Cimini C M, Weiss H R
Department of Physiology and Biophysics, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway 08854-5635.
Hypertension. 1990 Jul;16(1):35-42. doi: 10.1161/01.hyp.16.1.35.
The purpose of this study was to determine if hypertrophied myocardium was associated with diminished cardiac function, restricted oxygen supply, or oxygen consumption during tachycardia. Myocardial oxygen supply and oxygen consumption were determined during baseline and atrial pacing conditions 30 days after New Zealand White rabbits were prepared as one-kidney, one clip Goldblatt hypertensive or uninephrectomized sham control rabbits. Coronary blood flow and cardiac output, using radioactive microspheres, and small vessel oxygen saturations, using microspectrophotometry, were measured in hypertrophied and nonhypertrophied hearts. After 30 days, baseline blood pressure was significantly higher in the Goldblatt rabbits compared with sham controls, and hypertension was maintained during pacing. The myocardium was hypertrophied in the Goldblatt hypertensive rabbits compared with sham controls. Baseline heart rates were not different between animal groups (242 +/- 32 and 244 +/- 24 beats/min, respectively). Both groups were paced 35% above baseline heart rates; during pacing, cardiac output was similar to baseline values in the sham controls (304 +/- 99 versus 321 +/- 116 ml/min, respectively) but reduced in the hypertensive rabbits (248 +/- 43 versus 325 +/- 62 ml/min). Myocardial oxygen consumption increased twofold in both nonhypertrophied and hypertrophied ventricles during tachycardia. Oxygen extraction was significantly elevated, but coronary blood flow was not altered during pacing in either animal group. Therefore, at the pacing level chosen the diminished function in cardiac hypertrophy was not associated with reduced oxygen consumption. Conversely, reduced efficiency during pacing in the hypertrophied myocardium was suggested.
本研究的目的是确定肥厚心肌是否与心动过速时的心功能减退、氧供应受限或氧消耗有关。在将新西兰白兔制备成一侧肾、单夹Goldblatt高血压模型或单侧肾切除假手术对照兔30天后,于基线期和心房起搏条件下测定心肌氧供应和氧消耗。使用放射性微球测量肥厚和非肥厚心脏的冠状动脉血流量和心输出量,使用显微分光光度法测量小血管氧饱和度。30天后,Goldblatt兔的基线血压显著高于假手术对照组,且起搏期间高血压持续存在。与假手术对照组相比,Goldblatt高血压兔的心肌肥厚。动物组之间的基线心率无差异(分别为242±32和244±24次/分钟)。两组均以高于基线心率35%的频率起搏;起搏期间,假手术对照组的心输出量与基线值相似(分别为304±99和321±116毫升/分钟),但高血压兔的心输出量降低(248±43和325±62毫升/分钟)。心动过速期间,非肥厚和肥厚心室的心肌氧消耗均增加两倍。氧摄取显著升高,但两组动物在起搏期间冠状动脉血流量均未改变。因此,在所选择的起搏水平下,心肌肥厚时的心功能减退与氧消耗减少无关。相反,提示肥厚心肌在起搏期间效率降低。