Additive effect of cyclooxygenase and nitric oxide synthase blockade on the cerebrocortical microcirculation.

The contribution of vasodilator cyclooxygenase (COX) metabolites to the maintenance of the cerebrocortical blood flow (CBF) has been studied under physiological conditions and in nitric oxide (NO) deficiency. Inhibition of COX decreased resting CBF without changing arterial blood pressure. NO synthase blockade resulted in hypertension and CBF reduction as well as in enhanced cerebral prostacyclin and prostaglandin E2 production.

Carbon monoxide-prostaglandin E2 interaction in the hypothalamic circulation.

The heme oxygenase (HO)-carbon monoxide pathway was earlier shown to increase hypothalamic blood flow after inhibition of nitric oxide synthesis in rats. We hypothesized that this effect is mediated by prostaglandin E2 (PGE2). Inhibition of constitutive HO activity decreased cerebral PGE2 production and simultaneously increased hypothalamic nitric oxide synthase (NOS) activity without changing hypothalamic blood flow.

Surfactant protein D inhibits TNF-alpha production by macrophages and dendritic cells in mice.

Background: Surfactant protein (SP) D shares target cells with the proinflammatory cytokine TNF-alpha, an important autocrine stimulator of dendritic cells and macrophages in the airways.

Objective: We sought to study the mechanisms by which TNF-alpha and SP-D can affect cellular components of the pulmonary innate immune system.

Methods: Cytokine and SP-D protein and mRNA expression was assessed by means of ELISA, Western blotting, and real-time PCR, respectively, by using in vivo models of allergic airway sensitization.

Adaptation of the hypothalamic blood flow to chronic nitric oxide deficiency is independent of vasodilator prostanoids.

The aim of our study was to investigate the adaptation of the hypothalamic circulation to chronic nitric oxide (NO) deficiency in rats. Hypothalamic blood flow (HBF) remained unaltered during chronic oral administration of the NO synthase (NOS) inhibitor N(G)-nitro-l-arginine methyl ester (l-NAME, 1 mg/ml drinking water) although acute NOS blockade by intravenous l-NAME injection (50 mg/kg) induced a dramatic HBF decrease. In chronically NOS blocked animals, however, acute l-NAME administration failed to influence the HBF.