Laks M M, Garner D, Wong V
Am Heart J. 1979 Dec;98(6):732-5. doi: 10.1016/0002-8703(79)90471-x.
Five mongrel dogs with chronically implanted catheters in the left atrium, mid-thoracic aorta, and right atrium were continuously infused with subhypertensive doses of norepinephrine for 3 months. Left ventricular cineangiography, determinations of aortic pressure, and cardiac output were performed in the conscious dog. After 3 months of continuous norepinephrine infusion, stroke volume increased from 38 +/- 3.0 to 67 +/- 8.0 ml. (p less than .01), the left ventricular end-diastolic volume increased from 72 +/- 6.4 to 89 +/- 12.9 ml. (p less than .05), and the ejection fraction increased from 52 +/- 3.6 to 76 +/- 3.6% (p less than .005). We postulate that norepinephrine results in an increased myocardial function by producing physiological myocardial hypertrophy.
五只杂种狗的左心房、胸主动脉中部和右心房长期植入导管,连续3个月给予亚高血压剂量的去甲肾上腺素。在清醒的狗身上进行左心室电影血管造影、主动脉压力测定和心输出量测定。连续输注去甲肾上腺素3个月后,每搏量从38±3.0毫升增加到67±8.0毫升(p<0.01),左心室舒张末期容积从72±6.4毫升增加到89±12.9毫升(p<0.05),射血分数从52±3.6%增加到76±3.6%(p<0.005)。我们推测,去甲肾上腺素通过产生生理性心肌肥大导致心肌功能增强。