Objective To investigate the effect of different concentrations of propofol on tracheal smooth muscle (TSM) isolated from guinea pigs with induced asthma and the underlying mechanism. Methods Forty-eight guinea pigs of either sex weighing 150-200 g were randomly divided into 2 groups : normal group ( n = 20) and asthma group ( n = 28). Asthma was induced with ovoglobulin. The animals were sacrificed by a blow to the head without anesthesia. Trachea was immediately removed and cut into tracheal rings (3-5 mm in length) . 5-7 tracheal rings were prepared from each animal and suspended in organ bath filled with oxygenated (95% O2 , 5% CO2 ) KHB and stretched to an optimal resting tension which was measured by using a force-displacement transducer with a pen recorder. The two groups were further divided into six subgroups : control subgroup, 10 % intralipid subgroup and 4 propofol subgroups (10, 30, 100, 300?mol?L-1). The effect of different concentrations of propofol and their interaction with acetylcholine ( Ach ) and ryanodine on contraction of TSM were measured. Results (1) Effect of propofol on resting tension of TSM : in normal group propofol had no effect on TSM resting tension, while in asthma group propofol reduced TSM resting tension in a dose-dependent manner. 10% intralipid contracted TSM slightly and insignificantly as compared with control subgroup. (2) Effect of propofol on TSM contraction induced by Ach : propofol inhibited TSM contraction induced by Ach in a dose-dependent manner in both normal and asthma group. (3) Effect of propofol preconditioning on TSM contraction induced by Ach : pretreatment with propofol 100 and 300?mol?L-1 significantly inhibited TSM contraction induced by Ach in both normal and asthma group as compared with control subgroup. Pretreatment with even propofol 30?mol?L-1 was effective in asthma group. (4) There was no significant difference in propofol-inhibition of TSM contraction induced by Ach with or without ryanodine. Conclusion Pretreatment with clinical doses of propofol can significantly inhibit TSM contraction induced by Ach in guinea pigs with asthma and ryanodine receptor-mediated smooth muscle intracellular Ca2+ release is not involved.

Objective: To explore the peri-operative application of GLP-1 analogue and insulin on myocardial perfusion and clinical prognosis in patients of acute ST segment elevation myocardial infarction (STEMI) with stress-induced hyperglycemia. Methods: Our research was a prospective single center randomized control study. A total of 114 consecutive STEMI patients received percutaneous coronary intervention (PCI) within 12h of onset were enrolled, the patients had no diabetes while blood glucose ≥11.1mmol/L at immediate admission. Based on random number table, the patients were divided into 2 groups: Observation group, the patients received GLP-1 analogue, n=59 and Control group, the patients received insulin, n=55. The post-operative myocardial perfusion, indicators of myocardial damage and cardiac function, myocardial infarct area (MIA) and myocardial salvage index (MSI) were compared between 2 groups. The patients were followed-up for 6 months to record the incidence of major adverse cardiovascular events (MACE). Results: At peri-operative period, compared with Control group, Observation group had decreased peak values of creatine kinase isoenzyme (CK-MB) and troponin T (cTnT), P<0.05. At 6 months post-operation, compared with Control group, Observation group showed increased myocardial perfusion and left ventricular ejection fraction (LVEF), P<0.05, reduced MIA (15±12) g vs (20±14) g, P<0.05 and 12% elevated MSI as (0.64±0.13) vs (0.56±0.12), P<0.001. The MACE incidence was similar between 2 groups, P=0.217. Conclusion: In STEMI patients with stress-induced hyperglycemia, peri-operative application of GLP-1 analogue may safely regulate blood glucose, improve cardiac perfusion and function, reduce MIA; while it had no influence on myocardial perfusion at peri-operative period and no impact on MACE occurrence at 6 months post-operation.