Cardiac changes subseqent to experimental aortic lesions

Cardiac changes subseqent to experimental aortic lesions
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DOI:
10.1001/archinte.1927.00130040074007
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发表时间:
1927-04-01
影响因子:
--
通讯作者:
Hodges, FJ
Hodges, FJ
中科院分区:
其他
文献类型:
--
作者:
Eyster, JAE;Meek, WJ;Hodges, FJ

文献摘要

被引文献

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实验性主动脉瓣狭窄的方法是在19只狗的主动脉带和主动脉瓣的一个尖瓣平分在14只狗的主动脉瓣返流。这些程序在无菌条件下进行,并对动物进行长达7个月的观察。在病变形成之前和之后的不同时间,拍摄心脏大小(面积和横径)的远距X线片。最终处死动物,并在大多数情况下测定体重、心脏重量和心室重量比。结果表明,在病变产生后立即出现一段时间的初始心脏扩张,并持续几天,随后心脏恢复正常或甚至低于正常大小。第二个时期的扩大,表明肥大,逐渐发展,并在70-100天达到最大值。通过组织学检查和最终体重测定证实存在肥大。在整个观察过程中,频繁的心电图未能揭示电轴或各种波的任何显著变化。当实验产生急性和大量心室扩张时,情况也是如此。证实了主动脉瓣返流与血液实际回流到心室中相关的观点,并且进一步表明,主动脉瓣受损的心脏在动脉过载的条件下无法维持其输出,瓣膜完好的心脏也是如此。
Experimental aortic stenosis was produced by means of aortic bands in 19 dogs; and aortic regurgitation in 14 dogs by bisection of one of the cusps of the aortic valve. These procedures were carried out aseptically and the animals observed for periods up to 7 mo. Teleroentgenograms for heart size (area and transverse diameter) were made before and at various times subsequent to the production of the lesion. The animals were finally killed and in most cases body weight, heart weight, and ventricular weight ratios determined. The results indicated a period of initial heart dilatation immediately following the production of the lesion and persisting for a few days, subsequent to which the hearts returned to normal or even subnormal size. A 2nd period of enlargement, indicating hypertrophy, gradually developed and reached its maximum in 70-100 days. The presence of hypertrophy was confirmed histologically and by final weight determinations. Frequent electrocardiograms made throughout the observations failed to reveal any significant change in the electrical axis or in the various waves. This was also true when acute and massive ventricular dilatation was produced experimentally. The view that aortic regurgitation is associated with actual reflux of blood into the ventricle was confirmed, and it was further shown that a heart in which the aortic valve had been injured fails to maintain its output under conditions of arterial overload as well as a heart in which the valve is intact.