The object of this work was to try and advance our knowledge of the changes in the pulmonary vascular bed that lead to right ventricular hypertrophy in certain cases of cardiac and respiratory disease. We had noted in previous work some unexplained examples of right ventricular hypertrophy. Some cases of pulmonary heart disease had greatly hypertrophied right ventricles with apparently little gross change in the lungs. Other cases in congestive heart failure had gross changes in the lungs and apparently small right ventricles, but in some of these we were able to demonstrate relative right ventricular hypertrophy by weight when the ventricles were dissected, the left ventricle being very small, and the right ventricle the heavier of the two (Thomas and James, 1958). Histological changes in the pulmonary vascular bed have been described by many workers (Brenner, 1935; Parker, 1940; McKeown, 1952). Injection studies in conditions such as mitral stenosis and congenital heart disease have suggested that the pulmonary arterial bed is reduced (Short, 1957; Evans and Short, 1958). Physiological studies have shown that acute anoxia and some pharmacological agents can produce a transient restriction in the pulmonary vascular bed (Motley et al., 1947; Borst et al., 1957). Where does this " shut-down" take place, what is its character, and how much permanent effect does it produce? Lung injection studies in pulmonary angiography of mitral stenosis (Goodwin et al., 1952; Davies et al., 1953) and in post-mortem specimens (Short 1957), have shown the bare or pruned tree picture indicating that the smaller vessels of the pulmonary arterial bed have been narrowed or obliterated. The assessment of these pictures was visual and we have had no actual measure of the change: consequently in some cases of lesser degree it has been difficult to decide how much change has taken place. We considered this problem and have developed a method of injecting lung specimens in such a way as to obtain a measure of the volume of the arterial bed in the peripheral parts of these lungs (Thomas et al., 1959). We chose to study the peripheral portions because it is rare to find arteries exceeding 2 mm. in diameter in these parts and we were interested in the patency of the arteries of less than 2 mm. diameter.
[1]
A. Bell,et al.
Detection of pulmonary lesions in patients with congenital and acquired heart disease by wedge pulmonary arteriography.
,
1959,
Progress in cardiovascular diseases.
[2]
G. Owen,et al.
Method of measuring the volume of the arterial bed in the peripheral parts of cadaveric lungs.
,
1959,
Lancet.
[3]
W. Evans,et al.
PULMONARY HYPERTENSION IN CONGENITAL HEART DISEASE
,
1958,
British heart journal.
[4]
A. J. Thomas,et al.
THE RIGHT VENTRICLE AND THE SMALL PULMONARY ARTERIES IN COALWORKERS
,
1958,
British heart journal.
[5]
J. Goodwin.
I. The Nature of Pulmonary Hypertension
,
1958
.
[6]
D. Short.
The arterial bed of the lung in pulmonary hypertension.
,
1957,
Lancet.
[7]
M. Mcgregor,et al.
The effects of pharmacologic agents on the pulmonary circulation in the dog; studies on epinephrine, nor-epinephrine, 5-hydroxytryptamine, acetylcholine, histamine and aminophylline.
,
1957,
The Journal of clinical investigation.
[8]
J. Edwards,et al.
Pathology of the Pulmonary Vascular Tree: IV. Structural Changes in the Pulmonary Vessels in Chronic Left Ventricular Failure
,
1954,
Circulation.
[9]
J. Goodwin,et al.
THE CLINICAL AND RADIOLOGICAL ASSESSMENT OF THE PULMONARY ARTERIAL PRESSURE IN MITRAL STENOSIS
,
1953,
British heart journal.
[10]
L. Dexter,et al.
The dynamics of both right and left ventricles at rest and during exercise in patients with heart failure.
,
1953,
Transactions of the Association of American Physicians.
[11]
J. Goodwin,et al.
The pulmonary arteries in mitral stenosis demonstrated by angiocardiography.
,
1952,
The Journal of the Faculty of Radiologists. Faculty of Radiologists.
[12]
F. McKeown,et al.
THE PATHOLOGY OF PULMONARY HEART DISEASE
,
1952,
British heart journal.
[13]
A. Cournand,et al.
The influence of short periods of induced acute anoxia upon pulmonary artery pressures in man.
,
1947,
The American journal of physiology.
[14]
R. Parker.
PULMONARY EMPHYSEMA; A STUDY OF ITS RELATION TO THE HEART AND PULMONARY ARTERIAL SYSTEM
,
1940
.
[15]
P. White,et al.
The commonest cause of hypertrophy of the right ventricle—Left ventricular strain and failure
,
1936
.