The kidney is one of the organs that highly susceptible to age-related tissue damage. Several human and animal studies show decline in renal function with age. We examined the effect of endothelin-1 on age-related changes on renal function and whether this effect is mediated by ET-1 receptor types A or B. Also, we investigated the hemodynamic response to ET-1 and ET-1 receptor antagonist. Two age groups of male rats were used: young (4–5 months) and old (19–20 months). Each group was subdivided into four experiments in which hemodynamic and renal function data were measured after administration of saline (control group), acute intravenous injection of endothelin-1 (ET-1 group), administration of BQ-123, ETA receptor antagonist, 20 minutes before ET-1 (ETA antagonist group) and administration of BQ-788, ETB receptor antagonist, 20 minutes before ET-1(ETB antagonist group). We found that aging is associated with elevated mean arterial blood pressure and reduced renal function data. ET-1 injection resulted in more pressor response in old rats and more reduction of renal function data in young rats. Pretreatment with BQ-123 improved renal function with more augmentation in old rats while BQ-788 pretreatment has no effect on renal function. These results indicated that ET-1 and ET-1A receptor play a crucial role in age-related change in renal function.

The kidney is one of the organs that highly susceptible to age-related tissue damage. Several human and animal studies show decline in renal function with age. We examined the effect of endothelin-1 on age-related changes on renal function and whether this effect is mediated by ET-1 receptor types A or B. Also, we investigated the hemodynamic response to ET-1 and ET-1 receptor antagonist. Two age groups of male rats were used: young (4–5 months) and old (19–20 months). Each group was subdivided into four experiments in which hemodynamic and renal function data were measured after administration of saline (control group), acute intravenous injection of endothelin-1 (ET-1 group), administration of BQ-123, ETA receptor antagonist, 20 minutes before ET-1 (ETA antagonist group) and administration of BQ-788, ETB receptor antagonist, 20 minutes before ET-1(ETB antagonist group). We found that aging is associated with elevated mean arterial blood pressure and reduced renal function data. ET-1 injection resulted in more pressor response in old rats and more reduction of renal function data in young rats. Pretreatment with BQ-123 improved renal function with more augmentation in old rats while BQ-788 pretreatment has no effect on renal function. These results indicated that ET-1 and ET-1A receptor play a crucial role in age-related change in renal function.

Background: Acute lung injury (ALI) is a syndrome with a diagnostic criteria based on hypoxemia and a classical radiological appearance, with acute respiratory distress syndrome at the severe end of the disease. Facts recommended the occurrence of rupture of the basement membranes and interstitial matrix remodeling during ALI. Matrix metalloproteinase (MMPs) participate in tissue remodeling related with pathological conditions such as acute lung injury. We hypothesized the interrelationships between extracellular matrix (ECM) turnover as MMP-9 and indicator of angiogenesis such as angiopoietin-2 (Ang-2) as well as plasma von Willebrand factor (vWF) and their correlation with arterial partial pressure of oxygen (PaO2), oxygen saturation (SaO2) and mortality in ALI/ARDS. Materials and Methods: 88 mechanically ventilated patients [68 male, mean (SD) age 61 (10) years] were compared to 40 healthy controls [36 male, mean (SD) age 57 (10)]. All biomarkers were measured by Enzyme linked immunosorbeant assay (ELISA). Oxygenation, body temperature, leucocytes, and platelet counts were noted. Results: Plasma levels of all biomarkers were significantly different, among ALI/ARDS subjects (p0.001). They were inversely related to PaO2 and SaO2and positively related to mortality. In addition, increased MMP-9, Ang-2 and vWF levels were interrelated on the first day of admission. Conclusions: The observed diversity in plasma levels of MMP-9, Ang-2 and vWF in ALI/ARDS patients revealed the activity and severity of the disease, shedding more light onto the pathogenesis and/or presentation of ARDS.

