Ultrasound improves tissue perfusion in ischemic tissue through a nitric oxide dependent mechanism

被引:88
作者
Suchkova, VN
Baggs, RB
Sahni, SK
Francis, CW
机构
[1] Univ Rochester, Med Ctr, Hematol Oncol Unit, Sch Med & Dent,Dept Med, Rochester, NY 14642 USA
[2] Univ Rochester, Sch Med & Dent, Div Lab Anim Med, Rochester, NY USA
关键词
ultrasound; nitric oxide; nitric oxide synthase; ischemia;
D O I
10.1055/s-0037-1613315
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Ultrasound accelerates enzymatic fibrinolysis in vitro and in animal models and may be used as an adjunct to thrombolytic therapy. Ultrasound can also affect vascular tone directly, and we have now investigated the effect of ultrasound on tissue perfusion in a rabbit model of acute muscle ischemia to characterize the magnitude and temporal course of vasodilation and determine its mechanism. After ligation of the femoral artery of rabbits, tissue perfusion in the gracilis muscle as determined using a laser Doppler probe declined by 53% from 13.7 +/- 0.3 U to 6.4 +/- 0.2 U. The tissue became acidotic as pH declined from normal to 7.05 +/- 0.2. Application of 40 kHz ultrasound at intensities from 0.25 to 0.75 W/cm(2) progressively improved perfusion over 60 min and reversed acidosis, but, these effects were both completely blocked by pre-treatment with the nitric oxide synthase inhibitor L-NAME. Nitric oxide synthase activity in muscle was measured using an assay based on the conversion of radiolabeled L-arginine to L-citrulline and demonstrated an increase of 3.6-fold following ultrasound exposure. This effect was greatest at locations close to the transducer and declined progressively away from it. Histologic examination showed greater capillary circumference in ultrasound exposed muscle compared to unexposed tissue with no other histologic changes. We conclude that the application of 40 kHz at low intensity improves perfusion and reverses acidosis in acutely ischemic muscle through a nitric oxide dependent mechanism.
引用
收藏
页码:865 / 870
页数:6
相关论文
共 40 条
[1]   Production of oxidative products of nitric oxide in infarcted human heart [J].
Akiyama, K ;
Kimura, A ;
Suzuki, H ;
Takeyama, Y ;
Gluckman, TL ;
Terhakopian, A ;
Katagiri, T ;
Suh, KY ;
Roseto, J ;
Bing, RJ .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1998, 32 (02) :373-379
[2]   Nitric oxide synthase in atherosclerosis and vascular injury - Insights from experimental gene therapy [J].
Channon, KM ;
Qian, H ;
George, SE .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2000, 20 (08) :1873-1881
[3]   IMPAIRED VASODILATION OF FOREARM RESISTANCE VESSELS IN HYPERCHOLESTEROLEMIC HUMANS [J].
CREAGER, MA ;
COOKE, JP ;
MENDELSOHN, ME ;
GALLAGHER, SJ ;
COLEMAN, SM ;
LOSCALZO, J ;
DZAU, VJ .
JOURNAL OF CLINICAL INVESTIGATION, 1990, 86 (01) :228-234
[4]   FLOW-MEDIATED ENDOTHELIAL MECHANOTRANSDUCTION [J].
DAVIES, PF .
PHYSIOLOGICAL REVIEWS, 1995, 75 (03) :519-560
[5]   ULTRASONIC ENERGY - EFFECTS ON VASCULAR FUNCTION AND INTEGRITY [J].
FISCHELL, TA ;
ABBAS, MA ;
GRANT, GW ;
SIEGEL, RJ .
CIRCULATION, 1991, 84 (04) :1783-1795
[6]  
Fitzgerald PJ, 2001, CIRCULATION, V103, P1828
[7]   Signal transduction of eNOS activation [J].
Fleming, I ;
Busse, R .
CARDIOVASCULAR RESEARCH, 1999, 43 (03) :532-541
[8]   Ultrasound-enhanced thrombolysis [J].
Francis, CW .
ECHOCARDIOGRAPHY-A JOURNAL OF CARDIOVASCULAR ULTRASOUND AND ALLIED TECHNIQUES, 2001, 18 (03) :239-246
[9]   THE OBLIGATORY ROLE OF ENDOTHELIAL-CELLS IN THE RELAXATION OF ARTERIAL SMOOTH-MUSCLE BY ACETYLCHOLINE [J].
FURCHGOTT, RF ;
ZAWADZKI, JV .
NATURE, 1980, 288 (5789) :373-376
[10]   Targeting of nitric oxide synthase to endothelial cell caveolae via palmitoylation: Implications for nitric oxide signaling [J].
GarciaCardena, G ;
Oh, P ;
Liu, JW ;
Schnitzer, JE ;
Sessa, WC .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (13) :6448-6453