Antileukotrienes in asthma: present situation.
A single-blind, crossover study was carried out in 9 healthy subjects to investigate the effect of a single dose of 2 tablets of 400 mg pentoxifylline ('Trental' 400) or placebo on cerebral blood flow, cerebral perfusion quotient and mental functions under experimental hypobaric conditions. Subjects were exposed in a low pressure chamber to simulated atmospheric pressures at sea level, 4000 and 7000 metres, and tests were performed 2 hours after intake of the dose, using 99m technetium brain scintigraphy and psychometric tests, to assess acutely induced impairment of cerebral function. After placebo, cerebral blood flow was decreased, especially at the 7000 metre level, whereas there was significantly less decrease after pentoxifylline. The perfusion quotient was normal throughout the pentoxifylline period but was outside the normal range in 8 of the 9 subjects after placebo. Psychometric testing showed better performance by the subjects after drug than after placebo intake. The results suggest that pentoxifylline may protect cerebral blood flow, nutrition and function under impaired supply conditions.
Long-term pentoxyfylline therapy effectively achieves sustained biochemical improvement. This correlates well with histological resolution of the disease.
Pentoxifylline, an analogue of the methylxanthine theobromine, inhibits the proliferation and certain biosynthetic activities of fibroblasts derived from normal human skin. Fibroblasts from the skin of patients with keloids, scleroderma and morphoea were cultured in vitro in the presence and absence of pentoxifylline (100-1000 micrograms/ml) to determine whether it inhibits fibroblast proliferation and the production of collagen, glycosaminoglycans (GAG), fibronectin and collagenase activity. The exposure of subconfluent fibroblast cultures to pentoxifylline resulted in non-lethal, dose-dependent reductions in serum-driven fibroblast proliferation, with 1000 micrograms/ml pentoxifylline virtually negating the proliferative effect of serum on the cells. The fibroblasts assayed as confluent cultures produced reduced amounts, by up to 95%, of collagen and GAG, dependent on the concentration of pentoxifylline, both in the presence and absence of serum. Pentoxifylline similarly inhibited the fibronectin production by keloid and scleroderma fibroblasts, but had no effect on collagenase activity.
The objective of this study was to assess the pharmacokinetic characteristics and tolerability of a new oral syrup formulation of pentoxifylline as an adjunct to IVIG and ASA in the treatment of KD in children.
The interaction of immunocompetent cells with the vascular endothelium is of prime importance for the development of septic multiple organ failure. There is evidence from in-vitro studies that the methylxanthine derivative pentoxifylline can attenuate the extent of inflammatory reactions by amplification of cell-derived endogenous regulators. For instance, pentoxifylline potentiates the anti-inflammatory actions of adenosine, prostacyclin, and prostaglandins of the E series by its synergistic action on intracellular cyclic AMP. By this mechanism, pentoxifylline inhibits the oxygen-radical production of polymorphonuclear leukocytes, the aggregation of platelets, disseminated intravascular coagulation, and the production of cytokines. Consequently, pentoxifylline improves perfusion in the microcirculation as well as tissue oxygenation. Further studies will clarify whether the promising results obtained with pentoxifylline in experimental septic shock will be confirmed under clinical conditions.
This study shows that a novel route (via the pulmonary circulation) used to administer pentoxifylline after hemorrhagic shock leads to superior cardiac performance in comparison with administration via lactated Ringer's solution or i.v. systemic pentoxifylline.
Observational retrospective cohort study. One hundred twenty-seven patients with ISSHL, treated at outpatient clinics between the years 2000 and 2010, were studied. We evaluated the prognostic correlation of the type of treatment and time to treatment with glucocorticoids and ISSHL.
Whole blood impedance aggregometry using whole equine blood incubated with varying concentrations of PTX. Adenosine diphosphate (ADP) and collagen were used to initiate aggregation.
The mechanism of the early stage of metastasis formation by sticky blood-born cancer cells is discussed. Abnormal platelet aggregation to circulating and lodged cancer cells, as well as alterations of blood coagulation and fibrinolysis play an important role. The reducing effect of several platelet aggregation inhibitors on cancer cell stickiness and tumor embolism mortality has been investigated in rats after intravenous transplantation of 1 X 10(6) Walker-256 carcinosarcoma cells. The tested substances diminished platelet aggregation to circulating cancer cells, leading to a dose-dependent inhibition of cancer cell lodgment to the endothelium. Furthermore, some of the substances prevented lethal pulmonary tumor cell embolism which was observed in 60% of the controls. These results are interpreted by assuming an inhibition of disseminated intravascular coagulation which occured after intravenous transplantation of Walker-256 carcinosarcoma. On this basis a clinical long-term study for metastasis prophylaxis was started more than 4 years ago with one of the tested substances, the dipyridamole derivative RA 233, in 40 patients with sarcoma or malignant lymphoma of the head and neck region. The provisional results obtained in matched pairs are discussed.