The cerebral 'no-reflow' phenomenon after cardiac arrest in rats - Influence of low-flow reperfusion

被引:99
作者
Bottiger, BW
Krumnikl, JJ
Gass, P
Schmitz, B
Motsch, J
Martin, E
机构
[1] Department of Anesthesiology, University of Heidelberg, D-69120 Heidelberg
[2] Department of Neuropathology, University of Heidelberg, D-69120 Heidelberg
[3] Max-Planck-Inst. for Neurol. Res., Department of Experimental Neurology, D-50931 Cologne
关键词
cardiac arrest; cerebral blood flow; cerebral ischemia; no-reflow phenomenon; rats;
D O I
10.1016/S0300-9572(96)01029-5
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Objective: Experimental data indicate that early microcirculatory reperfusion is disturbed after cardiac arrest. We investigated the influence of prolonged cardiac arrest and basic life support (BLS) procedures on the quality of cerebral microcirculatory reperfusion. Materials and methods: In mechanically ventilated male Wistar rats anesthetized with N2O and halothane, cardiac arrest was induced by electrical fibrillation. Ten animals (group I) were subjected to 17 min of cardiac arrest (no-flow). Nine additional animals (group II) underwent only 12 min of cardiac arrest (no-flow), which was followed by a 5-min phase of BLS (i.e. mechanical ventilation and external cardiac compressions). In both groups, advanced resuscitation procedures including mechanical ventilation, external cardiac massage, 0.2 mg kg(-1) epinephrine, 0.5 mmol kg(-1) NaHCO3, and defibrillation were started 17 min after induction of cardiac arrest. The perfusion of the cerebral microcirculation was visualized by injection of 0.3 g kg(-1) 15% fluorescein isothiocyanate (FITC)-albumin 5 min after restoration of spontaneous circulation (ROSC), and the animals were decapitated 2 min later. The left hemispheres were fixed in 4% formalin, and coronal sections of 200 mu m thickness at three different standard levels of the rat brain were investigated using fluorescence microscopy. Areas without capillary filling (cerebral 'no-reflow') were identified and calculated. Results: ROSC could be achieved in five of 10 animals (50%) of group I, and in six of nine animals (67%) of group II (P = n.s.). The severity of cerebral 'no-reflow' was higher in group II compared with group I (6.9 +/- 7.6 vs. 0.7 +/- 0.7% of total sectional areas; P greater than or equal to 0.05). Two sham-operated animals showed homogeneous reperfusion. Conclusions: Wistar rats did not develop a marked cerebral 'no-reflow' phenomenon after circulatory arrest. A relevant degree of cerebral 'no-reflow' occurred, however, in animals subjected to a phase of BLS before circulatory stabilization. Therefore, low-flow states following prolonged cardiocirculatory arrest may aggravate early cerebral microcirculatory reperfusion disorders. (C) 1997 Elsevier Science Ireland Ltd.
引用
收藏
页码:79 / 87
页数:9
相关论文
共 37 条
[1]  
AMES A, 1968, AM J PATHOL, V52, P437
[2]  
[Anonymous], 1985, GUIDE CARE USE LAB A
[3]   ACTIVATION OF BLOOD-COAGULATION AFTER CARDIAC-ARREST IS NOT BALANCED ADEQUATELY BY ACTIVATION OF ENDOGENOUS FIBRINOLYSIS [J].
BOTTIGER, BW ;
MOTSCH, T ;
BOHRER, H ;
BOKER, T ;
AULMANN, M ;
NAWROTH, PP ;
MARTIN, E .
CIRCULATION, 1995, 92 (09) :2572-2578
[4]   THE EFFECTS OF GRADED DOSES OF EPINEPHRINE ON REGIONAL MYOCARDIAL BLOOD-FLOW DURING CARDIOPULMONARY-RESUSCITATION IN SWINE [J].
BROWN, CG ;
WERMAN, HA ;
DAVIS, EA ;
HOBSON, J ;
HAMLIN, RL .
CIRCULATION, 1987, 75 (02) :491-497
[5]   BENEFICIAL-EFFECTS OF TISSUE-TYPE PLASMINOGEN-ACTIVATOR IN ACUTE MYOCARDIAL-ISCHEMIA IN CATS [J].
DARIUS, H ;
YANAGISAWA, A ;
BREZINSKI, ME ;
HOCK, CE ;
LEFER, AM .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1986, 8 (01) :125-131
[6]   HISTOPATHOLOGICAL AND HEMODYNAMIC CONSEQUENCES OF COMPLETE VERSUS INCOMPLETE ISCHEMIA IN THE RAT [J].
DIETRICH, WD ;
BUSTO, R ;
YOSHIDA, S ;
GINSBERG, MD .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1987, 7 (03) :300-308
[7]   CORTICAL HYPOPERFUSION AFTER GLOBAL FOREBRAIN ISCHEMIA IN RATS IS NOT CAUSED BY MICROVASCULAR LEUKOCYTE PLUGGING [J].
DIRNAGL, U ;
NIWA, K ;
SIXT, G ;
VILLRINGER, A .
STROKE, 1994, 25 (05) :1028-1038
[8]   THE QUANTIFICATION OF CEREBRAL INFARCTION FOLLOWING FOCAL ISCHEMIA IN THE RAT - INFLUENCE OF STRAIN, ARTERIAL-PRESSURE, BLOOD-GLUCOSE CONCENTRATION, AND AGE [J].
DUVERGER, D ;
MACKENZIE, ET .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1988, 8 (04) :449-461
[9]   EFFECT OF CEREBRAL BLOOD-FLOW GENERATED DURING CARDIOPULMONARY-RESUSCITATION IN DOGS ON MAINTENANCE VERSUS RECOVERY OF ATP AND PH [J].
ELEFF, SM ;
KIM, H ;
SHAFFNER, DH ;
TRAYSTMAN, RJ ;
KOEHLER, RC .
STROKE, 1993, 24 (12) :2066-2073
[10]   REASSESSMENT OF CEREBRAL CAPILLARY CHANGES IN ACUTE GLOBAL ISCHEMIA AND THEIR RELATIONSHIP TO NO-REFLOW PHENOMENON [J].
FISCHER, EG ;
AMES, A ;
HEDLEYWHYTE, ET ;
OGORMAN, S .
STROKE, 1977, 8 (01) :36-39