The Journal of Physiological Sciences

, Volume 63, Issue 1, pp 55–62 | Cite as

Intravenous infusion of hyperosmotic NaCl solution induces acute cor pulmonale in anesthetized rats

  • Chikara Abe
  • Yoshiharu Tsuru
  • Chihiro Iwata
  • Ryosuke Ogihara
  • Hironobu MoritaEmail author
Original Paper


Intravenous hyperosmotic NaCl infusion is an effective treatment for circulatory shock. However, a fast infusion rate (2 mL/kg at the rate of 1 mL/s) induces transient hypotension. This response has been reported to be due to decreased total peripheral resistance and/or decreased cardiac performance. Although the hypotension is transient and recovers within 2 min without detrimental consequences, it is important to understand the associated hemodynamics and mechanisms. We found that the hypotensive effect was larger with intravenous NaCl infusion than with intra-aortic infusion, indicating that change in cardiac performance played a more significant role than change in peripheral resistance. NaCl infusion induced an increase in pulmonary vascular resistance and central venous pressure and a decrease in right ventricular dP/dt max, suggesting acute cor pulmonale. Diastolic ventricular crosstalk-induced left ventricular failure was also observed. Hyperosmotic NaCl-induced hypotension was therefore mainly due to a combination of acute cor pulmonale and left ventricular failure.


Arterial pressure Aortic flow Total systemic peripheral resistance Left ventricle Right ventricle dP/dt max 



This study was supported by The Salt Science Research Foundation, No. 1226, a Grant-in-Aid for Young Scientists (B), and a Grant-in-Aid for Scientific Research (C) from the Japan Society for the Promotion of Science.

Conflict of interest


Supplementary material

Supplementary material 1 (MPG 3410 kb)


  1. 1.
    de Felippe J, Jr., Timoner J, Velasco IT, Lopes OU and Rocha-e-Silva M, Jr. (1980) Treatment of refractory hypovolaemic shock by 7.5 % sodium chloride injections. Lancet 2(8202):1002–1004Google Scholar
  2. 2.
    Kreimeier U, Messmer K (2002) Small-volume resuscitation: from experimental evidence to clinical routine. Advantages and disadvantages of hypertonic solutions. Acta Anaesthesiol Scand 46(6):625–638PubMedCrossRefGoogle Scholar
  3. 3.
    Bitterman H, Triolo J, Lefer AM (1987) Use of hypertonic saline in the treatment of hemorrhagic shock. Circ Shock 21(4):271–283PubMedGoogle Scholar
  4. 4.
    Nakayama S, Kramer GC, Carlsen RC, Holcroft JW (1985) Infusion of very hypertonic saline to bled rats: membrane potentials and fluid shifts. J Surg Res 38(2):180–186PubMedCrossRefGoogle Scholar
  5. 5.
    Wright AR, Rees SA, Vandenberg JI, Twist VW, Powell T (1995) Extracellular osmotic pressure modulates sodium-calcium exchange in isolated guinea-pig ventricular myocytes. J Physiol 488(Pt 2):293–301PubMedGoogle Scholar
  6. 6.
    Orchard CH, Kentish JC (1990) Effects of changes of pH on the contractile function of cardiac muscle. Am J Physiol 258(6 Pt 1):C967–C981PubMedGoogle Scholar
  7. 7.
    Kien ND, Kramer GC, White DA (1991) Acute hypotension caused by rapid hypertonic saline infusion in anesthetized dogs. Anesth Analg 73(5):597–602PubMedGoogle Scholar
  8. 8.
    Zhang D, Sato T, Gong D, Fu L, Dai S, Xu H, Wu Q, Wang D, Peng Y, Sun Y (2009) Neural reflex hypotension induced by very small dose of hypertonic NaCl solution in rats. Chin J Physiol 52(1):8–15PubMedCrossRefGoogle Scholar
  9. 9.
    Andrade MV, Velasco IT, Moraes-Santos T, Melo JR, de Araujo GK, Cunha-Meio JR (2002) Cardiovascular and respiratory interactions of hyperosmolar saline, scorpion toxin, and veratridine in rats. Shock 18(5):407–414PubMedCrossRefGoogle Scholar
  10. 10.
    Raizner AE, Costin JC, Croke RP, Bishop JB, Inglesby TV, Skinner NS Jr (1973) Reflex, systemic, and local hemodynamic alterations with experimental hyperosmolality. Am J Physiol 224(6):1327–1333PubMedGoogle Scholar
  11. 11.
    Read RC, Johnson JA, Vick JA, Meyer MW (1960) Vascular effects of hypertonic solutions. Circ Res 8:538–548PubMedCrossRefGoogle Scholar
  12. 12.
    Ama R, Leather HA, Segers P, Vandermeersch E, Wouters PF (2006) Acute pulmonary hypertension causes depression of left ventricular contractility and relaxation. Eur J Anaesthesiol 23(10):824–831PubMedCrossRefGoogle Scholar
  13. 13.
    Atherton JJ, Moore TD, Lele SS, Thomson HL, Galbraith AJ, Belenkie I, Tyberg JV, Frenneaux MP (1997) Diastolic ventricular interaction in chronic heart failure. Lancet 349(9067):1720–1724PubMedCrossRefGoogle Scholar
  14. 14.
    Janicki JS, Weber KT (1980) The pericardium and ventricular interaction, distensibility, and function. Am J Physiol 238(4):H494–H503PubMedGoogle Scholar
  15. 15.
    Olsen CO, Tyson GS, Maier GW, Spratt JA, Davis JW, Rankin JS (1983) Dynamic ventricular interaction in the conscious dog. Circ Res 52(1):85–104PubMedCrossRefGoogle Scholar
  16. 16.
    Belenkie I, Dani R, Smith ER, Tyberg JV (1989) Effects of volume loading during experimental acute pulmonary embolism. Circulation 80(1):178–188PubMedCrossRefGoogle Scholar

Copyright information

© The Physiological Society of Japan and Springer Japan 2012

Authors and Affiliations

  • Chikara Abe
    • 1
  • Yoshiharu Tsuru
    • 2
  • Chihiro Iwata
    • 1
  • Ryosuke Ogihara
    • 2
  • Hironobu Morita
    • 1
    Email author
  1. 1.Department of PhysiologyGifu University Graduate School of MedicineGifuJapan
  2. 2.Primetech CorporationTokyoJapan

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