296 research outputs found
Exercise training and detraining process affects plasma adiponectin level in healthy and spontaneously hypertensive rats
BACKGROUND: Adiponectin levels with long-term swimming exercise have been never investigated in spontaneously hypertensive rats (SHR). OBJECTIVE: This study was aimed to investigate the effects of exercise and detraining process on the adiponectin plasma levels of spontaneously hypertensive rats (SHR) and healthy Wistar-Kyoto rats (WKY). MATERIAL AND METHODS: The rats in the exercise groups were swimming for 10 weeks, 5 days/week, one hour in a day. The detraining rats were left to be sedentary in their cages for 5 weeks after 10 weeks of exercise period. RESULTS: The plasma adiponectin levels decreased in E and SHRE groups compared to the SC and the SHR groups, respectively. In addition, blood pressure was decreased in the exercise groups vs their controls. The adiponectin level was not found to be significantly different in ED and SHRED groups compared to their controls. The blood pressure did not differ between SDC and ED groups, although in the SHRED group it was found to be lower than in SHRSD group rats. CONCLUSION: The results of this study showed that exercise reduced plasma levels of adiponectin in healthy and spontaneously hypertensive rats. However, this difference disappeared at the end of the training processes. Our results suggest, that changes in plasma adiponectin levels are not responsible for changes in blood pressure
Contribution of heme oxygenase 2 to blood pressure regulation in response to swimming exercise and detraining in spontaneously hypertensive rats
Background: We aimed to determine the effects of exercise followed by detraining on systolic blood pressure (SBP), heme oxygenase 2 (HO-2) expression, and carboxyhemoglobin (COHb) concentration in spontaneously hypertensive rats (SHR) to explain the role of carbon monoxide (CO) in this process. Material/Methods: Animals were randomized into exercised and detrained groups. Corresponding sedentary rats were grouped as Time 1–2. Swimming of 60 min/5 days/week for 10 weeks was applied. Detraining rats discontinued training for an additional 5 weeks. Gene and protein expressions were determined by real-time PCR and immunohistochemistry. Results: Aorta HO-2 histological scores (HSCORE) of hypertensive rats were lower, while SBP was higher. Swimming caused enhancement of HO-2 immunostaining in aorta endothelium and adventitia of SHR. Exercise induced elevation of blood COHb index in SHR. Synchronous BP lowering effect of exercise was observed. HO-2 mRNA expression, HSCORE, and blood COHb index were unaltered during detraining, while SBP was still low in SHR. Conclusions: CO synthesized by HO-2 at least partly plays a role in SBP regulation in the SHR-and BP-lowering effect of exercise. Regular exercise with short-term pauses may be advised to both hypertensives and individuals who are at risk. © Med Sci Monit
Increased systemic oxidative stress in patients with keratoconus
PurposeTo establish the effect of systemic oxidative stress on the pathogenesis of keratoconus by measuring serum total oxidant status (TOS) and total antioxidant status (TAS) in patients with keratoconus.MethodsTwenty-five patients with keratoconus (keratoconus group) and 25 age-sex-matched healthy subjects (control group) were enrolled in the study. Exclusion criteria were smoking habit, history of any other corneal pathology, systemic disease or inflammation, and current antioxidant or anti-inflammatory therapies. All participants underwent a detailed ophthalmological examination and corneal topography. Serum samples were obtained from all participants. Oxidative stress markers (TAS and TOS) were measured using a commercial kit and oxidative stress index (OSI) was calculated.ResultsThe study comprised 25 patients with keratoconus (mean age of 26.4±1.7 years) and 25 healthy control subjects (mean age of 26.6±1.7 years) (P>0.05). The serum TOS and OSI values were significantly higher in patients with keratoconus compared with those of the controls (P=0.036 and 0.037, respectively). However, serum TAS did not show significant difference between the keratoconus and control groups (P=0.497).ConclusionsThe higher levels of serum oxidant status and OSI in patients with keratoconus suggest that systemic oxidative stress might be involved in the pathogenesis of keratoconus. © 2014 Macmillan Publishers Limited
Neither a Nitric Oxide Donor Nor Potassium Channel Blockage Inhibit RBC Mechanical Damage Induced by a Roller Pump
Red blood cells (RBC) are exposed to various levels of shear stresses when they are exposed to artificial flow environments, such as extracorporeal flow circuits and hemodialysis equipment. This mechanical trauma affects RBC and the resulting effect is determined by the magnitude of shear forces and exposure time. It has been previously demonstrated that nitric oxide (NO) donors and potassium channel blockers could prevent the sub-hemolytic damage to RBC, when they are exposed to 120 Pa shear stress in a Couette shearing system. This study aimed at testing the effectiveness of NO donor sodium nitroprussid (SNP, 10-4 M) and non-specific potassium channel blocker tetraethylammonium (TEA, 10-7 M) in preventing the mechanical damage to RBC in a simple flow system including a roller pump and a glass capillary of 0.12 cm diameter. RBC suspensions were pumped through the capillary by the roller pump at a flow