title: The cerebral 'no-reflow' phenomenon after cardiac arrest in rats--influence of low-flow reperfusion.
abstract: 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.
  
  
  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 microns 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 < or = 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.
authors.affiliation: Department of Anesthesiology, University of Heidelberg, Germany.
authors.forename: B W
authors.initials: BW
authors.lastname: Böttiger
authors.forename: J J
authors.initials: JJ
authors.lastname: Krumnikl
authors.forename: P
authors.initials: P
authors.lastname: Gass
authors.forename: B
authors.initials: B
authors.lastname: Schmitz
authors.forename: J
authors.initials: J
authors.lastname: Motsch
authors.forename: E
authors.initials: E
authors.lastname: Martin
mesh_terms: D000818:Animals; D001921:Brain / Q000098:blood supply* / Q000473:pathology; D002560:Cerebrovascular Circulation / Q000502:physiology*; D046508:Culture Techniques; D004195:Disease Models, Animal; D005451:Fluorescein Angiography; D006323:Heart Arrest / Q000628:therapy; D002546:Ischemic Attack, Transient / Q000175:diagnosis / Q000503:physiopathology*; D008297:Male; D008833:Microcirculation / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D012016:Reference Values; D015427:Reperfusion Injury / Q000175:diagnosis / Q000473:pathology / Q000503:physiopathology*; D015203:Reproducibility of Results; D012121:Respiration, Artificial; D012151:Resuscitation / Q000379:methods*