The effect of swimming training on adrenomedullin levels, oxidative stress variables, and gastrocnemius muscle contractile properties in hypertensive rats.

Introduction/Aim: Regular exercise may have beneficial effects on high blood-pressure, as shown in different types of experimental hypertension models in rats. The present study aims to investigate the effects of 6-week swimming training on blood pressure, oxidative stress variables of selected tissues, serum adrenomedullin (ADM) levels, and in situ muscle contraction in rats with hypertension induced by Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME), an inhibitor of endothelial nitric oxide synthases (eNOs). Materials and Methods: Twenty-six male Sprague Dawley, 8 weeks of age, rats were randomly divided into four groups: (I) normotensive (C), (II) normotensive + exercise (E), (III) hypertensive (L), and (IV) hypertensive + exercise (LE). Hypertension was induced by the oral administration of L-NAME (60 mg/kg) for 6 weeks. Exercise was performed 5 times (1-h each) per week for 6 weeks. At the end of the experiment, blood and tissue samples (the gastrocnemius muscle, heart, kidney, and thoracic aorta) were collected following contractile properties of the gastrocnemius muscle in situ weredetermined. In the collected tissues, oxidative stress (e.g., lipid oxidation and antioxidant enzyme activity) and serum ADM levels were measured. 6-week L-NAME administration per se (Group L) led to a significant increase in systolic and diastolic blood pressure compared to other groups.  Results: Importantly, 6-week exercise caused a protective effect of high blood pressure in the rats received L-NAME (Group LE). The level of ADM was lower in the rats received L-NAME than that of the control group. L-NAME increased lipid peroxidation in the thoracic aorta and decreased superoxide dismutase in the heart, kidney and muscle, and decreased catalase and glutathione in the heart. However, the exercise intervention did not have protective effect on the L-NAME-mediated oxidative damage in the collected tissues.  Conclusion: In conclusion, 6-week exercise intervention rescued rats from high blood pressure, but did not have ameliorative effect on the decreased ADM levels.

Mice with diet-induced obesity demonstrate a relative prothrombotic factor profile and a thicker aorta with reduced ex-vivo function.

: Classical risk factors such as cholesterol and lipoproteins are currently not sufficient to explain all physiopathological processes of obesity-related vascular dysfunction as well as atherosclerosis and arteriosclerosis. Therefore, the discovery of potential markers involved in vascular dysfunction in the obese state is still needed. Disturbances in hemostatic factors may be involved in the developmental processes associated with obesity-related cardiovascular disorders. We hypothesized that alterations of several hemostatic factors in the obese state could correlate with the function and morphology of the aorta and it could play an important role in the development of vascular dysfunction. To test this, we fed mice with a high-fat diet for 18 weeks and investigated the relationships between selected hemostatic factors (in either plasma or in the liver), metabolic hormones and morphology, and ex-vivo function of the aorta. Here, we show that 18-week exposure to a high-fat diet results in a higher plasma fibrinogen and prolonged prothrombin time in diet-induced obese mice compared to the controls. In addition, liver levels or activities of FII, FX, activated protein C, AT-III, and protein S are significantly different in diet-induced obese mice as compared to the controls. Curiously, FII, FVIII, FX, activated protein C, PTT, and protein S are correlated with both the aorta histology (aortic thickness and diameter) and ex-vivo aortic function. Notably, ex-vivo studies revealed that diet-induced obese mice show a marked attenuation in the functions of the aorta. Taken together, aforementioned hemostatic factors may be considered as critical markers for obesity-related vascular dysfunction and they could play important roles in diagnosing of the dysfunction.

Effect of dietary probiotic and high stocking density on the performance, carcass yield, gut microflora, and stress indicators of broilers.

A study was carried out to evaluate the effect of dietary probiotic supplementation and stocking density on the performance, relative carcass yield, gut microflora, and stress markers of broilers. One-day-old Ross 308 male broiler chickens (n = 480) were allocated to 4 experimental groups for 42 d. Each treatment had 8 replicates of 15 chicks each. Two groups were subjected to a high stocking density (HSD) of 20 birds/m² and the other 2 groups were kept at low stocking density (LSD) of 10 birds/m². A basal diet supplemented with probiotic 1 and 0.5 g/kg of diet (in starter and finisher diets, respectively) was fed to 2 treatments, one with HSD and the other with LSD, thereby making a 2 × 2 factorial arrangement. There was no interaction between stocking density (LSD and HSD) and dietary probiotic (supplemented and unsupplemented) for all the variables. Feed intake and weight gain were significantly low and feed conversion ratio was poor in broilers at HSD. Dietary probiotic significantly enhanced the feed intake and weight gain in starter phase only. Dietary probiotic supplementation had no effect (P > 0.05) on total aerobs, Salmonella sp., and Lactobacilli populations in the intestines of broilers. However, HSD reduced the Lactobacilli population only (P < 0.05). Relative breast yields were significantly higher in broilers reared at LSD than HSD. Thigh meat yield was higher in broilers in HSD group compared to LSD. Dietary probiotic did not affect the relative carcass yield and weight of lymphoid organs. Serum malondialdehyde, corticosterone, nitric oxide, and plasma heterophil:lymphocyte ratio were not affected either by stocking density or dietary probiotic supplementation. In conclusion, HSD negatively affected the performance and intestinal Lactobacilli population of broilers only, whereas probiotic supplementation enhanced the performance of broilers during the starter phase only. Total aerobes, Salmonella, Lactobacilli carcass yield, and stress indicators of broilers were not affected by the dietary supplementation of probiotic under the conditions of the present study.

In vivo effects of leptin on lymphocyte subpopulations in mice.

Leptin, a hormone-cytokine mainly produced by the adipose tissue, has pleitropic effects on many biological system including metabolic, endocrine, and immune system. Although it is well known that leptin controls food intake on hypothalamic regions of brain, the role of leptin in hematopoietic and immune processes has been mainly investigated with in vitro and transgenic mouse studies. The aim of this study was to investigate the effects of peripheral leptin on lymphocyte subpopulation. Initially forty male Swiss albino mice were divided into five groups. Mice in group I (Control) were given serum physiologic (SP) and group L100, group L250, group L500, and group L1000 were given 100, 250, 500 and 1000 µg/kg/day recombinant mouse leptin, respectively. Leptin or SP was injected subcutaneously for the next 6 days. Daily food/water intake was recorded for each group. At the end of the study, whole blood samples (500 µl) were obtained via intracardiac punction in anesthetized mice. Leptin levels and lymphocyte subpopulations in blood samples were analyzed. We show that no in vivo dose-dependent effect of leptin is existed on lymphocyte subpopulations count in mice. Treatment of mice with high-dose leptin led to increase only CD4+ cells (P<0.05). In addition, high-dose leptin slightly increased CD3+ cells but this was not statistically confirmed (P=0.08). Notably, it was found that leptin caused insignificant changes on body weight and food intake in normal body weight mice. The data support that high-dose leptin has proliferative effect on CD4+ cells in vivo. However, more in vivo study needs to be examined to clarify how leptin affect lymphocyte subpopulations.