Background: Acute lung injury (ALI) is a syndrome with a diagnostic criteria based on hypoxemia and a classical radiological appearance, with acute respiratory distress syndrome at the severe end of the disease. Facts recommended the occurrence of rupture of the basement membranes and interstitial matrix remodeling during ALI. Matrix metalloproteinase (MMPs) participate in tissue remodeling related with pathological conditions such as acute lung injury. We hypothesized the interrelationships between extracellular matrix (ECM) turnover as MMP-9 and indicator of angiogenesis such as angiopoietin-2 (Ang-2) as well as plasma von Willebrand factor (vWF) and their correlation with arterial partial pressure of oxygen (PaO2), oxygen saturation (SaO2) and mortality in ALI/ARDS. Materials and Methods: 88 mechanically ventilated patients [68 male, mean (SD) age 61 (10) years] were compared to 40 healthy controls [36 male, mean (SD) age 57 (10)]. All biomarkers were measured by Enzyme linked immunosorbeant assay (ELISA). Oxygenation, body temperature, leucocytes, and platelet counts were noted. Results: Plasma levels of all biomarkers were significantly different, among ALI/ARDS subjects (p0.001). They were inversely related to PaO2 and SaO2and positively related to mortality. In addition, increased MMP-9, Ang-2 and vWF levels were interrelated on the first day of admission. Conclusions: The observed diversity in plasma levels of MMP-9, Ang-2 and vWF in ALI/ARDS patients revealed the activity and severity of the disease, shedding more light onto the pathogenesis and/or presentation of ARDS.

Background: Acute lung injury (ALI) is a syndrome with a diagnostic criteria based on hypoxemia and a classical radiological appearance, with acute respiratory distress syndrome at the severe end of the disease. Facts recommended the occurrence of rupture of the basement membranes and interstitial matrix remodeling during ALI. Matrix metalloproteinase (MMPs) participate in tissue remodeling related with pathological conditions such as acute lung injury. We hypothesized the interrelationships between extracellular matrix (ECM) turnover as MMP-9 and indicator of angiogenesis such as angiopoietin-2 (Ang-2) as well as plasma von Willebrand factor (vWF) and their correlation with arterial partial pressure of oxygen (PaO2), oxygen saturation (SaO2) and mortality in ALI/ARDS. Materials and Methods: 88 mechanically ventilated patients [68 male, mean (SD) age 61 (10) years] were compared to 40 healthy controls [36 male, mean (SD) age 57 (10)]. All biomarkers were measured by Enzyme linked immunosorbeant assay (ELISA). Oxygenation, body temperature, leucocytes, and platelet counts were noted. Results: Plasma levels of all biomarkers were significantly different, among ALI/ARDS subjects (p0.001). They were inversely related to PaO2 and SaO2and positively related to mortality. In addition, increased MMP-9, Ang-2 and vWF levels were interrelated on the first day of admission. Conclusions: The observed diversity in plasma levels of MMP-9, Ang-2 and vWF in ALI/ARDS patients revealed the activity and severity of the disease, shedding more light onto the pathogenesis and/or presentation of ARDS.

Introduction: Nervous system growth and differentiation are intimately interrelated with the presence of thyroid hormones (THs) in early development stages. Hypothyroidism during the fetal and postnatal life results in an irreversible mental retardation syndrome. Aim of the study: Assessment of the effect of 3,5,3‾-triiodo-L-thyronine (T3) on changes in the cerebral neurotransmitters level in hypothyroid rats male offspring and the possible role of Na+, K+-ATPase activity. Materials and methods: Hypothyroidism during pregnancy and lactation in one group (hypothyroid group) was induced by the antithyroid drug, methimazole (MMI) that was added to drinking water at a concentration of 0.02%. In the second group (T3-treated hypothyroid group), MMI was stopped and animal’s offsprings were given T3 (20 μg/100 g body weight in 0.01 N NaOH, i.p.) for one week. The third group is the control group; neither the mother nor the offspring received any drug. The hypothyroid state in mothers during pregnancy was confirmed by measuring total thyroxine (TT4) and total triiodothyronine (TT3) at gestational day 10. At the end of experiment, the offsptings were sacrificed and free thyroxine (FT4) and free triiodothyronine (FT3) in sera and neurotransmitters (dopamine, norepinephrine and serotonin) and Na+, K+-ATPase activity were measured in the cerebral homogenate. Results: Maternal hypothyroidism induced a significant decrease in the cerebral level of dopamine, norepinephrine, serotonin and Na+, K+-ATPase activity when compared with euthyroid group. Treatment with T3 significantly increased the cerebral level of neurotransmitters and Na+, K+-ATPase activity when compared with the hypothyroid group. Conclusion: T3 supplementation during the postnatal period through its effect on the cerebral Na+, K+-ATPase effectively reversed the effect of maternal methimazole-induced hypothyroidism on the cerebral level of dopamine, norepinephrine and serotonin.

