OBJECTIVE: To investigate the protective effect of target temperature management (TTM) combined with prostaglandin E₁ (PGE₁) on ischemia/reperfusion (I/R) injury of cerebral micro-vascular endothelium cell (CMEC) in the return of spontaneous circulation (ROSC) rats with successful cardiopulmonary resuscitation. METHODS: Transoesophageal cardiac pacing with alternating current was used to induce ventricular fibrillation in rats. Five groups were set: Sham group (S group), ROSC group (R group), PGE₁ group (P group), TTM group (T group) and PGE₁/TTM group (PT group). Cell edema and micro-thrombus formation in cerebral tissue were evaluated through HE staining. I/R injury of CMEC was evaluated through CD34/TUNEL and vascular endothelial (VE)-cadherin/VE growth factor receptor double fluorescent immunohistochemistry staining. VE-cadherin mRNA and vascular cell adhesion molecule-1 (VCAM-1) mRNA expression in cerebral tissue lysate was analyzed by fluorescence quantitative PCR. RESULTS: TTM, PGE₁ and PGE₁/TTM could significantly improve cerebral interstitial edema, micro-thrombus, and inflammatory cells infiltration in the brain tissue, and reduce the apoptosis and VE-cadherin protein loss of CMEC. PGE₁/TTM showed better protective effect. These 3 interventions also inhibited the rapid elevation of VE-cadherin mRNA (0. 5 h) and VCAM-1 mRNA (4 h and 8 h) expression (P < 0.05), which might indicate the less I/R injury of CMEC of ROSC rat. CONCLUSION: Both PGE₁ and TTM could alleviate I/R injury of CMEC from ROSC rat after CPR separately, while PGE₁/TTM combined intervention might have synergistic better effect.
OBJECTIVE: To investigate the protective effect of target temperature management (TTM) combined with prostaglandin E₁ (PGE₁) on ischemia/reperfusion (I/R) injury of cerebral micro-vascular endothelium cell (CMEC) in the return of spontaneous circulation (ROSC) rats with successful cardiopulmonary resuscitation. METHODS: Transoesophageal cardiac pacing with alternating current was used to induce ventricular fibrillation in rats. Five groups were set: Sham group (S group), ROSC group (R group), PGE₁ group (P group), TTM group (T group) and PGE₁/TTM group (PT group). Cell edema and micro-thrombus formation in cerebral tissue were evaluated through HE staining. I/R injury of CMEC was evaluated through CD34/TUNEL and vascular endothelial (VE)-cadherin/VE growth factor receptor double fluorescent immunohistochemistry staining. VE-cadherin mRNA and vascular cell adhesion molecule-1 (VCAM-1) mRNA expression in cerebral tissue lysate was analyzed by fluorescence quantitative PCR. RESULTS:TTM, PGE₁ and PGE₁/TTM could significantly improve cerebral interstitial edema, micro-thrombus, and inflammatory cells infiltration in the brain tissue, and reduce the apoptosis and VE-cadherin protein loss of CMEC. PGE₁/TTM showed better protective effect. These 3 interventions also inhibited the rapid elevation of VE-cadherin mRNA (0. 5 h) and VCAM-1 mRNA (4 h and 8 h) expression (P < 0.05), which might indicate the less I/R injury of CMEC of ROSC rat. CONCLUSION: Both PGE₁ and TTM could alleviate I/R injury of CMEC from ROSC rat after CPR separately, while PGE₁/TTM combined intervention might have synergistic better effect.