THE CEREBRAL NO-REFLOW PHENOMENON AFTER CARDIAC-ARREST IN RATS - INFLUENCE OF LOW-FLOW REPERFUSION

Citation
Bw. Bottiger et al., THE CEREBRAL NO-REFLOW PHENOMENON AFTER CARDIAC-ARREST IN RATS - INFLUENCE OF LOW-FLOW REPERFUSION, Resuscitation, 34(1), 1997, pp. 79-87
Citations number
37
Categorie Soggetti
Emergency Medicine & Critical Care
Journal title
ISSN journal
03009572
Volume
34
Issue
1
Year of publication
1997
Pages
79 - 87
Database
ISI
SICI code
0300-9572(1997)34:1<79:TCNPAC>2.0.ZU;2-G
Abstract
Objective: Experimental data indicate that early microcirculatory repe rfusion is disturbed after cardiac arrest. We investigated the influen ce of prolonged cardiac arrest and basic life support (BLS) procedures on the quality of cerebral microcirculatory reperfusion. Materials an d methods: In mechanically ventilated male Wistar rats anesthetized wi th N2O and halothane, cardiac arrest was induced by electrical fibrill ation. Ten animals (group I) were subjected to 17 min of cardiac arres t (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 BL S (i.e. mechanical ventilation and external cardiac compressions). In both groups, advanced resuscitation procedures including mechanical ve ntilation, external cardiac massage, 0.2 mg kg(-1) epinephrine, 0.5 mm ol kg(-1) NaHCO3, and defibrillation were started 17 min after inducti on of cardiac arrest. The perfusion of the cerebral microcirculation w as visualized by injection of 0.3 g kg(-1) 15% fluorescein isothiocyan ate (FITC)-albumin 5 min after restoration of spontaneous circulation (ROSC), and the animals were decapitated 2 min later. The left hemisph eres were fixed in 4% formalin, and coronal sections of 200 mu m thick ness at three different standard levels of the rat brain were investig ated using fluorescence microscopy. Areas without capillary filling (c erebral 'no-reflow') were identified and calculated. Results: ROSC cou ld be achieved in five of 10 animals (50%) of group I, and in six of n ine 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 0.0 5). Two sham-operated animals showed homogeneous reperfusion. Conclusi ons: Wistar rats did not develop a marked cerebral 'no-reflow' phenome non after circulatory arrest. A relevant degree of cerebral 'no-reflow ' occurred, however, in animals subjected to a phase of BLS before cir culatory stabilization. Therefore, low-flow states following prolonged cardiocirculatory arrest may aggravate early cerebral microcirculator y reperfusion disorders. (C) 1997 Elsevier Science Ireland Ltd.