The LLD of TM suppresses HMGB1-induced and TLR2-mediated myocardial reperfusion injury and apoptosis in vitro and in vivo.

No abstract

NO-production and K ATP-channel activation together may fully account for the steady-state hypercapnic flow response in mouse heart. However, chronic deletion of eNOS does not result in a reduced hypercapnic flow response. Enhanced activation of K ATP-channels and potentially Kv-channels contributes to the compensatory mechanisms involved in the hypercapnic flow response when eNOS activity is absent.

Inhaled anesthetics are inhaled via the lungs. They subsequently pass through the alveolocapillary membrane and diffuse into the blood to finally target the central nervous system and induce anesthesia. This principle of anesthesia induction was first described for diethylether in 1847. Nevertheless, the use of diethylether for anesthesia is obsolete and even the use of nitrous oxide (introduced for anesthesia in 1847) is declining in Germany. Almost all modern volatile anesthetics are halogenated methylethylethers in which fluorine is used as a halogen. All of these anesthetics depress myocardial contractility and induce hypotension. Depression of CO2 and hypoxia-induced respiration are other serious side effects. Further side effects are liver and kidney related but they are rare and not induced by anesthetics per se but preferentially by toxic metobolites. Another promising inhalative anesthetic is xenon which fulfils many aspects of an ideal inhalative anesthetic.