The Influence of Preoperative Anxiety, Optimism, and Pain Catastrophizing on Acute Postoperative Pain in Patients Undergoing Cardiac Surgery: A Cross-sectional Study.

BACKGROUND: Acute postoperative pain (APOP) may cause complications and delay healing. Analgesics alone cannot completely relieve APOP. Preoperative anxiety, optimism, and pain catastrophizing are predictors of APOP. No study author has examined the mediating effect of pain catastrophizing on APOP in patients undergoing cardiac surgery. OBJECTIVE: The aims of this study were to investigate the relationship between preoperative anxiety, optimism, pain catastrophizing, confounding factors (age, sex, type of surgery, and preoperative pain), and APOP and to examine the mediating effect of pain catastrophizing. METHODS: The authors of this cross-sectional study used a convenience sampling method and included 100 adults undergoing cardiac surgery in a southern Taiwanese medical center. The patients were asked to complete the State-Trait Anxiety Inventory-State subscale, Pain Catastrophizing Scale, and Life Orientation Test-Revised questionnaires before surgery. Postoperatively, the patients were asked to report their pain intensity on a numerical rating scale. Results were analyzed using SPSS version 22. RESULTS: Patients had a mild level of anxiety, a moderate level of optimism, and pain catastrophizing before surgery, as well as a moderate level of APOP. Men reported lower levels of APOP than women (z = -2.0, P < .05). APOP was significantly associated with preoperative anxiety (r = 0.48, P < .01), optimism (r = -0.45, P < .01), and pain catastrophizing (r = 0.65, P < .01). Only pain catastrophizing was a significant predictor of APOP (ß = 0.60, P < .001) and fully mediated the relationship between anxiety and APOP (z = 4.92, P < .001). The final model explained 42% of the variance in APOP. CONCLUSIONS: Pain catastrophizing should be assessed before surgery. Reducing pain catastrophizing would decrease APOP and improve the quality of pain management.

Effect of Geumgwe-Sinkihwan on Renal Dysfunction in Ischemia/Reperfusion-Induced Acute Renal Failure Mice.

Renal ischemia-reperfusion (I/R) injury is an important cause of acute renal failure (ARF). Geumgwe-sinkihwan (GSH) was recorded in a traditional Chines medical book named "Bangyakhappyeon" in 1884. GSH has been used for treatment for patients with diabetes and glomerulonephritis caused by deficiency of kidney yang and insufficiency of kidney gi. Here we investigate the effects of GSH in mice model of ischemic acute kidney injury. The mice groups are as follows; sham group: C57BL6 male mice, I/R group: C57BL6 male mice with I/R surgery, GSH low group: I/R + 100 mg/kg/day GSH, and GSH high group: I/R + 300 mg/kg/day GSH. Ischemia was induced by clamping both renal arteries and reperfusion. Mice were orally given GSH (100 and 300 mg/kg/day) during 3 days after surgery. Treatment with GSH significantly ameliorated creatinine clearance, creatinine, and blood urea nitrogen levels. Treatment with GSH reduced neutrophil gelatinase associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1), specific renal injury markers. GSH also reduced the periodic acid-Schiff and picro sirius red staining intensity in kidney of I/R group. Western blot and real-time RT-qPCR analysis demonstrated that GSH decreased protein and mRNA expression levels of the inflammatory cytokines in I/R-induced ARF mice. Moreover, GSH inhibited protein and mRNA expression of inflammasome-related protein including NLRP3 (NOD-like receptor pyrin domain-containing protein 3, cryoprin), ASC (Apoptosis-associated speck-like protein containing a CARD), and caspase-1. These findings provided evidence that GSH ameliorates renal injury including metabolic dysfunction and inflammation via the inhibition of NLRP3-dependent inflammasome in I/R-induced ARF mice.

Blackcurrant Improves Diabetic Cardiovascular Dysfunction by Reducing Inflammatory Cytokines in Type 2 Diabetes Mellitus Mice.

Diabetic cardiovascular dysfunction is a representative complication of diabetes. Inflammation associated with the onset and exacerbation of type 2 diabetes mellitus (T2DM) is an essential factor in the pathogenesis of diabetic cardiovascular complications. Diabetes-induced myocardial dysfunction is characterized by myocardial fibrosis, which includes structural heart changes, myocardial cell death, and extracellular matrix protein accumulation. The mice groups in this study were divided as follows: Cont, control (db/m mice); T2DM, type 2 diabetes mellitus mice (db/db mice); Vil.G, db/db + vildagliptin 50 mg/kg/day, positive control, dipeptidyl peptidase-4 (DPP-4) inhibitor; Bla.C, db/db + blackcurrant 200 mg/kg/day. In this study, Bla.C treatment significantly improved the homeostatic model evaluation of glucose, insulin, and insulin resistance (HOMA-IR) indices and diabetic blood markers such as HbA1c in T2DM mice. In addition, Bla.C improved cardiac function markers and cardiac thickening through echocardiography. Bla.C reduced the expression of fibrosis biomarkers, elastin and type IV collagen, in the left ventricle of a diabetic cardiopathy model. Bla.C also inhibited TD2M-induced elevated levels of inflammatory cytokines in cardiac tissue (IL-6, IL-1ß, TNF-α, and TGF-ß). Thus, Bla.C significantly improved cardiac inflammation and cardiovascular fibrosis and dysfunction by blocking inflammatory cytokine activation signals. This showed that Bla.C treatment could ameliorate diabetes-induced cardiovascular complications in T2DM mice. These results provide evidence that Bla.C extract has a significant effect on the prevention of cardiovascular fibrosis, inflammation, and consequent diabetes-induced cardiovascular complications, directly or indirectly, by improving blood glucose profile.