The NFSC is sensitive to clinical stress during surgical stimulation. Moreover, the combined use of SC and NFSC may have a potential to differentiate between situations of stress due to inadequate hypnotic effect vs. inadequate analgesic effect.

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The effects of clinically relevant concentrations of anti-hypertensive agents on lipopolysaccharide (LPS)-induced interleukin-1beta (IL-1β) secretion by polymorphonuclear leukocytes (PMNs) were investigated in vitro. Lipopolysaccharide-induced secretion of IL-1β by PMNs from 15 hypertensive and 15 normotensive subjects after incubation with losartan, captopril, amlodipine, atenolol, and hydrochlorothiazide were assessed. IL-1β secretion by PMNs markedly increased in hypertensive patients versus normotensive subjects. Losartan, captopril, and amlodipine caused a concentration-dependent attenuation of IL-1β levels in both groups. Losartan, captopril, and amlodipine demonstrated marked in vitro anti-inflammatory effects at clinically relevant serum concentrations but atenolol and hydrochlorothiazide did not.

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Purpose. The effects of pioglitazone on sildenafil responsiveness in men with erectile dysfunction (ED) and a history of poor response to sildenafil were assessed. Methods. In a double-blinded study, 38 men aged 47 ± 1.5 years with moderate-tosevere ED and poor response to sildenafil were randomly assigned to take a premedication of pioglitazone 30 mg (n=19) or placebo (n=19) once daily for 9 weeks along with on-demand use of sildenafil during the last month of pioglitazonetreatment. Erectile function (EF) scores, assessed by EF domain of International Index of Erectile Function (IIEF), along with responses to Global Assessment Questions (GAQs) were major outcome measures. Serum levels of total testosterone (T), dehydroepiandrosterone sulfate (DHEAS), glucose, lipid profile and liver function test were minor outcome measures. Results.Pioglitazone significantly improved major outcome measures compared with placebo. The decrease from baseline of total cholesterol level was more in pioglitazonethan in placebo-treated groups. In 84% (32 out of 38) of the sildenafil poor-responders, at least one of the associated risk factors of ED was found. There was undiagnosed hypercholesterolemia in 34% of the subjects. Serum levels of T, DHEAS, glucose and other parameters remained unchanged in both groups. The intervention was well tolerated. Conclusions. Pioglitazone increased sildenafil response to improve ED of men with prior sildenafil failure and seems to be safe based on the present preliminary study. This improvement is likely regardless of fasting glucose and sex hormones levels.

Human serum paraoxonase (PON1) is a high-density lipoprotein-associated esterase that protects against organophosphate neurotoxicity, and is proposed to play a role in lipid metabolism and the onset of cardiovascular disease. In the present study, paraoxonase activities and phenotype distribution in serum of 132 healthy Iranian individuals aged 17-68 years were assessed using dual substrate method. In the study population, a wide interindividual variability (up to 15-fold) of paraoxonase activity was found. The mean of basal, salt-stimulated paraoxonase and arylesterase activities were 81.8 ± 57 U/ml, 153.1 ± 117.5 U/ml and 80.7 ± 12.8 kU/l, respectively. The ratio of salt-stimulated paraoxonase activity to arylesterase activity was used for definition of phenotypes. Based on the observed ratios, three distinct phenotypes AA (low activity), AB (intermediate activity) and BB (high activity) were determined. The PON1 ratio varied from 0.5 to 6.8. The paraoxonase phenotype frequencies were approximately 48% (AA), 41% (AB) and 11% (BB). In this work, serum triglycerides had significant positive correlation ( r = 0.334, P < 0.05) with paraoxonase activity, whereas high-density lipoprotein did not. No significant decrease in paraoxonase activity by smoking was observed. Age and sex had no influences on PON1 activities. In conclusion, the distribution of paraoxonase phenotypes in this Iranian population was trimodal and comparable to that of Caucasians from North America; however, overall enzyme activity was lower than that reported for Caucasians.

It has been well established that oxidative stress and inflammation are involved in the pathogenesis of diabetic nephropathy. It has been shown that tropisetron exerts anti-inflammatory and immunomodulatory properties. The current study was designed to investigate protective effects of tropisetron on early diabetic nephropathy in streptozotocin-induced diabetic rats. Rats were divided into six groups: (i) untreated diabetic (streptozotocin group); (ii) untreated control; (iii) diabetic rats treated with tropisetron (3 mg/kg); (iv) normal rats treated with tropisetron (3 mg/kg); (v) diabetic rats treated with granisetron (3 mg/kg); and (vi) normal rats treated with granisetron (3 mg/kg); rats began receiving treatment at the time of diabetes induction for 2 weeks. At the termination of the experiments, bodyweight, kidney index, urinary albumin excretion, and glomerular filtration rate were measured. The levels of oxidative stress markers and tumour necrosis factor-α were also determined. Streptozotocin-treated animals showed significant loss of bodyweight and renal enlargement and dysfunction. Diabetic rats also exhibited an increase in malondialdehyde along with a significant decrease in glutathione, superoxide dismutase activity, and catalase activity. Furthermore, the diabetic animals demonstrated a significant rise in renal cortical, urinary tumour necrosis factor-α, and urinary albumin excretion. Both granisetron and tropisetron decreased blood glucose in diabetic animals, but this decrease was not significant for granisetron. Treatment with tropisetron, but not granisetron, prevented increases in oxidative stress and tumour necrosis factor-α, decreased urinary cytokine excretion and albuminuria, and improved renal morphological damage. In conclusion, the present study suggests that tropisetron may be a protective agent in early diabetic nephropathy, and its action is mediated, at least in part, by anti-oxidative and anti-inflammatory mechanisms that appear to be independent of the 5-HT3 receptor.