Abstract
The aim of this study was to investigate the influence of enhanced external counterpulsation (EECP) on the cardiac function of beagle dogs after prolonged ventricular fibrillation. Twenty-four adult male beagles were randomly divided into control and EECP groups. Ventricular fibrillation was induced in the animals for 12 min, followed by 2 min of cardiopulmonary resuscitation. They then received EECP therapy for 4 h (EECP group) or not (control group). The hemodynamics was monitored using the PiCCO2 system. Blood gas and hemorheology were assessed at baseline and at 1, 2, and 4 h after return of spontaneous circulation (ROSC). The myocardial blood flow (MBF) was quantified by 18F-flurpiridaz PET myocardial perfusion imaging at baseline and 4 h after ROSC. Survival time of the animals was recorded within 24 h. Ventricular fibrillation was successfully induced in all animals, and they achieved ROSC after cardiopulmonary resuscitation. Survival time of the control group was shorter than that of the EECP group [median of 8 h (min 8 h, max 21 h) vs median of 24 h (min 16 h, max 24 h) (Kaplan Meyer plot analysis, P=0.0152). EECP improved blood gas analysis findings and increased the coronary perfusion pressure and MBF value. EECP also improved the cardiac function of Beagles after ROSC in multiple aspects, significantly increased blood flow velocity, and decreased plasma viscosity, erythrocyte aggregation index, and hematocrit levels. EECP improved the hemodynamics of beagle dogs and increased MBF, subsequently improving cardiac function and ultimately improving the survival time of animals after ROSC.
Highlights
In the United States, approximately 300,000 people have an out-of-hospital cardiac arrest each year, and approximately 30–40% of those cases achieve return of spontaneous circulation (ROSC), with only 7% of patients surviving until hospital discharge [1,2]
We found that external counterpulsation (EECP) treatment after ROSC improved neurological function in beagle dogs, increased the release of vascular endothelial-derived relaxing factor NO-1, and increased brain microcirculation blood flow [14]
The survival time of the control group was a median of 8 h, which was significantly shorter than the median of 24 h of the EECP group (P=0.026)
Summary
In the United States, approximately 300,000 people have an out-of-hospital cardiac arrest each year, and approximately 30–40% of those cases achieve return of spontaneous circulation (ROSC), with only 7% of patients surviving until hospital discharge [1,2]. Myocardial dysfunction is an important cause of post-resuscitation circulatory failure that may lead to early mortality after ROSC [3,4]. It is defined as a reversible global dysfunction due to a stunned myocardium in the absence of coronary occlusion and microcirculation disorder of the coronary artery [5,6,7,8,9]. Clinical and experimental studies have found that, in some situations, persistent tissue hypoxia may lead to organ damage despite the restoration of global hemodynamic parameters (heart rate, mean artery pressure, and cardiac index) to their ‘‘normal’’ levels [10,11,12]. Clinical interventions to improve microcirculatory blood flow are still very limited
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