Studies of Pulmonary Hypertension I. Pulmonary Circulatory Dynamics in Patients With Pulmonary Emphysema at Rest 1

Yu, Paul N.; Lovejoy, Frank W.; Joos, Howard A.; Nye, Robert E.; McCann, William S.; Vernarelli, S. John; Gouverneur, Carol

doi:10.1172/jci102721

Cited by 63 publications

(7 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Despite early studies showing a relationship between partial pressure of carbon dioxide (PaCO 2 ) and mPAP in COPD subjects, 27 the role of hypercapnia in contributing to PHT in COPD is unclear. From a range of physiologic studies exploring this relationship 28 -30 it has become apparent that hypercapnia increases cardiac output, which drives an increase in mPAP.…”

Section: Hypercapnia/acidosismentioning

confidence: 99%

Mechanisms of pulmonary hypertension in chronic obstructive pulmonary disease: A pathophysiologic review

Wrobel

Thompson

Williams

2012

The Journal of Heart and Lung Transplantation

View full text Add to dashboard Cite

Section: Hypercapnia/acidosismentioning

confidence: 99%

Mechanisms of pulmonary hypertension in chronic obstructive pulmonary disease: A pathophysiologic review

Wrobel

Thompson

Williams

2012

The Journal of Heart and Lung Transplantation

View full text Add to dashboard Cite

“…Alveolar hypoxia undoubtedly contributes to pulmonary hypertension in COPD and there is a correlation, albeit poor, between the pulmonary artery pressure and the degree of arterial hypoxaemia [6,7]. Structural remodelling of the pulmonary vasculature as a consequence of chronic alveolar hypoxia is probably the main contributor to the pathogenesis of pulmonary hypertension in COPD [3,8] although a number of other factors may be involved, including hyperinflation and loss of alveolar capillaries in emphysema [9].…”

Section: Introductionmentioning

confidence: 99%

Pilot study of losartan for pulmonary hypertension in chronic obstructive pulmonary disease

et al. 2005

View full text Add to dashboard Cite

Background: Morbidity in COPD results from a combination of factors including hypoxia-induced pulmonary hypertension, in part due to pulmonary vascular remodelling. Animal studies suggest a role of angiotensin II and acute studies in man concur. Whether chronic angiotensin-II blockade is beneficial is unknown. We studied the effects of an angiotensin-II antagonist losartan, on haemodynamic variables, exercise capacity and symptoms.

show abstract

“…The methods of determining the cardiac output and recording blood pressures have been described in detail in several previous papers (11)(12)(13)(14). The formulae used to derive the resistances and ventricular work against pressures and mitral valve flow were adopted from the papers by Gorlin' and his co-workers (15,16).…”

Section: Clinical Materials and Methodsmentioning

confidence: 99%

Studies of Pulmonary Hypertension. Ix. The Effects of Intravenous Hexamethonium on Pulmonary Circulation in Patients With Mitral Stenosis1

Yu¹,

Nye²,

Lovejoy³

et al. 1958

J. Clin. Invest.

Self Cite

View full text Add to dashboard Cite

During the past five years, circulatory effects of intravenous hexamethonium have been studied in normal subjects and in patients with various cardiac diseases (1-10). With adequate doses of the drug a significant reduction of the systemic blood pressure was observed in almost all cases. In many patients, particularly those with pulmonary hypertension, a reduction of the pulmonary artery pressure was also seen. However, the pulmonary "capillary" or pulmonary artery wedge pressures were recorded in only a small number of cases and changes of resistances in the pulmonary circuit were seldom studied.The purposes of this paper are: 1) to report the hemodynamic effects of hexamethonium in a series of patients with mitral stenosis, 2) to discuss the probable mechanism of the changes of the resistances and pressures in the pulmonary circuit of these patients, and 3) to stress the therapeutic benefit of hexamethonium in patients with acute pulmonary edema secondary to mitral stenosis. CLINICAL MATERIAL AND METHODTwenty-seven patients with predominant mitral stenosis were studied. There were 10 males and 17 females. Their ages ranged from 13 to 58 years. None of the patients had a significant degree of mitral insufficiency, a demonstrable lesion of other valves, or systemic hypertension.1This study was supported in part by a grant-in-aid (H 222 C7) from the National Heart Institute of the National Institutes of Health, by a grant from the American Heart Association and New York Heart Assembly, and by the Hochstetter Fund and Ernest L. Woodward Fund.2Present address: Department of Physiology, Dartmouth Medical School, Hanover, N. H.8 Postdoctoral Research Fellow, National Heart Institute, United States Public Health Service (1956)(1957)(1958). 4 Trainee, National Heart Institute, United States Public Health Service (1956Service ( -1957.The patients were studied two to three hours after a light breakfast. In all cases 100 to 200 mg. of methyprylon (Noludar®) 5 was given by mouth as premedication.The methods of determining the cardiac output and recording blood pressures have been described in detail in several previous papers (11)(12)(13)(14). The formulae used to derive the resistances and ventricular work against pressures and mitral valve flow were adopted from the papers by Gorlin' and his co-workers (15, 16). The mean pressures were measured by planimetric integration. Pulmonary "capillary" pressure was substituted for pulmonary venous and left atrial pressures. Pulmonary vascular resistance is the resistance between pulmonary artery and pulmonary vein. Total pulmonary resistance is the resistance between pulmonary artery and a hypothetical sink at atmospheric pressure. The difference between total pulmonary resistance and pulmonary vascular resistance is termed "left heart resistance" instead of "mitral valve resistance" (17, 18). It includes the resistance at the mitral valve as well as the resistance to filling offered by the left ventricle in diastole. In patients with pure mitral stenosis, however, most of the ca...

show abstract

Studies of Pulmonary Hypertension I. Pulmonary Circulatory Dynamics in Patients With Pulmonary Emphysema at Rest 1

Cited by 63 publications

References 19 publications

Mechanisms of pulmonary hypertension in chronic obstructive pulmonary disease: A pathophysiologic review

Mechanisms of pulmonary hypertension in chronic obstructive pulmonary disease: A pathophysiologic review

Pilot study of losartan for pulmonary hypertension in chronic obstructive pulmonary disease

Studies of Pulmonary Hypertension. Ix. The Effects of Intravenous Hexamethonium on Pulmonary Circulation in Patients With Mitral Stenosis1

Contact Info

Product

Resources

About