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[Cancer Research 39, 17-23, January 1, 1979]
© 1979 American Association for Cancer Research

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Hemodynamic Characteristics in Microcirculatory Blood Channels during Early Tumor Growth1

Bernhard Endrich, Marcos Intaglietta2, Huibert S. Reinhold and Joseph F. Gross

Department of AMES-Bioengineering, M-005, University of California, San Diego, La Jolla, California, 92093 [B. E., M. I.]; Radiobiological Institutes, TNO Rijswijk, The Netherlands [H. S. R.]; and Department of Chemical Engineering, University of Arizona, Tucson, Arizona 85719 [J. F. G.]

Red blood cell (RBC) velocity was determined in the microcirculation of the BA 1112 rat sarcoma and in regions located outside the tumor (repairing tissue), which were used as a control and were assumed to be representative for the inflammatory-reparative reaction of a healing wound. Studies were carried out in modified Algire chamber preparations utilizing television techniques in situ during a period of 18 days.

RBC velocity in repairing tissue was of the order of 0.80 ± 0.15 (S.E.) mm/sec in terminal arterioles, 0.2 ± 0.09 mm/sec in postcapillary venules, and 0.2 ± 0.1 mm/sec in collecting venules and remained constant during the observation period. By comparison, RBC velocity in terminal arterioles of the tumor tissue increased from 0.72 ± 0.08 mm/sec to 0.95 ± 0.09 mm/sec and decreased slightly in postcapillary and collecting venules. Vasomotion in terminal arterioles of the malignant tissue portion could be demonstrated only until Day 22 after implantation.

Since vasomotion was observed only during the initial phase of tumor growth and the arteriolar RBC velocity increased during the same period, our findings indicate that blood is supplied to mesenchymal tumor by means of dilated arterioles. Our observations are related to control measurements in adjacent repairing tissue, which like tumor tissue exhibits continuous cellular replication.

In this tissue, the RBC velocity of postcapillary and collecting venules remained constant. By comparison, RBC velocity decreased in venular outflow vessels of the tumor, suggesting that venous drainage is facilitated during progressive spread of the BA 1112 sarcoma.

1 Supported by National Cancer Institute Contract N01-CB-63981.

2 To whom requests for reprints should be addressed at AMES-Bioengineering, M-005, University of California, San Diego, La Jolla, Calif. 92093.

Received 6/19/78. Accepted 9/25/78.




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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1979 by the American Association for Cancer Research.