Duration of endothelial dysfunction of mesenteric blood vessels of rats in influenza A(H3N2) virus infection

Marchenko V.A., Antonyuk I.A., Toropova Ya.G., Mukhametdinova D.V., Galagudza M.M., Zhilinskaya I.N.

North-Western State Medical University Named after I.I. Mechnikov, St. Petersburg, Russia
Almazov National Medical Research Centre, St. Petersburg, Russia

Objective of the study. To determine the duration of systemic endothelial dysfunction of blood vessels in influenza A(H3N2) virus infection.

Materials and methods. The study involved intranasal infection of Wistar rats with influenza A/Port Chalmers/1/1973 (H3N2) virus at a dose of 6.5 lg EID₅₀/mL. The animals were euthanized on days 30, 60, and 90 post-infection (n=5). The control group received intranasal DMEM and was euthanized at the same time intervals. Viral infectivity in lung and mesentery homogenates was assessed using embryonated chicken eggs. The level of endothelial NO-synthase (eNOS) expression in the endothelium of mesentery blood vessels in rats was studied using immunohistochemical analysis followed by morphometry. Vasomotor function of the mesenteric blood vessels endothelium was studied using myography.

Results. Influenza A(H3N2) virus was not detected in the lung or mesentery tissues of infected rats in the long-term period. A decrease in eNOS in the endothelium of mesenteric blood vessels of infected rats by 25.36% and 16.95% (p<0.05) was recorded on days 30 and 60, respectively. The maximum response of mesenteric blood vessels from infected rats to a vasoconstrictor decreased by 15.02% (p<0.05) on day 60 and increased by 32.39% (p<0.01) on day 90 compared to the control.

Conclusion. The data obtained indicates that influenza A(H3N2) virus causes prolonged systemic endothelial dysfunction in the blood vessels.