INTRACAVITARY ULTRASOUND IMPAIRS LEFT-VENTRICULAR PERFORMANCE - PRESUMED ROLE OF ENDOCARDIAL ENDOTHELIUM

被引:27
作者
GILLEBERT, TC
DEHERT, SG
ANDRIES, LJ
JAGENEAU, AH
BRUTSAERT, DL
机构
[1] ANTWERP STATE UNIV CTR,DEPT PHYSIOL,GROENERBORGERLAAN 171,B-2020 ANTWERP,BELGIUM
[2] ANTWERP STATE UNIV CTR,DEPT PHYSIOL & MED,B-2020 ANTWERP,BELGIUM
来源
AMERICAN JOURNAL OF PHYSIOLOGY | 1992年 / 263卷 / 03期
关键词
CARDIAC FUNCTION; CONTRACTILITY; DIASTOLE; RELAXATION;
D O I
10.1152/ajpheart.1992.263.3.H857
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Irradiation of isolated cardiac muscle by high-power, high-frequency, continuous wave ultrasound selectively damages endocardial endothelium (EE). We evaluated this ultrasound effect in vivo on the performance of the intact ejecting canine left ventricle (LV). A cylindrical ultrasound probe (0.9 MHz, 25 W), mounted on a catheter, was inserted in the LV cavity through an apical stab wound and was activated for 60, 120, and 240 s, followed each time by a recovery period of 10-15 min. Ultrasound transiently and repeatedly abbreviated the time interval from end diastole to peak (-)dP/dt (from 241 +/- 30 to 229 +/- 32 ms after 240 s; P < 0.001), accelerated LV pressure fall, did not alter peak (+)-dP/dt or peak systolic pressure, increased diastolic and systolic segment lengths, and decreased fractional shortening. Microscopic analysis revealed dispersed granulocytes attached to the EE. EE cells were visibly damaged only in a limited area surrounding the probe. Accordingly, high-power, high-frequency, continuous wave ultrasound reversibly modulated LV performance, presumably by transient alteration of EE function.
引用
收藏
页码:H857 / H865
页数:9
相关论文
共 25 条
[1]  
ANDRIES LJ, 1991, AM J PHYSIOL, V261, pH1636
[2]   END-SYSTOLIC MEASURES OF REGIONAL VENTRICULAR PERFORMANCE [J].
AVERSANO, T ;
MAUGHAN, WL ;
HUNTER, WC ;
KASS, D ;
BECKER, LC .
CIRCULATION, 1986, 73 (05) :938-950
[3]   EFFECTS OF DAMAGING THE ENDOCARDIAL SURFACE ON THE MECHANICAL PERFORMANCE OF ISOLATED CARDIAC-MUSCLE [J].
BRUTSAERT, DL ;
MEULEMANS, AL ;
SIPIDO, KR ;
SYS, SU .
CIRCULATION RESEARCH, 1988, 62 (02) :358-366
[4]   RELAXATION AND DIASTOLE OF THE HEART [J].
BRUTSAERT, DL ;
SYS, SU .
PHYSIOLOGICAL REVIEWS, 1989, 69 (04) :1228-1315
[5]   THE ENDOCARDIUM [J].
BRUTSAERT, DL .
ANNUAL REVIEW OF PHYSIOLOGY, 1989, 51 :263-273
[6]  
BRUTSAERT DL, 1986, MOL MECHANISMS MUSCL, P606
[7]   ENDOTHELIAL, PLATELET AND LEUKOCYTE INTERACTIONS IN ISCHEMIC-HEART-DISEASE - INSIGHTS INTO POTENTIAL MECHANISMS AND THEIR CLINICAL RELEVANCE [J].
DINERMAN, JL ;
MEHTA, JL .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1990, 16 (01) :207-222
[8]   MYOCARDIAL RELAXATION .2. HEMODYNAMIC DETERMINANTS OF RATE OF LEFT-VENTRICULAR ISOVOLUMIC PRESSURE DECLINE [J].
GAASCH, WH ;
BLAUSTEIN, AS ;
ANDRIAS, CW ;
DONAHUE, RP ;
AVITALL, B .
AMERICAN JOURNAL OF PHYSIOLOGY, 1980, 239 (01) :H1-H6
[9]   ASYNCHRONOUS (SEGMENTAL EARLY) RELAXATION OF THE LEFT-VENTRICLE [J].
GAASCH, WH ;
BLAUSTEIN, AS ;
BING, OHL .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1985, 5 (04) :891-897
[10]   INFLUENCE OF LOADING PATTERNS ON PEAK LENGTH-TENSION RELATION AND ON RELAXATION IN CARDIAC-MUSCLE [J].
GILLEBERT, TC ;
SYS, SU ;
BRUTSAERT, DL .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1989, 13 (02) :483-490