Influence of atrial natriuretic factor on intravascular volume displacement in pigs

D. L. Rutlen, G. Christensen, K. G. Helgesen and A. Ilebekk University of Oslo, Institute for Experimental Medical Research, Ullevaal Hospital, Norway. The present study was undertaken to quantitate the influences of transcapillary fluid loss, urine output, and the capacity vessels on volume displac...

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Veröffentlicht in:American journal of physiology. Heart and circulatory physiology 1990-11, Vol.259 (5), p.H1595-H1600
Hauptverfasser: Rutlen, D. L, Christensen, G, Helgesen, K. G, Ilebekk, A
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Sprache:eng
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Zusammenfassung:D. L. Rutlen, G. Christensen, K. G. Helgesen and A. Ilebekk University of Oslo, Institute for Experimental Medical Research, Ullevaal Hospital, Norway. The present study was undertaken to quantitate the influences of transcapillary fluid loss, urine output, and the capacity vessels on volume displacement toward and away from the right heart during atrial natriuretic factor (ANF) administration. In eight anesthetized pigs undergoing carotid denervation, cervical vagotomy, and splenectomy, blood was drained from the venae cavae to an extracorporeal reservoir and returned to the right atrium at a constant rate so that volume displacement toward and away from the heart could be recorded as change in reservoir volume. Human ANF-(99-126) (0.1 micrograms.kg-1.min-1) for 15 min was associated with a decrease in reservoir volume of 2.7 +/- 0.4 ml/kg (P less than 0.05), which resulted from a decrease in total blood volume of 8.6 +/- 1.0 ml/kg (P less than 0.05) and a displacement from the capacitance vasculature of 5.9 +/- 1.3 ml/kg (P less than 0.05). Since urine output increased only slightly, virtually all of the total blood volume decrement was due to a displacement of fluid into the extravascular space. Thus ANF acts to displace volume away from the right heart. The displacement is due almost entirely to an increase in transcapillary fluid loss; however, volume displacement from the capacity vessels to the right heart partially counteracts this transcapillary influence.
ISSN:0363-6135
0002-9513
1522-1539
DOI:10.1152/ajpheart.1990.259.5.h1595