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Objective:To apply real-time shear wave elastography to observe the effect of instrument-assisted soft tissue mobilization (IASTM) on Achilles tendons for healthy adults. Methods:From July to December, 2020, 52 healthy adults were assigned into control group (n = 15) and experimental group (n = 37) randomly. The experimental group received IASTM on left Achilles tendons, once another day for two weeks, while the control group received no treatment. The thickness and elastic modulus of the left Achilles tendons were measured with high-frequency ultrasound and shear wave ultrasound elastography on all the subjects, before treatment, immediately after the first treatment and three days after treatment, respectively. Results:Five cases dropped down in the experimental group. There was no significant difference in thickness and elastic Young's modulus of the left Achilles tendons between two groups before treatment (t < 0.630, P > 0.05). The thickness of the left Achilles tendons was less in the experimental group than in the control group immediately after the first treatment (t = 2.149, P < 0.05), while average and maximum elastic Young's modulus was less three days after treatment (t > 2.134, P < 0.05). Conclusion:Real-time shear wave elastography could quantify the thickness and elasticity of Achilles tendon, to evaluate the effect of IASTM.
RESUMO
Objective To observe the effect of 15-hydroxyeicosatetraenoic acid (15-HETE) on the intracellular calcium ion ([Ca2+]i) concentration of cerebral arterial smooth muscle and discuss the source of ([Ca2+]i) mobilization induced by 15-HETE to reveal the mechanism underlying the vasoconstriction aroused by 15-HETE. Methods First, papain and collagenase were employed to isolate the cerebral artery smooth muscle cells (SMCs) from the rats. The cells were separated into experimental group (treated with 15-HETE) and control group. Confocal laser scanning microscope was used to investigate the ([Ca2+]i) signaling in cultured SMCs. Then, Ca2+ channel blockers and Ca2+ store depletion agent were added to identify the source of Ca2+ transients in SMCs of the 2 groups. Finally, internal carotid artery (ICA) rings were used to observe the effect of non-Ca2+ solution on 15-HETE-induced ICA vasoconstriction on both groups. Results Compared with the control group, 15-HETE treatment group enjoyed a significantly increased level of ([Ca2+]i) in cultured SMCs (P＜0.05). After the addition of Ca2+channel blockers (nifedipine, lanthanum ion) and calcium-free solution, 15-HETE treatment group still enjoyed a significantly increased level of ([Ca2+]i) in cultured SMCs as compared with the control group (P＜0.05), while after the addition of Ca2+ store depletion agent (caffeine), no obvious difference was noted between the 2 groups (P＞0.05). Non-Ca2+ solution had no effect on 15-HETE induced vasoconstriction.Conclusion 15-HETE may activate Ca2+ releasing from intracellular stores to rise. ([Ca2+]i) level in SMCs, which subsequently induce the constriction of cerebral arterial smooth muscle.