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Present study was designed to examine the effectiveness of N-2-mercaptopropionyl glycine (MPG) on oxygen free radical (OFR) mediated reperfusion injury. Twenty dogs underwent 90 min of left anterior descending (LAD) coronary artery occlusion followed by 4 h of reperfusion. In control animals (n = 12), 115 ml of saline was infused through left atrium at the onset of reperfusion whereas treated animals (n = 8) received loading dose of MPG (40 mg/kg) infused through left atrium for 1 h followed by maintenance dose (25 mg/kg) for remaining 3 hours. Percentage area of necrosis vis-a-vis area at risk and percentage necrosis in left ventricular mass in MPG treated animals was significantly lower in comparison to control animals. Reperfusion in control group increased the lipid peroxidation and lowered glutathione (GSH) and superoxide dismutase (SOD) activity. MPG treatment significantly lowered the lipid peroxidation whereas GSH and SOD levels in necrotic zone were higher than in control. The above results suggest that MPG can offer a significant cardioprotection against oxidative stress in canine model.  相似文献   
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BACKGROUND: Transient ischemic dilation (TID) has been established as an important independent marker of severe and extensive coronary artery disease (CAD) in myocardial perfusion imaging (MPI). The accuracy of the TID index is dependent on a well-determined threshold (normal limits) between normal and abnormal values for each study protocol. To date, the effects of neither gender nor attenuation correction (AC) on TID normal limits have been established. Thus, the objectives of this study were to determine if AC processing changes the normal value of the TID index and if there were gender-related differences in the TID index of normal patients who had undergone rest/exercise-stress technetium-99m sestamibi MPI. METHODS AND RESULTS: Seventy-five patients (33 women, 42 men; mean age, 57.7 +/- 11.7 y and 55.9 +/- 10.0 y, respectively) with less than a 5% likelihood of CAD, who had undergone low-dose rest/high-dose exercise-stress Tc-99m sestamibi MPI, were studied. All studies were acquired using simultaneous emission/transmission scans and were corrected for attenuation, scatter, and resolution effects using the ExSPECT II method. Both the AC and non-AC studies were analyzed using the Emory Cardiac Toolbox (ECTb; Syntermed, Inc, Atlanta, Ga) quantitative software. The TID index was calculated automatically as the ratio of stress mean left ventricular volumes to rest mean left ventricular volumes by ECTb. Patients were grouped by gender and the TID indices from AC and non-AC studies were compared. Linear regressions of the TID index and body mass index were analyzed to exclude differences in body size between male and female patients as a confounding factor in gender-related differences in TID. The TID index upper normal limits were calculated as the mean value plus 2 standard deviations (SDs). AC processing did not change the TID index significantly whether the genders were combined or separated (AC TID = 0.97 +/- 0.14 vs non-AC TID = 0.98 +/- 0.12 for all patients). Female patients showed higher mean TID indices than male patients in both AC (1.01 +/- 0.15 vs 0.95 +/- 0.12) and non-AC studies (1.00 +/- 0.15 vs. 0.97 +/- 0.10), but this difference was statistically significant only in AC studies (p = .03). TID indices remained constant across the range of body mass index studied. The TID index upper normal limit was 1.31 for female and 1.18 for male patients. CONCLUSION: TID normal values for rest/exercise-stress Tc-99m sestamibi MPI are gender-dependent and not affected by AC processing. Thus, diagnosticians should take into account these gender-related differences, as compared with the traditional value generated from mostly male populations, to ensure both men and women have the same overall accuracy of using the TID index in the diagnosis and prognosis of CAD.  相似文献   
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BACKGROUND: A gender-independent stress normal database and criteria for abnormality for attenuation-corrected rest-stress technetium 99m sestamibi same-day myocardial perfusion imaging were developed by evaluation of 112 patients, validated against an obese population of 95 patients from four different clinical sites, and compared with conventional gender-matched database quantification of non-attenuation-corrected studies. METHODS AND RESULTS: These 95 validation patients (63 men) were used for prospective quantitative evaluation (mean weight, 213 +/- 57 lb; mean body mass index, 32 +/- 9 kg/m(2)). This group included 21 patients (12 men) with a lower than 5% likelihood of coronary artery disease (mean weight, 226 +/- 72 lb; mean body mass index, 34 +/- 13 kg/m(2)) and 74 who underwent cardiac catheterization within 2 months (35 with normal coronaries or coronary lesions <70%). These studies were processed twice, once by use of conventional reconstruction and gender-specific database quantification and a second time by use of attenuation correction and a single gender-independent attenuation-corrected normal database. The attenuation-corrected normal database and criteria for abnormality were developed by evaluation of 48 and 78 patients, respectively. No statistically significant differences were found when comparing attenuation-corrected perfusion distributions of normal men and women, whereas significant differences were found in the same uncorrected studies. Compared with quantitative analysis of the uncorrected studies, quantitative analysis of the attenuation-corrected studies by use of a gender-independent normal database demonstrated a significant improvement in normalcy rate (90% vs 52%, P =.006) and specificity (57% vs 29%, P =.015) in this obese population at no significant loss in sensitivity (90% vs 97%, P = not significant). CONCLUSION: Attenuation-corrected studies can be quantified with a single gender-independent normal database and a single criterion for abnormality without loss of sensitivity and with significantly better specificity and normalcy rate.  相似文献   
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Free radical injury is thought to play a significant role in the pathogenesis of several disease processes in low birth weight premature infants including retinopathy of prematurity and necrotizing enterocolitis. Because iron is a known catalyst in free radical-mediated oxidation reactions, the objectives of the present in vitro studies were to determine whether after exposure to air 1) iron present in infant formula, or that added to human milk or formula as medicinal iron or as iron contained in human milk fortifier, increases free radical and lipid peroxidation products; and 2) recombinant human lactoferrin added to formula or human milk attenuates iron-mediated free radical formation and lipid peroxidation. Before adding medicinal iron to formula and human milk, significantly more ascorbate and alpha-hydroxyethyl radical production and more lipid peroxidation products (i.e. thiobarbituric acid reactive substances, malondialdehyde, and ethane) were observed in formula. After the addition of medicinal iron to either formula or human milk, further increases were observed in free radical and lipid peroxidation products. When iron-containing human milk fortifier was added to human milk, free radicals also increased. In contrast, the addition of apo-recombinant human lactoferrin to formula or human milk decreased the levels of oxidative products when medicinal iron or human milk fortifier was present. We speculate that the presence of greater concentration of iron and the absence of lactoferrin in formula compared with human milk results in greater in vitro generation of free radicals and lipid peroxidation products. Whether iron-containing formula with lactoferrin administered enterally to preterm infants will result in less free radical generation in vivo has yet to be established.  相似文献   
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