Source:http://linkedlifedata.com/resource/pubmed/id/17933454
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
|
pubmed:dateCreated |
2008-2-25
|
pubmed:abstractText |
Recently, several reports have been published on ultrasonic vascular dilation produced with relatively low-frequency ultrasound. It has been speculated that nitric oxide (NO) is an important factor for this ultrasonic vascular dilation. However, a quantitative relationship between the ultrasound intensity and NO generation was not clarified in these reports. We investigated the quantity of NO generated by various ultrasonic intensities by means of real-time measurement of NO concentration in the adductor muscles of the thigh of New Zealand white rabbits exposed to a continuous-wave ultrasound (490 kHz). In the quantitative relationship between NO generation and ultrasonic intensity, the percent increase in NO concentration was 1.25% +/- 1.25%, 10.6% +/- 2.9% and 20.1% +/- 3.5%, with the maximum muscle temperature increase 0.5 +/- 0.2 degrees C, 0.7 +/- 0.2 degrees C, and 0.8 +/- 0.3 degrees C at the ultrasonic intensity (SPTA) of 0.21, 0.35 and 0.48 W/cm(2), respectively. The effect of ultrasound on NO generation was intensity-dependent with a progressive increase from 0.21 W/cm(2) to 0.48 W/cm(2) without significant thermal effect. Ultrasonic NO generation was partially reduced by NOS inhibitor of L-NMMA, clarifying that ultrasound can activate both NOS-dependent and NOS-independent NO generation. These new findings provided scientific basis for ultrasonic vasodilatation and support the potentiality of a new ultrasonic technology for the treatment and prevention of the ischemic tissue based on the new concept of NO generated angiogenesis. (E-mail: furuhata@jikei.ac.jp).
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical | |
pubmed:status |
MEDLINE
|
pubmed:month |
Mar
|
pubmed:issn |
0301-5629
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
34
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
487-93
|
pubmed:meshHeading |
pubmed-meshheading:17933454-Animals,
pubmed-meshheading:17933454-Electrodes,
pubmed-meshheading:17933454-Endothelium, Vascular,
pubmed-meshheading:17933454-Models, Animal,
pubmed-meshheading:17933454-Muscle, Skeletal,
pubmed-meshheading:17933454-NG-Nitroarginine Methyl Ester,
pubmed-meshheading:17933454-Nitric Oxide,
pubmed-meshheading:17933454-Nitric Oxide Synthase,
pubmed-meshheading:17933454-Rabbits,
pubmed-meshheading:17933454-Thigh,
pubmed-meshheading:17933454-Ultrasonic Therapy,
pubmed-meshheading:17933454-Vasodilation,
pubmed-meshheading:17933454-Wound Healing
|
pubmed:year |
2008
|
pubmed:articleTitle |
Nitric oxide generation directly responds to ultrasound exposure.
|
pubmed:affiliation |
Medical Engineering Laboratory, Jikei University School of Medicine, Tokyo, Japan.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|