Background: Oxidative stress has been implicated in the pathophysiology of cerebral ischemia. Pentraxin-3 plays an important role in innate immune responses and in inflammatory diseases. Our aim was to evaluate pentraxin-3 serum level on focal transient cerebral ischemia and reperfusion model in rabbits and to assess the anti-inflammatory and anti-oxidant effects of vagus nerve stimulation. Materials and Methods: Focal transient cerebral ischemia and reperfusion was induced by occlusion of the right common carotid artery for 2 hours followed by reperfusion for one hour. Stimulating electrodes were implanted on the cervical part of the right vagus nerve. Vagus nerve stimulation was started 30 min following right common carotid artery ligation for a period of one hour. The stimulation signals were delivered every five minutes for 30 seconds. All the procedures were duplicated but no stimulus was delivered in the control group. Serum level of pentraxin-3, lipid peroxide and total thiols were determined at baseline, at end of ischemia and at end of reperfusion and the animal decapitated and neuronal damage was evaluated. Results: We found that vagus nerve stimulation caused reduction of the ischemic features with revival of the cell shape and size. It also resulted in decreased serum levels of pentraxin-3 and lipid peroxide whereas the level of total thiols was increased. Conclusion: We concluded that the observed diversity in pentraxin-3, lipid peroxide and total thiols serum levels in cerebral ischemia and reperfusion may reflect relative roles in the biology. Anti-inflammatory and anti-oxidant role of vagus nerve stimulation in cerebral ischemia and reperfusion may represent a marker of altered cerebral function, and may provide potential therapeutic applications.

Background: Oxidative stress has been implicated in the pathophysiology of cerebral ischemia. Pentraxin-3 plays an important role in innate immune responses and in inflammatory diseases. Our aim was to evaluate pentraxin-3 serum level on focal transient cerebral ischemia and reperfusion model in rabbits and to assess the anti-inflammatory and anti-oxidant effects of vagus nerve stimulation. Materials and Methods: Focal transient cerebral ischemia and reperfusion was induced by occlusion of the right common carotid artery for 2 hours followed by reperfusion for one hour. Stimulating electrodes were implanted on the cervical part of the right vagus nerve. Vagus nerve stimulation was started 30 min following right common carotid artery ligation for a period of one hour. The stimulation signals were delivered every five minutes for 30 seconds. All the procedures were duplicated but no stimulus was delivered in the control group. Serum level of pentraxin-3, lipid peroxide and total thiols were determined at baseline, at end of ischemia and at end of reperfusion and the animal decapitated and neuronal damage was evaluated. Results: We found that vagus nerve stimulation caused reduction of the ischemic features with revival of the cell shape and size. It also resulted in decreased serum levels of pentraxin-3 and lipid peroxide whereas the level of total thiols was increased. Conclusion: We concluded that the observed diversity in pentraxin-3, lipid peroxide and total thiols serum levels in cerebral ischemia and reperfusion may reflect relative roles in the biology. Anti-inflammatory and anti-oxidant role of vagus nerve stimulation in cerebral ischemia and reperfusion may represent a marker of altered cerebral function, and may provide potential therapeutic applications.