B5），持续3小时。与基线测量值或对照（生理盐水处理）猪的值相比，内毒素血症猪的左心室收缩末期弹性（Ees）、收缩末期压力-容积关系的斜率、经左心室舒张末期容积标准化的收缩末期弹性（Ees norm）、左心室压力增加率（dP/dt max）和可预负荷性搏出功（PRSW，搏出功与舒张末期容积关系）均未改变。在对照组和内毒素处理组中，猪的左心室压力和容积存在明显的个体差异。在尾腔静脉球囊闭塞期间频繁出现室性早搏，进一步混淆了Ees、Ees norm和PRSW的测定。与对照猪相比，内毒素显著（P<0.05）降低了左心室舒张末期压力，与基线相比显著（P<0.01）降低了左心室舒张末期容积。内毒素降低了心脏指数和动脉血压，而心率、中心静脉压和平均肺动脉压升高。（摘要截短于250字）
