Archiv für Kreislaufforschung

, Volume 66, Issue 1–4, pp 66–79 | Cite as

Statischer Druck, Blutvolumen und zentralvenöser Druck bei renovaskulärer Hypertonie

  • R. Gotzen
  • C. Herberg
  • G. Schultze
  • F. W. Lohmann
Article
  • 33 Downloads

Zusamemnfassung

Bei hypertonen Ratten (9 Wochen nach Klammerung einer Nierenarterie) und normotonen Kontrolltieren wurden der statische Druck, das Erythrozyten- und Plasmavolumen und der zentralvenöse Druck bestimmt.

Es fanden sich folgende Ergebnisse:
  1. 1.

    Der statische Druck der Hochdruckratten war signifikant gegenüber den normotonen Kontrolliteren erhöht.

     
  2. 2.

    Das Blutvolumen der Hochdruckratten war bei Bezug auf das Körpergewicht signifikant gegenüber den normotonen Kontrolltieren verkleinert. Die Abnahme des Blutvolumens beruht auf einer überwiegenden Verkleinerung des Plasma-volumens.

     
  3. 3.

    Der zentralvenöse Druck zeigte im Mittel keinen Unterschied zwischen den Hoch-druckratten und den normotonen Kontrolltieren.

     

Die Erhöhung des statischen Drucks bei der renovaskulären Hypertonie der Ratte beruht auf einer Konstriktion des Kapazitätsgefäßsystems. Die gleichzeitige Steigerung des herzzeitvolumens dürfte bei normalem Füllungsdruck des Herzens auf eine Kontraktilitäts- und/oder Frequenzsteigerung des Herzens zurückzuführen sein. Diese Kreislaufveränderungen lassen an eine gesteigerte Sympathikusaktivität denken.

Summary

Mean circulatory filling pressure, red cell volume and plasma volume and central venous pressure were measured in rats with experimental renal hypertension due to unilateral stenosis of one renal artery (9 weeks later) and normotensive control rats.

The results are as following:
  1. 1.

    In hypertensive rats the mean circulatory filling pressure was significantly elevated compared with normotensive controll rats.

     
  2. 2.

    Blood volume related to body weight was significantly reduced in hypertensive rats compared with normotensive controll rats. The reduced blood volume was caused by lowered plasma volume.

     
  3. 3.

    In the two groups of rats, the hypertensive one and the normotensive control group, the central venous pressure was equally normal.

     

An increase in mean circulatory pressure in rats with experimental renal hypertension is caused by constriction of capacitance vessels. The simultaneous raise of cardiac output in absence of change in central venous pressure may result from inotropic or/and chronotopic influences on the heart.

These changes in circulation may be due to increased sympathetic activity.

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Copyright information

© Dr. Dietrich Steinkopff Verlag 1971

Authors and Affiliations

  • R. Gotzen
    • 1
  • C. Herberg
    • 1
  • G. Schultze
    • 1
  • F. W. Lohmann
    • 1
  1. 1.Medizinischen Klinik und Poliklinik der Freien Universität Berlin im Klinikum SteglitzBerlin 45

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