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Metoprolol impairs resistance artery function in mice.

Mostafa H El Beheiry1, Scott P Heximer, Julia Voigtlaender-Bolz

  • 1Department of Anesthesia, St. Michael's Hospital, Keenan Research Centre of the Li Ka Shing Knowledge Institute, University of Toronto, Canada.

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Acute metoprolol treatment may increase mortality by blocking beta-2 receptors, impairing blood vessel dilation and reducing oxygen delivery. This beta-blockade effect impacts cerebral blood flow and microvascular function.

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Area of Science:

  • Pharmacology
  • Cardiovascular Physiology
  • Neuroscience

Background:

  • Acute beta-blockade with metoprolol is linked to increased mortality through unknown mechanisms.
  • Metoprolol's high affinity for beta-2 adrenoreceptors suggests a potential role in its adverse effects.

Purpose of the Study:

  • To investigate if metoprolol-induced blockade of beta-2 adrenoreceptors impairs microvessel vasodilation, contributing to increased mortality.
  • To assess the impact of metoprolol on cardiovascular function and tissue oxygen delivery.

Main Methods:

  • Measurements in anesthetized mice included cardiac output, mean arterial pressure, cerebral blood flow, and brain tissue oxygenation.
  • Vasodilatory responses to beta-adrenergic agonists were tested in isolated mesenteric and cerebral arteries.
  • Myogenic responses of isolated arteries were also assessed.

Main Results:

  • Metoprolol reduced heart rate, stroke volume, cardiac output, cerebral blood flow, and brain oxygenation, while increasing systemic vascular resistance.
  • In isolated arteries, metoprolol impaired vasodilation induced by beta-adrenergic agonists.
  • Metoprolol did not affect basal tone or myogenic responses in mesenteric arteries.

Conclusions:

  • Acute metoprolol administration impairs beta-2 adrenergic agonist-mediated vasodilation.
  • This impairment reduces tissue oxygen delivery and may contribute to increased perioperative mortality.
  • The findings support the hypothesis that beta-2 adrenoreceptor blockade is a mechanism for metoprolol's adverse effects.