Physiologic response to hemorrhagic shock depends on rate and means of hemorrhage.

Background: Traditional models of shock classify severity based on the volume of hemorrhage. Clinically, hemorrhage occurs at a variable rate, usually slowing as blood pressure drops; however most animal experimental models use a constant rate of hemorrhage. Our hypothesis was that rapid bleeding followed by slower bleeding using a fixed total volume would result in a greater physiologic insult.

[Evaluation of aroeira (Schinus terebinthifolius Raddi) extract on the healing process of gastroraphy in rats].

Purpose: To evaluate the healing process of gastric suture in rats using hydroalcoholic aroeira (Schinus terebinthifolius Raddi) extract.

Methods: Forty adult male rats, divided into two groups of 20 animals were operated and named as follows: aroeira group (Ga), and the control group (Gc). Each group was divided into two subgroups (SG) of 10 animals (SGa and SGc) according to the time of provoked death (three and seven days).

LPS-induced acute lung injury is attenuated by phosphodiesterase inhibition: effects on proinflammatory mediators, metalloproteinases, NF-kappaB, and ICAM-1 expression.

Background: Acute endotoxemia is characterized by an enhanced inflammatory response. Pentoxifylline (PTX), a phosphodiesterase inhibitor, has been shown to decrease TNF-alpha levels and to down-regulate neutrophil activation, likely because of increases in intracellular cyclic AMP. Its effects on lipopolysaccharide (LPS) induced lung injury, more specifically on tissue neutrophil infiltration and degranulation, adhesion molecule expression, and transcriptional factor activation, have not been fully investigated.

Role of hypertonic saline and pentoxifylline on neutrophil activation and tumor necrosis factor-alpha synthesis: a novel resuscitation strategy.

Background: Hypertonic saline (HS) and pentoxifylline (PTX) have been shown to modulate polymorphonuclear neutrophil (PMN) functions after shock and sepsis. We hypothesized that a combination of HS and PTX (HSPTX) would down-regulate PMN functions and inflammatory mediator synthesis more effectively than each alone, possibly by acting at different steps of the signaling pathways, ultimately leading to an enhanced effect.

Methods: Whole blood from healthy volunteers was stimulated with lipopolysaccharide (LPS) (100 microg/mL), f-methionyl-leucyl-phenylalanine (1 micromol/L), and phorbol 12-myristate 13-acetate (1 microg/mL).

Nonspecific phosphodiesterase inhibition attenuates liver injury in acute endotoxemia.

Background: Endotoxemia is accompanied by pro-inflammatory cytokine production, generation of reactive oxygen species, and end-organ injury. Pentoxifylline (PTX), a methylxanthine derivative and phosphodiesterase inhibitor, is known for its anti-inflammatory properties, including down-regulation of interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha synthesis. Its effects on liver function and hepatic histology following acute endotoxemia have not been investigated fully.

LPS-stimulated PMN activation and proinflammatory mediator synthesis is downregulated by phosphodiesterase inhibition: role of pentoxifylline.

Background: Excessive production of reactive oxygen species by PMN is associated with tissue damage during inflammation. LPS interacts with the cell surface receptor CD14, which generates transmembrane signals through Toll-like protein 4 leading to mitogen activated protein kinase (MAPK) p38 activation, cytokine synthesis, PMN beta2-integrin expression and oxidative burst. Phosphodiesterase inhibition decreases proinflammatory cytokine production and tissue injury after LPS challenge.