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Carbon dioxide is a triple vasodilator.

Dragos A Duse1,2, Nathalie H Schröder1, Sotirios Akritidis3

  • 1Institute for Molecular Medicine III, University Hospital Düsseldorf, Heinrich Heine University; Düsseldorf, Germany.

Cardiovascular Research
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Carbon dioxide (CO2) acts as a triple vasodilator, influencing blood flow through nitric oxide, EDHF, and myogenic pathways. A novel NIRS-CO2 method reveals blunted CO2 responses in vascular disease, offering a new diagnostic tool.

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Area of Science:

  • Physiology
  • Vascular Biology
  • Medical Diagnostics

Background:

  • Carbon dioxide (CO2) is known to regulate blood flow and is used therapeutically for conditions like brain injury and peripheral arterial disease (PAD).
  • The precise mechanisms underlying CO2's vasoactive effects, particularly its role in different vascular beds and disease states, remain incompletely understood.
  • Understanding CO2's vasodilatory actions is crucial for optimizing its therapeutic applications and developing new diagnostic tools.

Purpose of the Study:

  • To elucidate the multifaceted vasodilatory mechanisms of carbon dioxide (CO2) in the vasculature.
  • To investigate the impact of vascular disease on CO2-mediated vasodilation in both animal models and human subjects.
  • To develop and validate a novel non-invasive method, Near Infrared Spectroscopy combined with CO2 (NIRS-CO2), for assessing microvascular reactivity.

Main Methods:

  • Vasoactive CO2 effects were assessed in isolated arteries from healthy, hypertensive, and soluble guanylyl cyclase (sGC) knockout mice using a myograph.
  • CO2-based Near Infrared Spectroscopy (NIRS-CO2) was developed to measure skin microcirculation vasoreactivity in healthy individuals and patients with PAD and coronary artery disease (CAD).
  • NIRS-CO2 measurements were compared with flow-mediated dilation (FMD) and analyzed for associations with disease status and cardiovascular risk factors.

Main Results:

  • CO2 was identified as a 'triple vasodilator,' mimicking endothelium-derived relaxing factor (nitric oxide, NO), endothelium-derived hyperpolarization factor (EDHF), and direct myogenic vasodilators.
  • CO2 engages endothelial NO/sGC, endothelial SKCa/IKCa channels, and myogenic KV and IKCa potassium channels.
  • CO2-evoked vasodilation was found to be blunted and delayed in diseased human and murine arteries; NIRS-CO2's time-to-intersection metric correlated with PAD/CAD status and identified individuals with cardiovascular risk factors.
  • CO2 vasodilation duration and extent were coupled to tissue metabolism via vascular carbonic anhydrases (CAs), indicating a mechanism for vasculometabolic coupling.

Conclusions:

  • NIRS-CO2 is a feasible method for assessing CO2-evoked microvascular responsiveness, demonstrating disease-associated alterations in PAD/CAD patients.
  • The study identified CO2 as a triple vasodilator with distinct molecular targets, offering insights into its therapeutic potential.
  • Further research is needed to validate NIRS-CO2 in broader vasculopathies and to clarify the roles of NO-sGC and K+ channel pathways for future therapeutic applications.