Flaim S F, Minteer W J, Nellis S H, Clark D P
Am J Physiol. 1979 May;236(5):H698-704. doi: 10.1152/ajpheart.1979.236.5.H698.
A model for high output heart failure (HCO) was developed in male, Sprague-Dawley rats using an abdominal aortocaval shunt equal to 50% of total cardiac output (CO) with 2 mo of postsurgical recovery. The model was evaluated by analysis of hemodynamics, peripheral blood flows (BF) (radioactive microspheres), and plasma catecholamine levels as well as mass and fluid content of organs. In HCO, CO and left ventricular end-diastolic pressure were increased with significant left and right ventricular hypertrophy. Mean blood pressure (BP) was unchanged, but pulse BP was increased in HCO. BF to skeletal muscle, cutaneous, and some splanchnic regions was reduced to HCO, whereas BF to the cerebral, coronary, and renal beds was protected. Plasma epinephrine and norepinephrine levels were significantly elevated in HCO suggesting enhanced sympathetic as well as adrenal catecholamine release. Tissue analysis indicated altered circulatory status secondary to HCO in liver, kidney, spleen, and lung. The results indicate that this model will be a relevant tool for studies of the circulatory effects of heart failure.
利用腹主动脉腔静脉分流术(分流血流量等于心输出量总量的50%),在雄性Sprague-Dawley大鼠中建立了高输出量心力衰竭(HCO)模型,并术后恢复2个月。通过血流动力学分析、外周血流量(BF)(放射性微球法)、血浆儿茶酚胺水平以及器官的质量和液体含量对该模型进行评估。在HCO模型中,心输出量和左心室舒张末期压力升高,伴有显著的左、右心室肥厚。平均血压(BP)未改变,但HCO模型中的脉压升高。流向骨骼肌、皮肤和一些内脏区域的血流量减少,但流向脑、冠状动脉和肾床的血流量得到保护。HCO模型中血浆肾上腺素和去甲肾上腺素水平显著升高,提示交感神经以及肾上腺儿茶酚胺释放增强。组织分析表明,HCO继发引起肝脏、肾脏、脾脏和肺循环状态改变。结果表明,该模型将成为研究心力衰竭循环效应的一个相关工具。