Introduction: Cardiac arrest (CA) triggers post-CA syndrome (PCAS) with complex pathophysiological mechanisms resembling sepsis. Hemoadsorption (HA) is a novel technique designed to remove circulating cytokines. HA in experimental sepsis removed cytokines and improved survival.
Hypothesis: (1) Experimental CA results in cytokine release, and (2) cytokines will be removed by HA in a dose-dependent manner per HA cartridge size.
Methods: Rats were subjected to 10 min ventricular fibrillation (VF) CA. After resuscitation, mean arterial pressure was kept >65 mmHg using epinephrine (EPI) and albumin (ALB) infusions. Veno-venous HA using different cartridge sizes (CA_HA1, CA_HA5 and CA_HA10, n=6/group) was performed between resuscitation time 1 h (RT1) and RT3 when the rats were sacrificed. Sham HA was performed via inactive cartridge (CA_S_HA, n=6). Concurrent controls (CA, n=3) were subjected to 10 min VF CA without HA or sham HA. Plasma cytokines were assessed using Luminex method. Data are displayed as means±SEM. One-way ANOVA with post-hoc Tukey’s test was used to compare the data.
Results: CA resulted in marked increases in interleukin (IL)-1a, IL-1b, and IL-10 that were reduced to sham levels by HA. However, the changes in IL-6, tumor necrosis alpha (TNFa), and interferon gamma (IFNg) over time were similar across groups (Figure 1). In contrast, other cytokines were not affected, e.g. IL-2 or IL-4. TNFa levels peaked early at RT1 prior to HA initiation, and decreased at RT3 in all groups including CA_S_HA, suggesting spontaneous decrease rather than an effect of HA. Increased total EPI and ALB requirements were seen in CA_HA10 group (p<0.05 vs. CA_S_HA or CA). ALB levels at RT3 were not different between groups.
Conclusions: HA reduced selected pivotal cytokines in a dose-dependent manner. However, several cytokines were still increasing at RT3, suggesting that a longer treatment may be needed to optimize the effect. HA seems to hold promise to attenuate PCAS.