The Pressure Myograph System - 114P is an ideal system used to study the structure and function of isolated sections of small vessels (diameter >40 μm) under near-physiological conditions. Vessel diameters can be measured in response to pharmacological and physiological stimuli.

A built-in heating system maintains the chamber temperature, eliminating the need for continuous and often costly superfusion. The chamber cover includes ports for superfusion, for rapid draining and filling, for cumulative addition of drugs and for oxygenation. To facilitate cleaning, the chamber is made of acid resistant stainless steel. Measurements are continuously recorded by a computer with dimension analysis software - MyoVIEW. As an option, the FlowMeter - 162FM can be added to the system to measure flows between 15-4000 μl/min. In studies requiring rapid freezing or fixation of the vessel segment, the Pressure Myograph for rapid freezing - 115FP can replace the standard 110P chamber.

Because of the nature of the technique, physiological responses such as the myogenic response and flow-mediated dilation can be examined. The state-of-the-art Pressure Myograph software MyoVIEW will collect data such as vessel wall thickness, changes in vessel and lumen diameter, intravascular pressure, and a host of other calculated parameters, such as shear stress and vascular resistance, setting pressure or perfusion myography apart from standard organ bath techniques.

The Myograph & Pressure package

Myograph chamber, Pressure Interface, chamber cover, calibration kit, internal and external tubing, set of polished cannulae.

The Acquisition & Analysis package

Upright Zeiss, Nikon microscope or Motic (contact DMT for further specifications) with USB camera, PC and MyoVIEW.

• Study the structure and function of small vessels >60 μm under near-physiological pressures

• Ergonomic design to facilitate easy and quick mounting of arteries Simplified precise cannula alignment

• Longitudinal force measurement

• Combine with fluorescence imaging to study intracellular Ca2+ or pH

Mascha Koenen, et al., “Ablation of Prdm16 and beige fat identity causes vascular remodeling and elevated blood pressure”, Science, 2026

Alessandro Mengozzi, “BET-induced metabolic reprogramming fuels inflammation at the vascular-fat interface in mice and patients with cardiometabolic disease”, Cell Reports, 2026

Steven D Brooks, et al., “Sickle Trait and Alpha Thalassemia Increase NOS-Dependent Vasodilation of Human Arteries Through Disruption of Endothelial Hemoglobin-eNOS Interactions:, Circulation, 2025

Luisa Rubinelli, et al., “Suppression of endothelial ceramide de novo biosynthesis by Nogo-B contributes to cardiometabolic diseases”, Nature Communications, 2025

Qingqing Chu, et al., “Oxysterol Sensing Through GPR183 Triggers Endothelial Senescence in Hypertension”, Circulation Research,2024