Search

Vasomotor function (constriction, dilation) can be assessed ex vivo using the pressure myograph technique, also referred to as perfusion myography in older literature. The technique involves isolating an artery (or any other blood vessel/lymphatic vessel) from an animal research model or from surgery-resected human tissue. The vessel preparation is mounted between two tiny glass pipettes through which a physiological saline solution (usually Krebs') is perfused while superfusing the preparation with the same solution. The inner and outer diameter of the vessel can be measured in real time, giving valuable information about the vessel reactivity in response to various vasoconstrictor or vasodilator stimuli in different research models or treatments. In addition, by measuring the passive (100% relaxed) inner and outer diameters of the vessel, important structural information is obtained, which is used to assess the degree of structural remodeling in a disease model or treatment. This technique is not a high-throughput technique and requires highly dedicated and trained personnel to carry out experiments. The reward, however, is highly physiologically relevant data, which can be used to assess the vascular function/dysfunction in almost any vascularized tissue of any human disease model., (© 2025. The Author(s), under exclusive license to Springer Science+Business Media, LLC, part of Springer Nature.)

Evidence is emerging that disruption of the endothelial glycocalyx might contribute importantly to arterial dysfunction in the context of diabetes. One approach to assess the integrity of the endothelium and the vascular smooth muscle cell layer, in the absence of neural, humoral, and mechanical influences, is by measuring arterial vasomotion ex vivo. Here we describe a procedure to assess non-receptor-mediated vasoconstriction, receptor-mediated vasoconstriction, and endothelium-dependent and -independent vasodilation, in resistance and conductance arteries pressurized to 60 mmHg. In addition to evaluating vasoreactivity using isobaric approaches, the same experimental set-up can be used to initiate a pressure gradient across the artery such that intraluminal, flow-mediated vasodilation can be measured. After recording endothelium-dependent vasodilation using isobaric or flow-mediated approaches, identical interventions can be completed in the presence of enzymes that cleave biologically active heparan sulfates into inactive disaccharide and oligosaccharide fragments to assess the contribution from: (a) endothelial-derived substances (e.g., nitric oxide via nitric oxide synthase inhibition); or (b) important components of the glycocalyx (e.g., removal of heparan sulfate via heparitinase III treatment). Here, we show that acute disruption of a predominant glycosaminoglycan i.e., heparan sulfate impairs intraluminal flow-mediated vasodilation in murine resistance arteries., (© 2022. Springer Science+Business Media, LLC, part of Springer Nature.)