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Influence of timolol, benzalkonium-preserved timolol, and benzalkonium-preserved brimonidine on oxidative stress biomarkers in the tear film.
Sedlak, L, Wojnar, W, Zych, M, Wyględowska-Promieńska, D
Cutaneous and ocular toxicology. 2020;(3):260-268
Abstract
PURPOSE The objective of this study was to investigate the influence of topical preservative-free timolol, benzalkonium chloride(BAC)-preserved timolol, BAC-preserved timolol, and BAC-preserved brimonidine on total protein concentration, advanced oxidation protein products (AOPP) content, total sulfhydryl groups content, the activity of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), as well as Total Oxidant Status (TOS), Total Antioxidant Response, and Oxidative Stress Index (OSI) in the tear film. METHODS The patients were divided into four groups: group C (n = 25)-control group-subjects who did not use topical antiglaucoma medications, group T (n = 17)-patients using topical preservative-free timolol, group T + BAC (n = 24)-patients using topical BAC-preserved timolol, and group BR + BAC (n = 19)-patients using topical BAC-preserved brimonidine. RESULTS The SOD, CAT, and GPx activities as well as AOPP, TOS, and OSI were found to be higher in the tear film of patients treated with BAC-preserved topical timolol or brimonidine in comparison with patients treated with preservative-free timolol or patients who did not use antiglaucoma topical medications. CONCLUSIONS This indicates that using BAC-preserved topical medications increases oxidative stress in the tear film and may, in the long-term, contribute to the clinical presentation of dry eye disease.
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Assist devices fail to reverse patterns of fetal gene expression despite beta-blockers.
Lowes, BD, Zolty, R, Shakar, SF, Brieke, A, Gray, N, Reed, M, Calalb, M, Minobe, W, Lindenfeld, J, Wolfel, EE, et al
The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation. 2007;(11):1170-6
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Abstract
BACKGROUND Heart failure is associated with reversal to a fetal gene expression pattern of contractile and metabolic genes. Substantial recovery of ventricular function with assist devices is rare. Our goal was to evaluate the effects of assist devices on fetal gene expression and hypoxia inducible factor-1 alpha (HIF-1 alpha), a transcriptional factor in hypoxic signaling. METHODS Human heart tissue was obtained from the left ventricular apex at the time of assist device implantation and again from the left ventricular free wall during cardiac transplantation. Non-failing tissue was obtained from unused hearts from human donors. Gene expression was measured with the Affymetrix 133 plus 2 Array. HIF-1 alpha was measured by Western blotting with commercially available antibodies. RESULTS Heart failure was associated with a decrease in alpha-myosin heavy chain and sarcoplasmic reticulum-Ca(2+) adenosine triphosphatase messenger RNA expression along with an increase in skeletal tropomyosin. This pattern persisted after assist device therapy. Heart failure was also associated with abnormalities in regulatory metabolic genes including glucose transporter 1 (GLUT1). These patterns also persisted after assist device therapy despite a reduction in atrial natriuretic peptide expression and normalization of HIF-1 alpha. CONCLUSIONS Failure of assist devices to produce sustained recovery of myocardial contractile function may be due in part to persistent fetal transcriptional patterns of contractile and metabolic genes.
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Effect of sesame oil on diuretics or Beta-blockers in the modulation of blood pressure, anthropometry, lipid profile, and redox status.
Sankar, D, Rao, MR, Sambandam, G, Pugalendi, KV
The Yale journal of biology and medicine. 2006;(1):19-26
Abstract
The study was undertaken to investigate the effect of sesame oil in hypertensive patients who were on antihypertensive therapy either with diuretics (hydrochlorothiazide) or Beta-blockers (atenolol). Thirty-two male and 18 female patients aged 35 to 60 years old were supplied sesame oil (Idhayam gingelly oil) and instructed to use it as the only edible oil for 45 days. Blood pressure, anthropometry, lipid profile, lipid peroxidation, and enzymic and non-enzymic antioxidants were measured at baseline and after 45 days of sesame oil substitution. Substitution of sesame oil brought down systolic and diastolic blood pressure to normal. The same patients were asked to withdraw sesame oil consumption for another 45 days, and the measurements were repeated at the end of withdrawal period. Withdrawal of sesame oil substitution brought back the initial blood pressure values. A significant reduction was noted in body weight and body mass index (BMI) upon sesame oil substitution. No significant alterations were observed in lipid profile except triglycerides. Plasma levels of sodium reduced while potassium elevated upon the substitution of sesame oil. Lipid peroxidation (thiobarbituric acid reactive substances [TBARS]) decreased while the activities of superoxide dismutase (SOD), catalase (CAT), and the levels of vitamin C, vitamin E, Beta-carotene, and reduced glutathione (GSH) were increased. The results suggested that sesame oil as edible oil lowered blood pressure, decreased lipid peroxidation, and increased antioxidant status in hypertensive patients.
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[The treatment of coronary heart disease by beta-adrenoblockers or tiazide diuretics preparation in combination with vegetarian diet].
