BACKGROUND: It has been well documented that ATP activates NOS enzymes and causes increased NO production in several cell types. Although RBC known to possesses eNOS enzyme activity, it has not been investigated whether RBC eNOS could be induced by e

BACKGROUND: Rho-kinase, an effector of the small GTPase RhoA, is known to be a novel inhibitory regulator of eNOS in endothelial cells under basal conditions and disease states. However, although RBC possesses active RhoA/Rho-kinase pathway, Rho-kina

Backround: Possible toxic effects of hyperoxia have been reported previously. However, the number of studies investigating the influence of hyperoxia on blood cells is limited and there are no data regarding its hemorheological effects. Objective: Th

Background: Hypotension is a common adverse effect associated with the use of propofol and sodium thiopental. The objective of this study was to examine the impact of thiopental and propofol on erythrocyte (RBC) nitric oxide (NO) synthase activity and RBC-mediated NO release. Methods: A prospective, interventional in vitro trial. Male patients aged between 18 and 45 years with a classification of American Society of Anesthesiologists (ASA) class I, defined as healthy individuals, were included in this study. Venous blood samples (20 mL) were obtained from patients who met the inclusion criteria. Measurements were performed using the specific fluorescent probes for NO and calcium (Ca²⁺). Propofol and sodium thiopental were added to the suspensions at doses of 100, 250, 500, and 1000 μM and incubated for 30 min. All suspensions were proceeded to flow cytometric analysis. Nitrite/nitrate concentration was measured in the supernatant of RBC suspensions after centrifugation. RBC deformability and aggregation were measured by laser diffraction analysis using an ektacytometer. The primary outcome was to evaluate the effects of sodium thiopental and propofol on RBC-NOS activity. Results: Sodium thiopental caused significant increase in intracellular NO concentrations at all doses studied (p < 0.001). Importantly, the intracellular NO concentration increment was positively correlated with sodium thiopental concentration in the suspensions. The presence of L-N-acetylmethyl-arginine in the experimental medium abolished NO production in RBCs in response to sodium thiopental. Sodium thiopental caused increased nitrite and nitrate levels in the suspension medium in a dose-dependent manner. Incubation with thiopental caused an increase in intracellular free Ca⁺² levels while propofol induced no change. Sodium thiopental and propofol caused significant decrement in RBC aggregation. Conclusions: This study presents the initial evidence of augmented RBC-mediated NO production and release in response to sodium thiopental administration. In contrast to the effects observed with sodium thiopental, our results demonstrated that propofol had no impact on RBC-mediated NO production.

Background/aim: Diabetes is manifested by endothelial dysfunction and an imbalance between vasoconstriction and vasodilation. The aim of our study is to examine the effect of vitK2 application on vascular and rheological parameters in a rat diabetes model. Materials and methods: A total of 60 male Wistar Albino rats were used to examine vascular responses and hemorheological parameters. A total of 6 groups were: control (C), control+vehicle (Cv), control+vitK2 administered (C + K2), diabetes (D), diabetes+vehicle (Dv), and diabetes+vitK2 (D + K2) group. After the animals were sacrificed, blood and vascular samples were taken and the contraction and relaxation responses of the aorta and erythrocyte deformability and aggregation were examined. Results: When KCl dose-response curves are evaluated; Increased vasoconstriction response was found in the Dv group compared to the Cv group. The increase in vasoconstriction observed in the Dv group decreased with the application of vit K2. D+vitK2 group thoracic aorta contraction responses returned to Cv group levels. In response to increasing cumulative doses of Phe, a significant increase in vasoconstriction response was observed in the Dv group compared to the Cv group. VitK2 application reduced the Phe-mediated contractile response, which was increased in the Dv group, and returned the contraction response to Cv conditions except for two intermediate Phe doses. In the Dv + K2 group, a significant decrease was observed in the aggregation index, which was tended to increase. Conclusion: Considering the cardiovascular complications frequently observed in diabetes, it can be suggested that vitK2 therapy may yield positive outcomes in diabetes.