EFFECTS OF PRESSURE AND DURATION OF HYPERKALEMIC INFUSIONS ON ENDOTHELIAL FUNCTION

被引:24
作者
CARTIER, R
PELLERIN, M
HOLLMANN, C
PELLETIER, LC
机构
[1] Department of Cardiovascular Surgery, Montreal Heart Institute, Montreal, Que.
关键词
D O I
10.1016/0003-4975(93)90278-P
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Infusions of crystalloid hyperkalemic cardioplegic solutions (CHCSs) are known to impair endothelium-dependent coronary relaxation. This impairment might also be influenced by high perfusion pressure and duration of CHCS infusion. To verify this hypothesis, we designed experiments to study the influence of pressure and duration of CHCS infusion as modulating factors in CHCS-related endothelial impairment. Isolated hearts of Sprague-Dawley rats were studied in a Langendorff apparatus for coronary endothelial function. Hearts (n = 6) were exposed to four different CHCSs containing 12, 24, 40, or 100 mmol/L of potassium chloride (KCl). Endothelial and smooth muscle functions were respectively tested by infusion of 5-hydroxytryptamine (1 x 10-6 mol/L) and sodium nitroprusside (1 x 10(-5) mol/L) before and after CHCS perfusion. In group I (n = 24), 37-degrees-C CHCSs were perfused at 80 cm H2O of pressure for 30 minutes. In group II (n = 24), the same CHCSs were perfused at 160 cm H2O for 30 minutes. In group III (n = 18), CHCSs containing 24, 40, and 100 mmol/L of KCl were infused at 160 cm H2O for 10 minutes. In all groups, response to sodium nitroprusside was unaltered by CHCS infusion, indicating that smooth muscle function was preserved. However, in group II, 5-hydroxytryptamine-induced vasodilatation was significantly impaired in hearts perfused with CHCS containing 24 mmol/L of KCl or more, suggesting endothelial damage. This study demonstrates that, in addition to KCl concentration, pressure and duration of infusion are two major determinants in CHCS-mediated endothelial damage.
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收藏
页码:700 / 705
页数:6
相关论文
共 24 条
[1]  
CARPENTIER S, 1981, CIRCULATION, V64, P90
[2]  
FOLLETTE DM, 1980, SURG FORUM, V31, P253
[3]   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
[4]   ENDOTHELIUM-DERIVED RELAXING FACTOR INHIBITS INVITRO PLATELET-AGGREGATION [J].
FURLONG, B ;
HENDERSON, AH ;
LEWIS, MJ ;
SMITH, JA .
BRITISH JOURNAL OF PHARMACOLOGY, 1987, 90 (04) :687-692
[5]   THE NATURE OF ENDOTHELIUM-DERIVED VASCULAR RELAXANT FACTOR [J].
GRIFFITH, TM ;
EDWARDS, DH ;
LEWIS, MJ ;
NEWBY, AC ;
HENDERSON, AH .
NATURE, 1984, 308 (5960) :645-647
[6]  
HARJULA A, 1984, J CARDIOVASC SURG, V25, P147
[7]  
HASHIMOTO K, 1991, J THORAC CARDIOV SUR, V102, P688
[8]  
HEARSE D J, 1986, British Journal of Pharmacology, V87, p12P
[9]  
Hearse DJ, 1981, PROTECTION ISCHEMIC
[10]  
Langendorff O., 1895, PFLUEGERS ARCH, V61, P291, DOI [DOI 10.1007/BF01812150, 10.1007/BF01812150]