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At least 19 recordsLinked to original sources

PubMed1979

Effect of pentoxifylline on red cell flexibility and cation transport in healthy subjects and patients with hereditary spherocytosis.

The effect of pentoxifylline (3,7-dimethyl-1-(5-oxo-hexyl)-xanthine) on the flexibility of red cells was studied using a filtration method in which the red cells are forced, at a constant flow-rate, through a porous polycarbonate membrane. The filtration pressure reflects red cell rigidity and the amount of Hb released from the disrupted cells ('free Hb') red cell fragility. The advantage of this method is that it allows the two important determinants of red cell flexibility, rigidity and fragility, to be studied simultaneously. Pentoxifylline significantly improved normal red cell flexibility both in vivo and in vitro as judged by this method. The impaired flexibility of red cells from patients with congenital or hereditary spherocytosis (HS) was aggravated by pentoxifylline in vitro. A similar effect of pentoxifylline was also observed on red cells from relatives of HS patients. The effect of pentoxifylline on Ca2+ transport and Ca2+-Mg2+-ATPase activity in red cells from normal and HS patients was investigated. Under in vitro conditions pentoxifylline did not affect the Ca2+-Mg2+-ATPase activity of or Ca2+ efflux from normal and HS red cells. Neither the influx of monovalent cations (Na+, Rb+) or the osmotic resistance of normal or HS red cells was affected by pentoxifylline.

Adenosine Triphosphatases↗

PubMed1992

Pentoxifylline modulates activation of human neutrophils by amphotericin B in vitro.

The antifungal agent amphotericin B (AmB) alters neutrophil (polymorphonuclear leukocyte [PMN]) function, and this may be the mechanism for some of the adverse effects caused by AmB. AmB is a potent inhibitor of PMN migration, increases PMN adherence and aggregation, and primes PMN for increased oxidative activity in response to a second stimulus. AmB also stimulates mononuclear leukocytes (MNLs) to release inflammatory mediators which augment the effects of AmB on PMN function. In the present study, we observed that the methylxanthine derivative pentoxifylline decreased the effects of AmB on PMN function. AmB (2 micrograms/ml) priming doubled PMN chemiluminescence stimulated by fMet-Leu-Phe. In the presence of MNLs, AmB priming increased fMet-Leu-Phe-stimulated PMN chemiluminescence to 622% of unprimed PMN activity. Pentoxifylline (100 microM) blunted the rise in AmB-augmented PMN chemiluminescence in the presence of MNLs to 282% of unprimed PMN activity, and pentoxifylline metabolites were active at 10 microM. Pentoxifylline (100 microM) also blocked AmB-augmented PMN oxidative activity in whole blood, as measured by nitroblue tetrazolium reduction. In the presence of MNL, AmB (2 micrograms/ml) doubled the expression of the important PMN adherence factor Mac-1. Pentoxifylline (1 mM) decreased AmB-stimulated PMN Mac-1 expression back to unstimulated amounts. In the presence of MNLs, AmB (2 micrograms/ml) decreased PMN nondirected and directed migration to fMet-Leu-Phe to 40 and 38% of control PMN migration, respectively. Pentoxifylline (300 microM) counteracted AmB inhibition of nondirected and directed migration to fMet-Leu-Phe, resulting in migration that was 71 and 87% of control PMN migration, respectively. In contrast, the methylxanthine caffeine (100 muM) increased AmB-enhanced chemiluminescence but did not affect AmB-inhibited PMN migration. Pentoxifylline should be evaluated as adjunctive therapy to lessen the inflammatory damage caused by AmB.

Amphotericin B↗

PubMed1992

Pentoxifylline preserves small-intestine microvascular blood flow during bacteremia.

BACKGROUND: Intestinal mucosal ischemia with subsequent mucosal dysfunction has been implicated in the pathogenesis of ongoing sepsis and multiple systems organ failure. We have previously reported vasoconstriction and hypoperfusion in the intestinal microcirculation during sepsis. Efforts to improve microcirculatory blood flow during sepsis may lead to more effective treatment or prevention of multiple systems organ failure. Pentoxifylline improves survival and visceral organ perfusion in experimental sepsis and hemorrhage. The purpose of this study was to determine whether pentoxifylline would improve microvascular blood flow in the small intestine during bacteremia. METHODS: In vivo videomicroscopy was used to quantitate alterations of the small-intestine microcirculation during Escherichia coli bacteremia in rats pretreated with either intravenous pentoxifylline or saline solution. Systemic hemodynamic and microvascular variables were measured every 15 minutes for 2 hours. RESULTS: Tachycardia and increased cardiac output developed in bacteremic rats while they remained normotensive. Intestinal vasoconstriction and hypoperfusion occurred in bacteremic rats treated with saline solution. Microvessel diameters and blood flow remained within 5% to 10% of baseline in bacteremic rats pretreated with pentoxifylline. Pentoxifylline in nonbacteremic rats resulted in intestinal vasodilation and increased blood flow. CONCLUSIONS: Pentoxifylline prevented small-intestine vasoconstriction and preserved microvascular blood flow during hyperdynamic sepsis. Pentoxifylline in nonbacteremic rats increased microvascular blood flow.

