Ischemic stroke (IS) is one of the leading causes of mortality and disability worldwide and is frequently associated with secondary complications such as pneumonia (PN), which worsens clinical status and prognosis. The pathophysiology of IS involves oxidative stress and an exacerbated inflammatory response, contributing to blood-brain barrier disruption and neuronal damage. In addition, IS can induce immunosuppression, making individuals more susceptible to infections. Post-stroke pneumonia, a frequent complication, is associated with increased mortality and morbidity, but the exact mechanisms are not fully understood. The objective of this study was to evaluate the influence of pneumonia after IS on cerebral oxidative response in rats. Forty male Wistar rats, 60 days old, were used. Animals were subjected to middle cerebral artery occlusion (MCAO) to induce IS, or sham surgery (control). After 72 hours, pneumonia was induced by intratracheal administration of Klebsiella pneumoniae or saline. The groups were: sham+saline, sham+PN, MCAO+saline and MCAO+PN, with n = 10 per group. Twenty-four hours after PN induction, animals were euthanized and hippocampus and frontal cortex were collected for assessment of myeloperoxidase (MPO) activity, nitrite/nitrate (N/N) levels, oxidative damage to lipids and proteins, and activity of the antioxidant enzyme catalase (CAT). Data showed that the MCAO+PN group had more intense alterations compared with the other groups. There was a significant increase in MPO activity in the brain and elevated nitrite/nitrate levels in the frontal cortex. Lipid peroxidation was markedly increased in all three regions analyzed (hippocampus, frontal cortex and lung) in the MCAO+PN group. Significant reductions were also detected in the integrity of sulfhydryl-containing proteins and in CAT activity, especially in the frontal cortex, reinforcing impairment of the antioxidant system in the setting of combined injury. Post-stroke pneumonia exacerbates cerebral inflammatory and oxidative damage, highlighting a systemic impact and the need for careful attention to infectious comorbidities after ischemic injury.
Yoshii et al. (Sun,) studied this question.