Thermally-mediated ultrasound-induced contraction of equine muscular arteries in vitro and an investigation of the associated cellular mechanisms.

The research article investigates how exposure to MHz frequency ultrasound causes contraction in horse mesenteric arteries and the cellular mechanisms associated with it. The study revealed that the ultrasound exposure resulted in repeatable contraction of the arteries in proportion to the acoustic power and was found to be mediated by heat.

Research Methodology and Findings

• The research extends a previous study which found that MHz frequency ultrasound could cause contraction of carotid artery in vitro. In the current study, this investigation was applied to equine mesenteric arteries, specifically the large lateral cecal mesenteric artery.
• In the experiment, the artery was exposed to 4-minute periods of 3.2 MHz continuous wave ultrasound with acoustic powers up to 145 mW. The results showed that the ultrasound exposure led to reversible repeatable contraction of the artery.
• Additionally, the response’s magnitude was found to be directly proportional to the acoustic power. At 145 mW, the mean increase in wall stress was identified to be 0.020 ± 0.017 mN/mm(2) in 34 tests.
• These test results were found to be consistent with the hypothesis and previous findings that the ultrasound-induced contraction was thermally mediated.

Cellular Mechanisms and Impact

• Exposure to a 2°C temperature rise led to an increase in intracellular calcium, which was measured by Fluo-4 fluorescence.
• Inhibition of the inward-rectifier potassium ion channel with BaCl(2) at 4 μM enhanced the ultrasound response by 55% ± 49%, suggesting a similar electrophysiologic basis to responses in mild hyperthermia.
• In smaller mesenteric arteries, no notable vasoconstriction or rise in intracellular calcium was observed from the ultrasound exposure or heating. This suggested a lack or inactivity of temperature-sensitive channels in these smaller vessels.
• The study concludes that the responsiveness of blood vessels to ultrasound is dependent on not only the thermal properties of the vessels themselves and the surrounding tissues but also the electrophysiology within the smooth muscle cells.