Vasopressin decreases neuronal apoptosis during cardiopulmonary resuscitation

Epinephrine has been shown to be a first-choice drug for cardiopulmonary resuscitation. Nevertheless, its β-adrenergic effect probably increases myocardial oxygen consumption and leads to severe cardiac and cerebral injuries; moreover, epinephrine does not elevate long-term survival rates. The American Heart Association and the European Resuscitation Council recently recommended that vasopressin can be used for cardiopulmonary resuscitation, instead of epinephrine. However, the guidelines do not discuss the effects of vasopressin during cerebral resuscitation. According to a recent study reported in the Neural Regeneration Research, Chinese scholars found that vasopressin alone or the vasopressin and epinephrine combination suppress the activation of mitogen-activated protein kinase and c-Jun N-terminal kinase signaling pathways and reduce neuronal apoptosis during cardiopulmonary resuscitation, which is of great significance for improving the successful rate of cardiopulmonary resuscitation.

Immunohistochemical staining revealed that the c-Jun N-terminal kinase level gradually increased in the hippocampi of rats undergoing cardiopulmonary resuscitation after combined injection of epinephrine and vasopressin.

(Photo Credit: Neural Regeneration Research)

Source: Neural Regeneration Research