The inflammatory milieu of acute myocardial infarction (MI) is theoretically conducive to
enhanced cytokine synthesis within the brain. We tested the hypothesis that synthesis of …

Within minutes of acute myocardial infarction (MI), proinflammatory cytokines increase in the
brain, heart, and plasma. We hypothesized that cardiac afferent nerves stimulated by …

The expression of proinflammatory cytokines increases in the hypothalamus of rats with
heart failure (HF). The pathophysiological significance of this observation is unknown. We …

Exogenous tumor necrosis factor-α (TNF-α) induces delayed myocardial depression in vivo
but promotes rapid myocardial depression in vitro. The temporal relationship between …

The expression of proinflammatory cytokines increases in hypothalamus of rats with
myocardial infarction (MI) and heart failure. We used central gene transfer of human …

Previous studies have shown that 1 wk after permanent coronary artery ligation in rats, some
cellular mechanisms involving TNF-α occur and contribute to the development of cardiac …

Patients experiencing an acute myocardial infarction (AMI) have a three times higher chance
to develop depression. Vice versa, depressive symptoms increase the risk of cardiovascular …

The purpose of this study was to investigate the significance of the sequential changes in
proinflammatory cytokines observed in the plasma of patients early after myocardial infarct: a …

Tumor necrosis factor alpha (TNFα) is a pleiotrophic cytokine with diverse proinflammatory
actions. Focal cerebral ischemia induces rapid and dramatic increases in TNFα levels within …

Ischemic preconditioning (IP) and prior exposure to lipopolysaccharides (LPS) reduce infarct
size (IS) and serum tumor necrosis factor-α (TNF-α) concentration resulting from myocardial …