rate that maintains 200 mmHg hydrostatic pressure at the entrance of the capillary. An aliquot of 10 ml of RBC suspension of 0.4 L/L hematocrit was re-circulated through the capillary for 30 minutes. Plasma hemoglobin concentrations were found to be significantly increased (~7 folds compared to control aliquot which was not pumped through the system) and neither SNP nor TEA prevented this hemolysis. Alternatively, RBC deformability assessed by laser diffraction ektacytometry was not altered after 30 min of pumping and both SNP and TEA had no effect on this parameter. The results of this study indicated that, in contrast with the findings in RBC exposed to a well-defined magnitude of shear stress in a Couette shearing system, the mechanical damage induced by a roller pump could not be prevented by NO donor or potassium channel blocker
Nitric oxide synthetic pathway and cGMP levels are altered in red blood cells from end-stage renal disease patients
Red blood cells (RBCs) enzymatically produce nitric oxide (NO) by a functional RBC-nitric oxide synthase (RBC-NOS). NO is a vascular key regulatory molecule. In RBCs its generation is complex and influenced by several factors, including insulin, acetylcholine, and calcium. NO availability is reduced in end-stage renal disease (ESRD) and associated with endothelial dysfunction. We previously demonstrated that, through increased phosphatidylserine membrane exposure, ESRD-RBCs augmented their adhesion to human cultured endothelium, in which NO bioavailability decreased. Since RBC-NOS-dependent NO production in ESRD is unknown, this study aimed to investigate RBC-NOS levels/activation, NO production/bioavailability in RBCs from healthy control subjects (C, N = 18) and ESRD patients (N = 27). Although RBC-NOS expression was lower in ESRD-RBCs, NO, cyclic guanosine monophosphate (cGMP), RBC-NOS Serine1177 phosphorylation level and eNOS/Calmodulin (CaM)/Heat Shock Protein-90 (HSP90) interaction levels were higher in ESRD-RBCs, indicating increased enzyme activation. Conversely, following RBCs stimulation with insulin or ionomycin, NO and cGMP levels were significantly lower in ESRD- than in C-RBCs, suggesting that uremia might reduce the RBC-NOS response to further stimuli. Additionally, the activity of multidrug-resistance-associated protein-4 (MRP4; cGMP-membrane transporter) was significantly lower in ESRD-RBCs, suggesting a possible compromised efflux of cGMP across the ESRD-RBCs membrane. This study for the first time showed highest basal RBC-NOS activation in ESRD-RBCs, possibly to reduce the negative impact of decreased NOS expression. It is further conceivable that high NO production only partially affects cell function of ESRD-RBCs maybe because in vivo they are unable to respond to physiologic stimuli, such as calcium and/or insulin
Spontaneously Hypertensive Rats
https://stars.library.ucf.edu/cfm-ch-register-vol13/1230/thumbnail.jp
Effect of sulfite on red blood cell deformability ex vivo and in normal and sulfite oxidase-deficient rats in vivo.
The effect of sulfite, a widely used food additive, on red blood cell deformability ex vivo and in vivo was investigated. Ex vivo experiments were conducted in human blood exposed to sulfite (5, 10 and 20 mM). In vivo experiments were carried out in sulfite oxidase-competent (SOXC) and sulfite oxidase-deficient (SOXD) rats. In the in vivo experiments, sulfite was administered in the form of sodium metabisulfite (Na(2)S(2)O(5), 25 mg/kg/day) via drinking water. Vitamin E dissolved in olive oil at a dose of 50 mg/kg was administered by gastric gavages. Red blood cell (RBC) deformability was determined at various fluid shear stresses using an ektacytometer. Ex vivo sulfite exposure to RBC did not affect RBC deformability. In the in vivo experiments, although RBC deformability was not affected by sulfite treatment in SOXD rats, it was found to be significantly increased in SOXC rats. Vitamin E treatment in combination with sulfite caused impairment in RBC deformability in both SOXC and SOXD rats. We suggest that sulfite needs to be oxidized in order to improve RBC deformability
Effect of sulfite treatment on erythrocyte deformability in young and aged rats.
It is known that aging is associated with marked effects on integrity and function of cell membrane. These effects may also be exacerbated by exogenous chemicals, e.g. sulfite. Thus, the aim of this paper is to examine the influence of sulfite on hemorheological and related hematological parameters in rats of various ages. In this study, male Wistar rats at the age of 3 and 18 months were used and the following parameters were evaluated: Mean Cell Volume (MCV), Mean Corpuscular Hemoglobin Concentration (MCHC), Red blood Cell (RBC) deformability and aggregation. The results show that aging is associated with a decrease in RBC deformability and MCHC, an increase in MCV. Sulfite administration significantly increased RBC deformability in both young and aged rats. Although MCHC was decreased in young rats, it was increased in aged rats in response to sulfite exposure. Additionally, sulfite induced a decrement in MCV of aged rats. Neither aging nor sulfite treatment caused significant alterations in RBC aggregation parameters in all experimental groups. In conclusion, these findings suggest that RBC deformability impairs with age and sulfite has ameliorating effects on RBC deformability in both young and aged rats
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