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  • Nygren, Andreas,1967Gothenburg University,Göteborgs universitet,Institutionen för kliniska vetenskaper,Institute of Clinical Sciences (författare)

Vasopressors and intestinal mucosal perfusion after cardiac surgery: Norepinephrine vs. phenylephrine.

  • Artikel/kapitelEngelska2006

Förlag, utgivningsår, omfång ...

  • 2006

Nummerbeteckningar

  • LIBRIS-ID:oai:gup.ub.gu.se/53717
  • https://gup.ub.gu.se/publication/53717URI
  • https://doi.org/10.1097/01.CCM.0000201879.20281.C6DOI

Kompletterande språkuppgifter

  • Språk:engelska

Ingår i deldatabas

Klassifikation

  • Ämneskategori:ref swepub-contenttype
  • Ämneskategori:art swepub-publicationtype

Anmärkningar

  • OBJECTIVES: To evaluate the potential differential effects of norepinephrine, an alpha1-, beta1-, and beta2-receptor agonist, to the alpha1-agonist phenylephrine on jejunal mucosal perfusion, gastric-arterial PCO2 gradient, and the global splanchnic oxygen demand-supply relationship after cardiac surgery. DESIGN: A randomized, prospective, interventional crossover study. SETTING: A university cardiothoracic intensive care unit. PATIENTS: Ten patients were studied during propofol sedation and mechanical ventilation after uncomplicated coronary artery bypass surgery. INTERVENTIONS: Each patient received randomly and sequentially norepinephrine (0.052+/-0.009 microg/kg/min) and phenylephrine (0.50+/-0.22 microg/kg/min) to increase mean arterial blood pressure by 30%. MEASUREMENTS AND MAIN RESULTS: Data on jejunal mucosal perfusion, jejunal mucosal hematocrit, and red blood cell velocity (laser Doppler flowmetry) as well as gastric-arterial Pco2 gradient (tonometry) and splanchnic oxygen extraction were obtained before (control) and during a 30-min drug infusion period after the target mean arterial blood pressure was reached. The procedure was sequentially repeated for the second vasopressor. Both drugs induced a 40-46% increase in systemic vascular resistance with no change in cardiac index. Neither jejunal mucosal perfusion, jejunal mucosal hematocrit, red blood cell velocity, nor gastric-arterial Pco2 gradient was affected by any of the vasopressors. Splanchnic oxygen extraction increased from 38.2% to 43.1% (p<.001) with norepinephrine and from 39.3% to 47.5% (p<.001) with phenylephrine. This increase was significantly more pronounced with phenylephrine compared with norepinephrine (p<.05). Mixed venous-hepatic vein oxygen saturation gradient increased with both drugs (p<.01), and the increase was more pronounced with phenylephrine (p<.05). Splanchnic lactate extraction was not significantly affected by any of the vasopressors. CONCLUSIONS: Phenylephrine induced a more pronounced global alpha1-mediated splanchnic vasoconstriction compared with norepinephrine. Neither of the vasoconstrictors impaired perfusion of the gastrointestinal mucosa in postcardiac surgery patients. The lack of norepinephrine-induced, alpha1-mediated impairment of gastrointestinal perfusion is not explained by a beta2-mediated counteractive vasodilation but instead by possible mucosal autoregulatory escape.

Ämnesord och genrebeteckningar

  • Aged
  • Analysis of Variance
  • Cardiac Surgical Procedures
  • Cross-Over Studies
  • Female
  • Gastric Mucosa
  • blood supply
  • Hemodynamic Processes
  • Humans
  • Intestinal Mucosa
  • blood supply
  • drug effects
  • Jejunum
  • blood supply
  • Laser-Doppler Flowmetry
  • Male
  • Microcirculation
  • Middle Aged
  • Norepinephrine
  • pharmacology
  • Phenylephrine
  • pharmacology
  • Shock
  • Surgical
  • prevention & control
  • Splanchnic Circulation
  • drug effects
  • Vasoconstrictor Agents
  • pharmacology

Biuppslag (personer, institutioner, konferenser, titlar ...)

  • Thorén, Anders,1955Gothenburg University,Göteborgs universitet,Institutionen för kliniska vetenskaper,Institute of Clinical Sciences(Swepub:gu)xthand (författare)
  • Ricksten, Sven-Erik,1953Gothenburg University,Göteborgs universitet,Institutionen för kliniska vetenskaper,Institute of Clinical Sciences(Swepub:gu)xricsv (författare)
  • Göteborgs universitetInstitutionen för kliniska vetenskaper (creator_code:org_t)

Sammanhörande titlar

  • Ingår i:Critical care medicine34:3, s. 722-90090-3493

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