ABSTRACT
<p><b>OBJECTIVE</b>To study protective effect of ulinastatin on perioperative cardiac function in elderly patients undergoing major gastrointestinal surgery.</p><p><b>METHODS</b>Sixty elderly patients (32 male and 28 female patients) aged 60-82 years scheduled for major gastrointestinal surgery were randomized into ulinastatin group and control group. The patients in ulinastatin group received 2×10(5) U ulinastatin rapidly administered via a intravenous pump immediately before operation with subsequent continuous infusion at the rate of 1×10(5) U until the completion of surgery, and those in the control group received the same amount of saline instead. In both groups, the mean arterial pressure (MAP), heart rate (HR), left ventricular ejection fraction (LVEF), and cardiac output (CO) were monitored immediately before surgery (T0) and at 1 h (T1), 2 h (T2) and 3 h (T3) after the start of surgery. The total dopamine dose used was recorded at the end of surgery, and blood samples were collected at T0 and at 6 h (T4) and 12 h (T5) after the operation for determination of serum levels of cTn, CK-MB and BNP.</p><p><b>RESULTS</b>In both groups, MAP, LVEF and CO were significantly decreased at T2 and T3 (P<0.05) and serum levels of cTn, CK-MB and BNP significantly increased at T4 and T5 compared to those at T0 (P<0.05). Compared with the control group, the patients in ulinastatin group showed significantly higher MAP, LVEF and CO at T2 and T3 and lower serum levels of cTn, CK-MB and BNP at T4 and T5.</p><p><b>CONCLUSION</b>Ulinastatin offers effective perioerative cardiac protection in elderly patients undergoing major gastrointestinal surgery.</p>
Subject(s)
Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Cardiotonic Agents , Pharmacology , Creatine Kinase, MB Form , Metabolism , Digestive System Surgical Procedures , Glycoproteins , Pharmacology , Intraoperative Period , Natriuretic Peptide, Brain , Metabolism , Stroke VolumeABSTRACT
Objective To research the effect ofparecoxib on hippocampal nerve cell apoptosis and expressions of B cell lymphoma/lewkmia-2 (Bcl-2),Bcl-2 associated X protein (Bax) and caspase-3 of epilepsy rats.Methods Thirty SD male rats were randomly divided into three groups (n=10):control group,parecoxib treatment group and epilepsy group.The rats in the parecoxib treatment group and epilepsy group were injected with 4 mg/kg of parecoxib and same volume of saline,respectively,and 3 d after that,they both were injected intraperitoneally with 3 mmol/kg of lithium chloride,and then,20 h after that,they were injected intraperitoneally with 30 mg/kg ofhydrochloride pilocarpine; while rats in the control group were only injected intraperitoneally with the same volume of saline.The behavior changes of rats in the three groups were observed.After 7 d,terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL) was used to evaluate the neuronal apoptosis and Western blotting was employed to evaluate the expressions of Bcl-2,Bax and caspase-3 in the hippocarnpus of all groups.Results All epilepsy rats were very irritable; spontaneous seizures (SRS) times of precoxib treatment group were significantly reduced as compared with those of epilepsy group (P＜0.05).As compared with those in the control group,the Bcl-2,Bax and caspase-3 expressions and Bcl-2/Bax ratio in the epilepsy group were increased with statistically significant differences (P＜0.05); As compared with those in the epilepsy group,the Bcl-2,Bax and caspase-3 expressions and Bcl-2/Bax ratio in the precoxib treatment group were decreased with statistically significant differences (P＜0.05).As compared with that in the control group,the number of TUNEL positive cells in hippocampus of rats in the precoxib treatment group and epilepsy group were significantly increased (P＜0.05); as compared with that in the epilepsy group,the number of TUNEL positive cells in the hippocampus of precoxib treatment group was statistically reduced (P＜0.05).Conclusion Parecoxib can reduce the apoptosis of hippocampus neurons through inhibiting the protein expressions of Bax and caspase-3 to affect the Bcl-2 protein expression,whose mechanism may be related to the pathways of Bcl-2/Bax and Caspase-3 proteins.