Propofol-induced rhabdomyolysis: a case report.

OBJECTIVE: To report a case of propofol-induced rhabdomyolysis. In this case, widespread myolysis was detected after induction of anesthesia. CASE SUMMARY: A 54-year-old female patient was scheduled for a hysterectomy. Beginning shortly after the induction of anesthesia with propofol, several episodes of ventricular fibrillation occurred. Despite intensive care, the patient failed to recover. During most episodes of ventricular fibrillation, marked hyperthermia or hyperkalemia were not observed. Unexplained, widespread myolysis affecting both skeletal and cardiac muscle was observed at autopsy. DISCUSSION: In this patient, the evidence for rhabdomyolysis is robust. Clinical characteristics are similar to those observed in propofol infusion syndrome. The absence of a body temperature over 40 °C precludes the possibility of malignant hyperthermia. Widespread rhabdomyolysis locations cannot be explained by precordial electric shocks. Propofol is the only drug used in this case that has been reported to induce rhabodomyolysis. CONCLUSIONS: Signs of propofol-induced rhabdomyolysis may be different from those of malignant hyperthermia. Even a regular induction dose of propofol for adults could possibly trigger rhabdomyolysis similar to what is observed in children diagnosed with propofol infusion syndrome. Though rare, care should still be taken when administering propofol.

Interaction between ROS and p38MAPK contributes to chemical hypoxia-induced injuries in PC12 cells.

The present study investigated whether there is an interaction between reactive oxygen species (ROS) and p38 mitogen-activated protein kinase (MAPK) during chemical hypoxia-induced injury in PC12 cells. The results of the present study showed that cobalt chloride (CoCl2), a chemical hypoxia agent, markedly induced ROS generation and phosphorylation of p38MAPK, as well as neuronal injuries. N-acetylcysteine (NAC), a ROS scavenger, blocked CoCl2-induced phosphorylation of p38MAPK. In addition, SB203580, an inhibitor of p38MAPK attenuated not only CoCl2-induced activation of p38MAPK, but also ROS production. These results suggest that ROS and p38MAPK are capable of interacting positively during chemical hypoxia. Furthermore, NAC and SB203580 markedly prevented CoCl2-induced cytotoxicity, apoptosis and a loss of mitochondrial membrane potential. Taken together, our findings suggest that the positive interaction between CoCl2 induction of ROS and p38MAPK activation may play a significant role in CoCl2-induced neuronal injuries. We provide new insights into the mechanisms responsible for CoCl2-induced injuries in PC12 cells.