DOSE-DEPENDENT REDUCTION OF MYOCARDIAL INFARCT SIZE WITH THE PERFLUOROCHEMICAL FLUOSOL-DA

被引:21
作者
RICE, HE [1 ]
VIRMANI, R [1 ]
HART, CL [1 ]
KOLODGIE, FD [1 ]
FARB, A [1 ]
机构
[1] ARMED FORCES INST PATHOL,DEPT CARDIOVASC PATHOL,WASHINGTON,DC 20306
关键词
D O I
10.1016/0002-8703(90)90115-E
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The perfluorochemical Fluosol-DA has been shown to reduce infarct size. However, the dose-response relationship of the agent is unknown. Because perfluorochemicals (PFC) can potentially saturate the reticuloendothelial system and decrease carbon clearance as well as cause a transient elevation in liver enzymes, the present study was conducted to determine the lowest effective dose. New Zealand White rabbits (n = 73) were randomly selected prior to infarction to receive 10, 15, 20, 25, or 30 ml/kg PFC or an equivalent volume of 5% dextran (control) intravenously. Animals underwent 30 minutes of coronary artery occlusion with PFC or dextran infused over a 30-minute period starting at 20 minutes into the occlusion. Animals were put to death at 24 hours and infarct size was determined histologically and quantitated by computerized planimetry. Neutrophil infiltration into the ischemic myocardium was evaluated semiquantitatively. No hemodynamic differences were noted within groups. Infarct size was similar to that of controls in animals treated with 10 or 15 ml/kg PFC. Significant infarct size reduction, however, was noted in animals treated with 20, 25, and 30 ml/kg PFC versus controls; (p = 0.05, 0.04, and 0.02, respectively). Maximal infarct size reduction was seen with 30 ml/kg PFC (35%). Neutrophil infiltration was significantly decreased in all groups treated with PFC. These results show that intravenous Fluosol-DA significantly reduces infarct size at a minimal dose of 20 ml/kg. © 1990.
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页码:1039 / 1046
页数:8
相关论文
共 44 条
[31]  
PITARYS CJ, 1989, CIRCULATION, V80, P397
[32]   WAVEFRONT PHENOMENON OF ISCHEMIC CELL-DEATH .1. MYOCARDIAL INFARCT SIZE VS DURATION OF CORONARY-OCCLUSION IN DOGS [J].
REIMER, KA ;
LOWE, JE ;
RASMUSSEN, MM ;
JENNINGS, RB .
CIRCULATION, 1977, 56 (05) :786-794
[33]   REDUCTION OF THE EXTENT OF ISCHEMIC MYOCARDIAL INJURY BY NEUTROPHIL DEPLETION IN THE DOG [J].
ROMSON, JL ;
HOOK, BG ;
KUNKEL, SL ;
ABRAMS, GD ;
SCHORK, MA ;
LUCCHESI, BR .
CIRCULATION, 1983, 67 (05) :1016-1023
[34]   SELECTIVE ACCUMULATION OF THE 1ST COMPONENT OF COMPLEMENT AND LEUKOCYTES IN ISCHEMIC CANINE HEART-MUSCLE - A POSSIBLE INITIATOR OF AN EXTRA MYOCARDIAL MECHANISM OF ISCHEMIC-INJURY [J].
ROSSEN, RD ;
SWAIN, JL ;
MICHAEL, LH ;
WEAKLEY, S ;
GIANNINI, E ;
ENTMAN, ML .
CIRCULATION RESEARCH, 1985, 57 (01) :119-130
[35]   EFFECTS OF INTRAVENOUS FLUOROCARBONS DURING AND WITHOUT OXYGEN ENHANCEMENT ON ACUTE MYOCARDIAL ISCHEMIC-INJURY ASSESSED BY MEASUREMENT OF INTRAMYOCARDIAL GAS TENSIONS [J].
RUDE, RE ;
GLOGAR, D ;
KHURI, SF ;
KLONER, RA ;
KARAFFA, S ;
MULLER, JE ;
CLARK, LC ;
BRAUNWALD, E .
AMERICAN HEART JOURNAL, 1982, 103 (06) :986-995
[36]   OXYGEN RADICALS MEDIATE ENDOTHELIAL CELL DAMAGE BY COMPLEMENT-STIMULATED GRANULOCYTES - INVITRO MODEL OF IMMUNE VASCULAR DAMAGE [J].
SACKS, T ;
MOLDOW, CF ;
CRADDOCK, PR ;
BOWERS, TK ;
JACOB, HS .
JOURNAL OF CLINICAL INVESTIGATION, 1978, 61 (05) :1161-1167
[37]   INFLUENCE OF COLLATERAL BLOOD-FLOW AND OF VARIATIONS IN MVO2 ON TISSUE-ATP CONTENT IN ISCHEMIC AND INFARCTED MYOCARDIUM [J].
SCHAPER, W ;
BINZ, K ;
SASS, S ;
WINKLER, B .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1987, 19 (01) :19-37
[38]  
SCHAPER W, 1984, THERAPEUTIC APPROACH, P79
[39]   PASSIVE MECHANICAL-PROPERTIES OF HUMAN-LEUKOCYTES [J].
SCHMIDSCHONBEIN, GW ;
SUNG, KLP ;
TOZEREN, H ;
SKALAK, R ;
CHIEN, S .
BIOPHYSICAL JOURNAL, 1981, 36 (01) :243-256
[40]   NEUTROPHIL-MEDIATED INJURY TO ENDOTHELIAL-CELLS - ENHANCEMENT BY ENDOTOXIN AND ESSENTIAL ROLE OF NEUTROPHIL ELASTASE [J].
SMEDLY, LA ;
TONNESEN, MG ;
SANDHAUS, RA ;
HASLETT, C ;
GUTHRIE, LA ;
JOHNSTON, RB ;
HENSON, PM ;
WORTHEN, GS .
JOURNAL OF CLINICAL INVESTIGATION, 1986, 77 (04) :1233-1243