Medkova, IL, Ieromuzo, AA, Ivanov, AN, Mosiakina, LI, Biriukova, LS
Voprosy pitaniia. 2005;(3):39-41
Abstract
Work make on 84 patients with coronare heart diseases were divided into two groups, equal quantity. The first groups were given athenolol (50 mg daily), the second--hypotiazide (25 mg daily). In every groupspart patients received an antiatherogenic lactoovovegetetarian diet, part--an standard antiatherogenic diet 10c. Time observation--24 daily. By the end of the treatment period with athenolol in backoground the vegetarian diet the level of total cholesterol decreased by 16%, low-density lipoproteins cholesterol decreased by 18%. In groups patients received an standard antiatherogenic diet these parameters practically did'nt change. In the vegetarian group the atherogenic coefficient (KA) decreased by 31%., while in the patients on standard antiatherogenic diet KA showed only a tendency for decreasing. By the end to the treatment period with hypotiazide the slight decrease in total cholesterol, KA levels and a slight increase in HDL cholesterol were observed only the vegetarian group.
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Use of thallium-201 myocardial scintigraphy for the prediction of the response to beta-blocker therapy in patients with dilated cardiomyopathy.
Hara, Y, Hamada, M, Ohtsuka, T, Ogimoto, A, Saeki, H, Suzuki, J, Matsunaka, T, Nakata, S, Shigematsu, Y
Circulation journal : official journal of the Japanese Circulation Society. 2002;(12):1139-43
Abstract
This study was performed to evaluate whether thallium-201 myocardial scintigraphy (Tl-201) and iodine-123-metaiodobenzylguanidine (MIBG) myocardial scintigraphy could predict the usefulness of beta-blocker therapy in patients with dilated cardiomyopathy (DCM). Tl-201 and MIBG were performed in 47 patients before beta-blocker therapy. Patients were classified into group A, if their cardiac function improved, and group B, whose function remained unchanged. Two types of extent score (ES) by Tl-201 were proposed to quantitate myocardial damage, mean-2SD (ES-2) and mean-3SD (ES-3). The ES difference between ES-2 and ES-3 was calculated, and according to ES and ES difference, DCM cases were classified into 3 groups: mild-defect type (mild-type), moderate-defect type (moderate-type) and severe-defect type (severe-type). The heart-to-mediastinum (H/M) MIBG uptake ratio was evaluated, and the percent washout ratio of myocardial MIBG was obtained from these data. Group A comprised 18 mild-type, 14 moderate-type and 1 severe-type cases, and group B comprised 5 mild-type, 4 moderate-type and 5 severe-type cases. A significant relation was observed between the defect type on Tl-201 and the response to beta-blocker therapy (p=0.0090). Both H/M MIBG uptake ratios and washout ratio were not significantly different in the 2 groups. Tl-201 may be useful for predicting the response to beta-blocker therapy in patients with DCM.
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Limited effect of systemic beta-blockade on sympathetic outflow.
Tank, J, Diedrich, A, Schroeder, C, Stoffels, M, Franke, G, Sharma, AM, Luft, FC, Jordan, J
Hypertension (Dallas, Tex. : 1979). 2001;(6):1377-81
Abstract
Central beta-adrenoreceptors may augment sympathetic outflow. We tested the hypothesis that beta-blockade attenuates central sympathetic outflow by inhibiting central adrenoreceptors. We studied 18 healthy controls (4 female, 14 male; age, 26+/-6 years, body mass index, 23+/-3 kg/m(2)). ECG, brachial, and finger arterial blood pressure, muscle sympathetic nerve activity, and respiration were measured continuously before and during complete beta-blockade. Subjects received a total intravenous dose of 0.21 mg/kg of propranolol in 15 minutes. Spontaneous baroreflex slopes were calculated using the sequence technique (BRSup, BRSdown). The sympathetic baroreflex slope was determined at baseline using phenylephrine and sodium nitroprusside infusions. The subjects underwent cold pressor testing before and during beta-blockade. The R-R interval increased from 861+/-119 ms at baseline to 952+/-141 ms during beta-blockade (P<0.01). Blood pressure was 117+/-9/65+/-8 mm Hg at baseline and 117+/-10/67+/-8 mm Hg during beta-Blockade (P=NS). beta-Blockade did not affect baroreflex sensitivity (BRSup: 21+/-10 versus 28+/-11 ms/mmHg, P<0.1; BRSdown: 17+/-8 versus 20+/-8 ms/mmHg, P=NS). Muscle sympathetic nerve activity increased significantly during beta-blockade (number of bursts/100 beats: 32+/-9 versus 40+/-14, P<0.05), compared with baseline. However, the operating points of the parasympathetic and sympathetic baroreflex during beta-blockade were on the baroreflex curves obtained at baseline. beta-Blockade blunted the heart rate response to cold pressor testing; blood pressure and muscle sympathetic nerve activity responses were similar. Our study demonstrates that propranolol does not cause an acute decrease in sympathetic activity in normotensive young subjects. This, observation is not consistent with an important tonic stimulatory effect of beta-adrenoreceptors in the brain.