Hydrogen sulfide prevents the vascular dysfunction induced by severe traumatic brain injury in rats by reducing reactive oxygen species and modulating eNOS and H 2 S-synthesizing enzyme expression

• Published in: Life sciences (1973) Vol. 312; p. 121218
• Main Authors: López-Preza, Félix I, Huerta de la Cruz, Saúl, Santiago-Castañeda, Cindy, Silva-Velasco, Diana L, Beltran-Ornelas, Jesus H, Tapia-Martínez, Jorge, Sánchez-López, Araceli, Rocha, Luisa, Centurión, David
• Format: Journal Article
• Language: English
• Published: Netherlands 01.01.2023
• Subjects: Animals; Body Weight; Brain Injuries, Traumatic - complications; Brain Injuries, Traumatic - drug therapy; Hydrogen Sulfide - pharmacology; Hypertension - metabolism; NG-Nitroarginine Methyl Ester - adverse effects; Rats; Reactive Oxygen Species - metabolism; Water; Hydrogen sulfide; Traumatic brain injury; HS-synthesizing enzymes; Endothelial function; Vascular dysfunction
• ISSN: 1879-0631

To assess the effects of subchronic administration with NaHS, an exogenous H S donor, on TBI-induced hypertension and vascular impairments. Animals underweministration does not prevent the body weight loss but slightly imnt a lateral fluid percussion injury, and the hemodynamic variables were measured in vivo by plethysmograph method. The vascular function in vitro, the ROS levels by the DCFH-DA method and the expression of H S-synthesizing enzymes and eNOS by Western blot were measured in isolated thoracic aortas at day 7 post-TBI. The effect of L-NAME on NaHS-induced effects in vascular function was evaluated. Brain water content was determined 7 days after trauma induction. Body weight was recorded throughout the experimental protocol, whereas the sensorimotor function was evaluated using the neuroscore test at days -1 (basal), 2, and 7 after the TBI induction. TBI animals showed: 1) an increase in hemodynamic variables and ROS levels in aortas; 2) vascular dysfunction; 3) sensorimotor dysfunction; and 4) a decrease in body weight, the expression of H S-synthesizing enzymes, and eNOS phosphorylation. Interestingly, NaHS subchronic administration (3.1 mg/kg; i.p.; every 24 h for six days) prevented the development of hypertension, vascular dysfunction, and oxidative stress. L-NAME abolished NaHS-induced effects. Furthermore, NaHS treatment restored H S-synthesizing enzymes and eNOS phosphorylation with no effect on body weight, sensorimotor impairments, or brain water content. Taken together, these results demonstrate that H S prevents TBI-induced hypertension by restoring vascular function and modulating ROS levels, H S-synthesizing enzymes expression, and eNOS phosphorylation.