Biventricular cardiac dysfunction after acute massive pulmonary embolism in the rat

D. Matthew Sullivan, John A. Watts, Jeffrey A. Kline

Research output: Contribution to journalArticle

18 Scopus citations

Abstract

Cardiac dysfunction has been documented in vivo after acute massive pulmonary embolism (AMPE). The present study tests whether intrinsic ventricular dysfunction occurs in rat hearts isolated after AMPE. AMPE was induced in spontaneously breathing ketaminexylazine-anesthetized rats by thrombus infusion until mean arterial blood pressure (MAP) was ∼40% of basal measurement. A hypotensive control group underwent controlled blood withdrawal to produce MAP ∼40% of basal levels. Shams underwent identical surgical and anesthesia preparation but without pulmonary embolization. Hearts were perfused in isovolumetric mode, and simultaneous right ventricular (RV) and left ventricular (LV) pressures were measured. AMPE caused arterial hypotension with hypoxemia (Po2 = 50 ± 14 Torr), acidemia (pH = 7.26 ± 0.11), and high lactate concentration (6.9 ± 1.7 mM). Starling curves from both ventricles demonstrated that AMPE significantly reduced ex vivo systolic contractile function in the RV (P = 0.031) and LV (P = 0.008) compared with both the hypotensive control and sham hearts. AMPE did not alter coronary flow or compliance in either ventricle. Soluble tumor necrosis factor-α decreased in the RV (P = 0.043) and LV (P = 0.005) tissue. These data support the hypothesis that AMPE produces intrinsic biventricular dysfunction and suggest that arterial hypotension is not the principal mechanism of this dysfunction.

Original languageEnglish (US)
Pages (from-to)1648-1656
Number of pages9
JournalJournal of Applied Physiology
Volume90
Issue number5
StatePublished - May 3 2001

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Keywords

  • Animal model
  • Fibrinolysis
  • Myocardial contraction
  • Pulmonary heart disease
  • Shock
  • Tumor necrosis factor-α

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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