Application of midazolam and propofol in esophagogastroduodenoscopy: a triple-blind, randomized controlled trial

The use of intravenous sedatives is common in gastrointestinal endoscopy. This study is to evaluate the safety and efficacy of propofol and/or midazolam in induction of proper sedation in esophagogastroduodenoscopy [EGD] compared with a control group, which does not receive sedation for EGD. Four groups [A, B, C and D] of 30 patients each for whom EGD had been indicated were defined. Group A received no sedative, whereas groups B, C and D received midazolam, propofol and midazolam plus propofol intravenously, respectively. The four groups were compared with each other regarding heart rate [HR], oxygen saturation [O2S], systolic blood pressure [SBP], diastolic blood pressure [DBP], duration of endoscopy [DE], patient compliance [CM], retrograde amnesia [RA], antegrade amnesia [AA], patient activity [PA], skin color [SC], patient consciousness [CS], blood flow [BF], respiration state [RS] and pain. Patient compliance, retrograde amnesia, antegrade amnesia, patient activity, patient consciousness and pain were significantly different in our patient groups. On the contrary, no significant difference was found among the four groups regarding heart rate, oxygen saturation, systolic and diastolic blood pressures, duration of endoscopy, skin color, blood flow and respiratory state. Based on our findings, no sedation is necessary for EGD unless the patient feels anxious and therefore can not cooperate appropriately. For this case, the administration of propofol alone is a priority over midazolam alone and propofol plus midazolam

Endotheilal function in adolescents with a history of premature coronary artery disease in one parent

In young adults, a family history of premature coronary artery disease [CAD], as well as genetic and environmental factors are independent risk factors for coronary artery disease. Endothelial function was studied in 30 children [21 boys and 9 girls with mean age of 14.9 +/- 2.3 years old]of patients with documented CAD [men .45 and women .50 years old]. Chidren did not have any history of diabetes mellitus, dyslipidemia, hypertension, and smoking [active/passive]. Using vascular ultrasound, we measured resting Basal Brachial artery Diameter [BBD] and Endothelium-Dependent Dilatation [EDD] in response to increased flow and sublingual glyceryltrinitrate [GTN], an Endothelium-Independent Dilation [EID]. These parameters were also measured in 30 control subjects with normal parents [18 boys and 12 girls with mean age of 14.2 +/- 2/5years old] and results were compared with each other. Adolescents in CAD group had abnormal Endothelial Dependent Dilatation or EDD/BBD [8.5 +/- 3.4% vs 11.8 +/- 4.5% in control subjects; P= 0.003].Endothelial Independent Dilatation [EID/BBD] in the positive fimily history group was significantly more than control subjects [18.5 +/- 6.7% vs 11.9 +/- 5.2%; P <0.001]. EDD/EID or the index of endothelial function was significantly lower in the positive family history group [0.92 +/- 0.05 vs 1 +/- 0.03; P<0.001]. There was no difference in EDD/EID index between those with history of premature CAD in mother [7 cases] and those with history of premature CAD in father [23 cases] [0.92 +/- 0.04 vs 0.91 +/- 0.05]. Normal adolescents without any cardiovascular risk factors but a history of premature coronary artery disease in one parent may have endothelial dysfunction, and there is no difference whether the CAD is in mother or father

Endothelial function in male body builders taking androgenic steroids

Adverse cardiovascular events have been reported in body builders taking anabolic steroids. Adverse effects of AAS on endothelial function can initiate atherosclerosis. This study evaluates endothelial function in body builders using AAS, compared with non-steroids using athletes as controls. We recruited 30 nonsmoking male body builders taking AAS, 14 in build up phase, 8 in work out phase, and 8 in post steroid phase, and 30 nonsmoking male athletes who denied ever using steroids. Serum lipids and fasting plasma glucose were measured to exclude dyslipidemia and diabetes. Brachial artery diameter was measured by ultrasound at rest, after cuff inflation, and after sublingual glyceriltrinitrate [GTN] to determine flow mediated dilation [FMD], nitro mediated dilation [NMD] and ratio of FMD to NMD [index of endothelial function]. Use of AAS was associated with higher body mass index [BMI] and low density lipoprotein-cholesterol [LDL-C]. Mean ratio of flow mediated dilatation after cuff deflation to post GTN dilatation of brachial artery [index of endothelial function] in body builders taking AAS was significantly lower than control group [0.96[0.05] versus 1[0.08]; p=0.03]. After adjusting BMI, age and weight, no significant difference was seen in index of endothelial function between two groups [p=0.21]. Our study indicates that taking AAS in body builders doesn't have direct effect on endothelial function. Future study with bigger sample size and measurement of AAS metabolites is recommended