β-Blockade attenuates renal blood flow in experimental endotoxic shock by reducing perfusion pressure

Lex M. van Loon*, Gerard A. Rongen, Johannes G. van der Hoeven, Peter H. Veltink, Joris Lemson

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

25 Downloads (Pure)

Abstract

Clinical data suggests that heart rate (HR) control with selective β1-blockers may improve cardiac function during septic shock. However, it seems counterintuitive to start β-blocker infusion in a shock state when organ blood flow is already low or insufficient. Therefore, we studied the effects of HR control with esmolol, an ultrashort- acting β1-selective adrenoceptor antagonist, on renal blood flow (RBF) and renal autoregulation during early septic shock. In 10 healthy sheep, sepsis was induced by continuous i.v. administration of lipopolysaccharide, while maintained under anesthesia and mechanically ventilated. After successful resuscitation of the septic shock with fluids and vasoactive drugs, esmolol was infused to reduce HR with 30% and was stopped 30-min after reaching this target. Arterial and venous pressures, and RBF were recorded continuously. Renal autoregulation was evaluated by the response in RBF to renal perfusion pressure (RPP) in both the time domain and frequency domain. During septic shock, β-blockade with esmolol significantly increased the pressure dependency of RBF to RPP. Stopping esmolol showed the reversibility of the impaired renal autoregulation. Showing that clinical diligence and caution are necessary when treating septic shock with esmolol in the acute phase since esmolol reduced RPP to critical values thereby significantly reducing RBF.

Original languageEnglish
Article numbere14301
JournalPhysiological Reports
Volume7
Issue number23
DOIs
Publication statusPublished - 9 Dec 2019

Keywords

  • acute kidney injury
  • beta-blocker
  • renal autoregulation
  • renal blood flow
  • sepsis

Fingerprint

Dive into the research topics of 'β-Blockade attenuates renal blood flow in experimental endotoxic shock by reducing perfusion pressure'. Together they form a unique fingerprint.

Cite this