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<p>While the majority of rodent resuscitation studies prioritize neurologic outcomes, research into the long-term effects of global ischemia and reperfusion on cardiac function is scarce, generally limited to morphologic assessments. Extracorporeal cardiopulmonary resuscitation (ECPR) is a promising strategy for highly selected patients with refractory cardiac arrest (CA). We aimed to investigate the impact of ventricular fibrillation CA (VFCA) and subsequent ECPR on cardiac recovery in rats. Adult male Sprague-Dawley rats were subjected to either 6–8&#xa0;min VFCA, followed by ECPR and compared to sham animals. The primary outcome parameter was cardiac function assessment at 14 days after CA. The hearts of rats surviving for 14 days were isolated and mounted onto an erythrocyte-perfused, isolated working heart (WH) system. Cardiac output (CO), left ventricular systolic pressure (LVSP), and coronary flow were measured. To assess the heart adaptation to hemodynamic stress, the afterload was gradually increased in 10 mmHg increments while CO and LVSP were monitored. Additionally, the hearts from all animals surviving at least 36&#xa0;h were assessed histologically. Of 15 rats that achieved ROSC after 6&#xa0;min of CA, 7 could be evaluated in the WH setup 14 days after CA. In the 8&#xa0;min CA group, 15 animals achieved ROSC, of which 2 were investigated in WH at 14 days after CA. Compared to the hearts of 7 sham animals, no significant differences in cardiac hemodynamics were observed at a set afterload (60&#xa0;mm Hg; baseline) in the 6&#xa0;min CA group. However, the two investigated 8&#xa0;min CA animals exhibited a trend towards reduced CO and LVSP levels. Notably, both CA groups showed impaired hemodynamic performance to hemodynamic stress. Survivors at 14 days consistently showed significant myocardial pathology, with both 6&#xa0;min and 8&#xa0;min CA groups exhibiting fibrosis, inflammation, and edema most pronounced in the interventricular septum and right ventricle of the 8&#xa0;min CA group. Animals that died prematurely displayed time-dependent acute changes, progressing from hypereosinophilic degeneration (36&#xa0;h survivors) to myocardial necrosis, calcification, and the formation of cell-rich granulation tissue (48–108&#xa0;h survivors). VFCA led to impaired left ventricular hemodynamic function in 8&#xa0;min CA rats resuscitated with ECPR at rest and with increasing afterload. The isolated WH system may offer a valuable tool for assessing long-term cardiac function and performance after resuscitation.</p>

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Post-resuscitation left ventricular dysfunction in a rat model of ventricular fibrillation and extracorporeal cardiopulmonary resuscitation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月20日

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  • Wolfgang Weihs,
  • Matthias Mueller,
  • Ingrid Anna Maria Magnet,
  • Alexander Franz Szinovatz,
  • Ouafa Hamza,
  • Laurenz Wolner,
  • Petra Kodajova,
  • Benjamin Ullram,
  • Roman Brock,
  • Michael Holzer,
  • Bruno K. Podesser,
  • Attila Kiss,
  • Alexandra-Maria Stommel,
  • Sandra Högler

摘要

While the majority of rodent resuscitation studies prioritize neurologic outcomes, research into the long-term effects of global ischemia and reperfusion on cardiac function is scarce, generally limited to morphologic assessments. Extracorporeal cardiopulmonary resuscitation (ECPR) is a promising strategy for highly selected patients with refractory cardiac arrest (CA). We aimed to investigate the impact of ventricular fibrillation CA (VFCA) and subsequent ECPR on cardiac recovery in rats. Adult male Sprague-Dawley rats were subjected to either 6–8 min VFCA, followed by ECPR and compared to sham animals. The primary outcome parameter was cardiac function assessment at 14 days after CA. The hearts of rats surviving for 14 days were isolated and mounted onto an erythrocyte-perfused, isolated working heart (WH) system. Cardiac output (CO), left ventricular systolic pressure (LVSP), and coronary flow were measured. To assess the heart adaptation to hemodynamic stress, the afterload was gradually increased in 10 mmHg increments while CO and LVSP were monitored. Additionally, the hearts from all animals surviving at least 36 h were assessed histologically. Of 15 rats that achieved ROSC after 6 min of CA, 7 could be evaluated in the WH setup 14 days after CA. In the 8 min CA group, 15 animals achieved ROSC, of which 2 were investigated in WH at 14 days after CA. Compared to the hearts of 7 sham animals, no significant differences in cardiac hemodynamics were observed at a set afterload (60 mm Hg; baseline) in the 6 min CA group. However, the two investigated 8 min CA animals exhibited a trend towards reduced CO and LVSP levels. Notably, both CA groups showed impaired hemodynamic performance to hemodynamic stress. Survivors at 14 days consistently showed significant myocardial pathology, with both 6 min and 8 min CA groups exhibiting fibrosis, inflammation, and edema most pronounced in the interventricular septum and right ventricle of the 8 min CA group. Animals that died prematurely displayed time-dependent acute changes, progressing from hypereosinophilic degeneration (36 h survivors) to myocardial necrosis, calcification, and the formation of cell-rich granulation tissue (48–108 h survivors). VFCA led to impaired left ventricular hemodynamic function in 8 min CA rats resuscitated with ECPR at rest and with increasing afterload. The isolated WH system may offer a valuable tool for assessing long-term cardiac function and performance after resuscitation.