Effect of Low-Intensity Cavitation on the Isolated Human Thoracic Artery In Vitro
| Autor: | Vytautas Jurėnas, Jonas Navickas, Saulius Giedraitis, Algimantas Bubulis, Vida Garalienė |
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| Rok vydání: | 2017 |
| Předmět: |
Male
0301 basic medicine Agonist Carbachol Acoustics and Ultrasonics medicine.drug_class Biophysics Isometric exercise In Vitro Techniques 030204 cardiovascular system & hematology 03 medical and health sciences Thoracic Arteries 0302 clinical medicine Isometric Contraction Muscarinic acetylcholine receptor Myocardial Revascularization medicine Humans Radiology Nuclear Medicine and imaging Diltiazem Aged Radiological and Ultrasound Technology Voltage-dependent calcium channel business.industry Chemistry Calcium channel Ultrasound 030104 developmental biology Ultrasonic Waves Radiology Nuclear Medicine and imaging Anesthesia Female business Biomedical engineering medicine.drug |
| Zdroj: | Ultrasound in Medicine & Biology. 43:1040-1047 |
| ISSN: | 0301-5629 |
| DOI: | 10.1016/j.ultrasmedbio.2016.12.007 |
| Popis: | Reported here are the results of an experimental study on the response to low-intensity cavitation induced by low-frequency (4-6 W/cm2, 20 kHz and 32.6 kHz) ultrasound of isolated human arterial samples taken during conventional myocardial revascularization operations. Studies have found that low-frequency ultrasound results in a significant (48%-54%) increase in isometric contraction force and does not depend on the number of exposures (10 or 20) or the time passed since the start of ultrasound (0, 10 and 20 min), but does depend on the frequency and location (internal or external) of the blood vessels for the application of ultrasound. Diltiazem (an inhibitor of slow calcium channels) and carbachol (an agonist of muscarinic receptors) used in a concentration-dependent manner did not modify the relaxation dynamics of smooth muscle affected by ultrasound. Thus, ultrasound conditioned to the augmentation of the isometric contraction force the smooth muscle of blood vessels and did not improve endothelial- and calcium channel blocker-dependent relaxation. |
| Databáze: | OpenAIRE |
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