AJP Legacy AJP: Advances in Physiology Education
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol 204: 619-625, 1963;
0002-9513/63 $5.00
This Article
Right arrow Full Text (PDF)
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Hyland, J. W.
Right arrow Articles by Dexter, L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hyland, J. W.
Right arrow Articles by Dexter, L.

Effect of selective embolization of various sized pulmonary arteries in dogs

John W. Hyland 1, George T. Smith 1, Lockhart B. McGuire 1, Donald C. Harrison 1, Florence W. Haynes 1, and Lewis Dexter 1

1 Departments of Medicine and Pathology, Peter Bent Brigham Hospital, and Harvard Medical School, Boston, Massachusetts

Pulmonary embolism was produced in 30 closed-chest 8-kg dogs with polystyrene spheres, glass beads, or blood clots of precise graded size. The sizes matched selectively the internal diameter of pulmonary arteries from lobar branches (5–6 mm) down to atrial arteries (0.17 mm). Emboli were injected into the right atrium until the pressure in the pulmonary artery rose 5–10 mm Hg. The number of emboli of a given size required to produce this incipient pulmonary hypertension was compared with the number of vessels of that same size as determined from the literature as well as by postmortem injection with Schlesinger mass. The number of emboli bore a constant relation to the number of vessels of that same size. With each size, the majority of vessels had to be occluded before pulmonary hypertension appeared. This was true even in the absence of anesthesia. The results support the thesis that mechanical blockade rather than vasoconstriction is the mechanism by which pulmonary hypertension is produced by emboli occluding pulmonary arterial (as opposed to arteriolar) vessels.

Submitted on August 6, 1962




This article has been cited by other articles:


Home page
 JBJSHome page
J. Krebs, S. J. Ferguson, S. P. Hoerstrup, B. G. Goss, A. Haeberli, and N. Aebli
Influence of Bone Marrow Fat Embolism on Coagulation Activation in an Ovine Model of Vertebroplasty
J. Bone Joint Surg. Am., February 1, 2008; 90(2): 349 - 356.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Neuroradiol.Home page
J. Krebs, N. Aebli, B.G. Goss, K. Wilson, R. Williams, and S.J. Ferguson
Cardiovascular Changes after Pulmonary Cement Embolism: An Experimental Study in Sheep
AJNR Am. J. Neuroradiol., June 1, 2007; 28(6): 1046 - 1050.
[Abstract] [Full Text] [PDF]

Home page
 VASC ENDOVASCULAR SURGHome page
E. Duran, H. Y. Karagoz, A. Isimer, N. Dogan, A. Kocailik, K. Balkanli, and M. Sungun
Prostacyclin--Thromboxane Ratio as a Noninvasive Screening Test for Pulmonary Embolism
Vascular and Endovascular Surgery, May 1, 1992; 26(4): 317 - 321.
[Abstract] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 1963 by the American Physiological Society.