Cardiocerebral protective effects of dexmedetomidine as anesthetic in colorectal cancer surgery.

OBJECTIVE: To explore the cardiocerebral protective effect of dexmedetomidine as an anesthetic in colorectal cancer surgery. PATIENTS AND METHODS: A total of 246 colorectal cancer patients were enrolled in this retrospective analysis. Those patients were admitted to the Affiliated Hospital of Qingdao University and underwent surgery from July 2014 to July 2016. The patients were divided into observation group and control group according to the anesthetic used in surgery. The conventional anesthetic was administered to patients in control group, whereas conventional anesthetic supplemented with dexmedetomidine was administered to patients in the observation group. The heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), jugular venous oxygen saturation (Sj-vO2), cerebral oxygen extraction ratio (ERO2), and cerebral arterial partial pressure of oxygen (PaO2) were recorded before dexmedetomidine administration (T0), 30 min after start of surgery (T1), and 2 h after surgery (T2). Central venous blood (4 ml) was withdrawn 6 hours and 24 hours after surgery. Following centrifugation, the serum was collected and stored at -70°C. After collection of all the blood samples, concentrations of creatine kinase (CK-MB), troponin I (cTnI), TNF-α and S100ß in serum were measured using ELISA, and differences between the two groups were compared. RESULTS: Differences of the parameters measured at T0 were not statistically significant between observation group and control group (p>0.05), whereas the parameters measured at T1 and T2 were significantly better in the observation group than those in the control group (p<0.05). The post-surgery blood test showed that indicators of cardiocerebral hemodynamics were better in the observation group than those in the control group (p<0.05). CONCLUSIONS: Administration of dexmedetomidine in colorectal cancer surgery can provide effective cardiocerebral protection and it is worth popularizing in clinical practice.

Expression of cyclooxygenase-2 in human and an animal model of rheumatoid arthritis.

An inducible form of cyclooxygenase-2 (COX-2) has been shown to be upregulated in vitro by various pro-inflammatory agents, such as lipopolysaccharide, IL-1 and TNF, COX-2 appears to be responsible for the increase in prostaglandin synthesis at the site of inflammation. To examine the involvement of COX-2 in inflammation, we analysed the expression of this gene in human rheumatoid arthritis (RA) and in rat adjuvant-induced arthritis. Immunocytochemical studies of synovial membrane biopsies from human RA, osteoarthritic (OA) and normal joints using a COX-2 specific antibody showed positive staining in RA, but not in normal synovial membranes. Specifically, expression of COX-2 was detected in synovial lining cells, lymphoid aggregates and endothelial cells of blood vessels. Although some positive staining was observed in the OA joints, the number of stained cells was dramatically lower and the staining of the cells was less intense than in the rheumatoid tissue. By reverse transcription and polymerase chain reaction analysis, COX-2 mRNA was detected in the rat adjuvant arthritic limb, whereas no COX-2 mRNA was detectable in the normal limb. These observations indicate that COX-2 expression is upregulated in inflammatory joint disease and that COX-2 is a potential therapeutic target for specific inhibition.