[Protective effects of high-dose ulinastatin on vital organs in patients receiving total arch replacement for type A aortic dissection].

OBJECTIVE: To investigate the protective effects of high-dose ulinastatin on the vital organs in patients undergoing total arch replacement for type A aortic dissection. METHODS: Between September 2014 and March 2016, 66 patients with type A aortic dissection underwent total arch replacement at our center. Thirty-six of the patients received ulinastatin treatment at 300 000 U/8 h from admission to 3 days postoperatively and at 300 000 U/2 h during cardiopulmonary bypass surgery (UTI group), and the other 30 patients did not receive perioperative ulinastatin treatment (control group). The surgical data and blood biochemistry profiles on days 1, 3, and 5 postoperatively were compared between the two groups, and the postoperative ICU stay, re-operation for bleeding, ventilation for over 7 days, ultrafiltration for postoperative renal failure, tracheotomy, incidences of pulmonary and neurological complications and hospital death were also compared. RESULTS: s The operating time, cardiopulmonary bypass time, ACP time, cardiac arrest time, the lowest rectal temperature and frequency of bilateral and unilateral antegrade selective cerebral perfusion were similar between the two groups (P>0.05). Compared with those in the control group, patients in UTI group had lower lactate, S-100 and neuron specific enolase levels on the first postoperative day and higher OI on the 1st, 3rd, and 5th postoperative days (P<0.05), but serum creatinine, blood urea nitrogen, total bilirubin, and alanine aminotransferase levels were comparable between the two groups (P>0.05). No significant differences were found in the frequency of re-operation for bleeding, ultrafiltration for renal failure, tracheotomy, neurological complications or hospital death after the operation between the two groups, but the patients in UTI group had a shorter ICU time, a less frequent long-term ventilation and a lower incidence of pulmonary infection (P<0.05). CONCLUSION: High-dose ulinastatin offers protection on pulmonary function and lowers the specific brain injury markers in patients with type A aortic dissection after total arch replacement, but its protective effects on brain is uncertain.

Inhibition of acid sensing ion channel by ligustrazine on angina model in rat.

Ligustrazine, a compound extracted from roots of Ligusticum chuanxiong, is widely used in Chinese traditional medicine to treat cardiac and cerebrovascular diseases and pain, including angina. The mechanism(s) of ligustrazine's effect to reduce angina is not clear. Angina is mediated by cardiac afferent sensory neurons. These neurons display a large acid-evoked depolarizing sodium current that can initiate action potentials in response to acidification that accompanies myocardial ischemia. Acid-sensing ion channels (ASICs) mediate this current. Here we tested the hypothesis that ligustrazine reduces ischemia-induced cardiac dysfunction and acid-evoked pain by an action to inhibit ASIC-mediated current. The effects of ligustrazine to attenuate ischemia-induced ST-segment depression, T wave changes, and myocardial infarct size in hearts of anesthetized rats were determined. Effects of ligustrazine on currents mediated by ASICs expressed in cultured Chinese hamster ovary cells, and effects of the drug on acid-induced nociceptive behavior and acid-induced currents in isolated dorsal root ganglions cells were measured. Ligustrazine significantly attenuated acid-induced ASIC currents, reduced cardiac ischemia-induced electrical dysfunction and infarct size, and decreased the nociceptive response to injection of acid into the paw of the rat hindlimb. The ASIC channel inhibitor A-317567 similarly reduced electrical dysfunction, infarct size, and nociceptive behavior in the rat. Inhibition of ASICs by ligustrazine may explain at least in part the beneficial effects of the drug that are observed in patients with ischemic heart disease and angina.

Protective effects of osthole against myocardial ischemia/reperfusion injury in rats.

Osthole, a bioactive simple coumarin derivative extracted from a number of medicinal plants, such as Cnidium monnieri and Angelica pubescens, has been shown to exert a variety of pharmacological activities and is considered to have potential therapeutic applications. In this study, we investigated the protective effects of osthole against myocardial ischemia/reperfusion (I/R) injury in rats. Male Sprague-Dawley rats were randomly assigned to 1 of 5 groups: the sham-oeprated control group (control), the vehicle group (vehicle), and 3 treatment groups, which were treated with osthole at the concentration of 1, 10 or 50 mg/kg (intraperitoneally), respectively, upon the initiation of myocardial ischemia. Treatment with osthole suppressed the formation of lipid peroxidation products, enhanced the capacities of antioxidant enzymes and inhibited the expression of inflammatory cytokines following myocardial I/R injury. Moreover, treatment with osthole reduced high-mobility group box protein 1 (HMGB1) and phosphorylated nuclear factor (NF)-κB expression in ischemic myocardial tissue. These results demonstrate the protective effects of osthole against myocardial I/R injury in rats and suggest that these effects may be associated with its antioxidant and anti-inflammatory activities.