OBJECTIVES: The aim of this study was to investigate whether early enhanced external counter pulsation therapy after cardiopulmonary resuscitation improved neurological outcome in a mongrel dog cardiac arrest model. DESIGN: Randomized, animal study. SETTING: Assisted circulation laboratory. SUBJECTS: Twenty-four healthy male adult dogs (12-14 kg). INTERVENTIONS: After minutes of untreated ventricular fibrillation followed by 2 minutes of cardiopulmonary resuscitation, the dogs were randomized to receive 4 hours of enhanced external counter pulsation therapy, to receive 4 hours of hypertension with over 140 mm Hg or to be a control. MEASUREMENTS: Blood pressure and left ventricular ejection fraction were recorded. Cerebral flow was assessed using magnetic resonance imaging. Arterial blood gases and endothelium-derived vasoactive substances were assessed before cardiac arrest and 4 hours after the return of spontaneous circulation. Neurological outcome was assessed by the neurologic deficit score and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling staining. RESULTS: Enhanced external counter pulsation significantly improved the left ventricular ejection fraction and increased common carotid artery blood flow and shear stress. Enhanced external counter pulsation increased both relative cerebral blood volume (RCBV, p = 0.043) and relative cerebral blood flow (RCBF, p = 0.012) in animals 4 hours after return of spontaneous circulation. Enhanced external counter pulsation therapy promoted the production of nitric oxide and tissue plasminogen activator and decreased the release of endothelin-1 (p = 0.013) after return of spontaneous circulation. Treatment with norepinephrine in the high mean artery pressure also increased common carotid artery blood flow and shear stress. However, no effects on the left ventricular ejection fraction, the production of nitric oxide and tissue plasminogen activator, or the release of endothelin-1 were found. The neurologic deficit scores of the animals were significantly lower at 24, 48, 72, and 96 hours in the enhanced external counter pulsation group, as well as at 24, 72, and 96 hours compared with animals in the control group after return of spontaneous circulation. Fewer apoptotic neurons were observed in the animals in the enhanced external counter pulsation group compared with the animals in the control and hypertension groups. CONCLUSIONS: These data indicated that the treatment of early enhanced external counter pulsation improved neurological outcome by both increasing cerebral blood flow and improving the recovery of microcirculation after return of spontaneous circulation. The treatment of early enhanced external counter pulsation can be a good option for protecting the brain after return of spontaneous circulation.
OBJECTIVES: The aim of this study was to investigate whether early enhanced external counter pulsation therapy after cardiopulmonary resuscitation improved neurological outcome in a mongrel dogcardiac arrest model. DESIGN: Randomized, animal study. SETTING: Assisted circulation laboratory. SUBJECTS: Twenty-four healthy male adult dogs (12-14 kg). INTERVENTIONS: After minutes of untreated ventricular fibrillation followed by 2 minutes of cardiopulmonary resuscitation, the dogs were randomized to receive 4 hours of enhanced external counter pulsation therapy, to receive 4 hours of hypertension with over 140 mm Hg or to be a control. MEASUREMENTS: Blood pressure and left ventricular ejection fraction were recorded. Cerebral flow was assessed using magnetic resonance imaging. Arterial blood gases and endothelium-derived vasoactive substances were assessed before cardiac arrest and 4 hours after the return of spontaneous circulation. Neurological outcome was assessed by the neurologic deficit score and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling staining. RESULTS: Enhanced external counter pulsation significantly improved the left ventricular ejection fraction and increased common carotid artery blood flow and shear stress. Enhanced external counter pulsation increased both relative cerebral blood volume (RCBV, p = 0.043) and relative cerebral blood flow (RCBF, p = 0.012) in animals 4 hours after return of spontaneous circulation. Enhanced external counter pulsation therapy promoted the production of nitric oxide and tissue plasminogen activator and decreased the release of endothelin-1 (p = 0.013) after return of spontaneous circulation. Treatment with norepinephrine in the high mean artery pressure also increased common carotid artery blood flow and shear stress. However, no effects on the left ventricular ejection fraction, the production of nitric oxide and tissue plasminogen activator, or the release of endothelin-1 were found. The neurologic deficit scores of the animals were significantly lower at 24, 48, 72, and 96 hours in the enhanced external counter pulsation group, as well as at 24, 72, and 96 hours compared with animals in the control group after return of spontaneous circulation. Fewer apoptotic neurons were observed in the animals in the enhanced external counter pulsation group compared with the animals in the control and hypertension groups. CONCLUSIONS: These data indicated that the treatment of early enhanced external counter pulsation improved neurological outcome by both increasing cerebral blood flow and improving the recovery of microcirculation after return of spontaneous circulation. The treatment of early enhanced external counter pulsation can be a good option for protecting the brain after return of spontaneous circulation.