Whole-body hyperthermia attenuates experimental autoimmune myocarditis in the rat.

Background: Heat stress prior to induction of various forms of cardiac injury has been shown to result in preconditioning and attenuation of subsequent damage. We evaluated the effects of whole-body hyperthermia (WBH) on experimental autoimmune myocarditis (EAM) induced either by injection of myosin or by adoptive transfer of lymphocytes.

Methods And Results: Lewis rats were pretreated with WBH either 24 h prior to EAM induction (Group A1) or 14 days following EAM induction (Group A2).

The effect of tyrphostin AG-556 on intimal thickening in a mouse model of arterial injury.

Background: Inflammation has been shown to play an important role in promoting the response to arterial injury and proinflammatory cytokines, such as tumor necrosis factor (TNF) alpha, are candidate mediators. AG-556 is a tyrosine kinase inhibitor proven to be effective in a model of multiple sclerosis-like syndrome in mice due to its immunomodulating effect. In the current study, we investigated the effect of the tyrphostin AG-556 on neointimal thickening and cytokine profile in a model of arterial injury in the mouse.

The effect of early and late treatment with the tyrphostin AG-556 on the progression of experimental autoimmune myocarditis.

Experimental autoimmune myocarditis (EAM) in rats is a T-cell-mediated disorder; the involvement of TNF-alpha in this disorder has been demonstrated. EAM represents a model for human autoimmune myocarditis, a condition for which no optimal treatment is currently available. Tyrphostins AG-126 and AG-556 were previously shown to reduce TNF-alpha production and its end-organ cytotoxicity, thus proving beneficial in animal models of septic shock and experimental autoimmune encephalomyelitis.

Inhibition of intimal thickening in the rat carotid artery injury model by a nontoxic Ras inhibitor.

Background: Neointimal formation with and without previous vascular injury is common after balloon dilation and in transplant arteriosclerosis. It involves proliferation and migration of medial smooth muscle cells and inflammation, processes that are regulated by Ras proteins and their down-stream effectors. Farnesylthiosalicylate (FTS) is a Ras inhibitor that interferes with Ras membrane anchorage and affects Ras proteins in their active state.

Relation of preexisting anti-beta2GPI antibodies to infarct size in a rat model.

Background: Anti-beta2-glycoprotein I (beta2GPI) antibodies (a subpopulation of antiphospholipid (aPL) antibodies) are associated with a procoagulant state in humans and with enhanced atherosclerosis in experimental animal models. Moreover, the presence of high titers of aPL antibodies in relatively young patients is associated with higher incidence of subsequent myocardial infarction. Herein, we evaluated the role of preexisting high levels of aPL antibodies in determining the size of the infarct induced by permanent ligation of the left anterior descending artery (LAD) in a rat model.