Animals↗

PubMed1992

Effects of pentoxifylline on equine neutrophil function and flow properties.

Pentoxifylline has been reported to improve peripheral vascular circulation by altering the flow properties of blood. To determine if the hemorrheological effects of pentoxifylline were mediated by alterations in neutrophil function and/or flow properties, we evaluated the drug's effects on equine neutrophils in vitro. Pentoxifylline, at a concentration of 1 x 10(-1) M, but not at concentrations of 1 x 10(-6) M to 1 x 10(-2) M, markedly suppressed neutrophil superoxide production, zymosan phagocytosis and adherence to nylon wool. Pentoxifylline failed to improve neutrophil filterability through 3 mu polycarbonate filters at any concentration tested. We conclude that equine neutrophil function and flow properties are unlikely to be affected by pentoxifylline concentrations achievable in vivo.

Animals↗

PubMed1992

Effects of phosphodiesterase inhibitors caffeine and pentoxifylline on spontaneous and stimulus-induced acrosome reactions in human sperm.

OBJECTIVE: To determine whether the phosphodiesterase inhibitors caffeine and pentoxifylline influence the acrosome reaction in the conditions in which they are currently used as sperm movement enhancers. DESIGN: The frequency of acrosome reaction occurring spontaneously in capacitating media or induced by physiological (follicular fluid [FF]) and artificial (ionophore A23187) stimuli was compared in the presence and absence of the phosphodiesterase inhibitors. SETTING: Private hospital and research laboratory. PATIENTS, PARTICIPANTS: Patients undergoing routine semen examination before in vitro fertilization (no pathology detected) and healthy sperm donors. INTERVENTIONS: None. MAIN OUTCOME MEASURE: Percentage of acrosome-reacted sperm determined with the use of fluorescein-labeled Pisum sativum agglutinin as acrosomal stain. RESULTS: Caffeine alone augmented the frequency of acrosome reaction, but this effect was not observed with pentoxifylline alone. However, pentoxifylline increased sperm responsiveness to the acrosome reaction-inducing stimuli, FF and ionophore A23187. CONCLUSIONS: The promotion of spontaneous acrosome reaction may counteract the benefits from application of caffeine as motility stimulant. On the other hand, the sensitization to physiological acrosome reaction stimuli is expected to contribute to the improvement of sperm fertilizing ability by pentoxifylline and make this drug a potential candidate for the treatment of acrosome reaction anomalies.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMedDate not supplied

The effect of pentoxifylline ('Trental') on cerebral blood flow: a double-blind study.

A double-blind, placebo controlled crossover study was carried out in 20 geriatric patients with cerebrovascular insufficiency ot asses the effect of pentoxifylline on cerebral blood flow. Using 99m Tc cerebral scinitigraphy and a gamma comera/computer system, the pattern of blood flow in 5 brain areas was manitored after a single intravenous infusion of 200 mg pentoxifylline (10 ml) and after 10 ml saline solution. The results showed that, with the exception of one brain area, there was a statistically significant increase both in regional and hemispheric cerebral blood flow after pentoxifylline. It is of particular interst that global hemispheric blood flow, which gives an indication of total blood supply to the brain, showed approximately the same percentage increase on both sides with pentoxifylline.

Aged↗

PubMed1978

The effect of pentoxifylline on the flow properties of human blood.

Recent investigations have revealed that erythrocytes from patients with chronic arterial occlusive disease are significantly less deformable than red blood cells from healthy subjects. The influence of pentoxifylline on red blood cell fluidity was measured by a standard filtration technique using 8 micron membrane filters. Impaired deformability of erythrocytes was significantly improved in patients suffering from peripheral vascular disorders following intravenous injection of 200 mg pentoxifylline. Studies on reduced red cell deformability induced by hyperosmolarity in vitro showed that pentoxifylline (4 and 20 microgram/ml) produced a dose-dependent improvement both in blood from healthy subjects and from patients with peripheral arterial occlusive disease. The results suggest that the positive therapeutic effect of pentoxifylline in peripheral arterial occlusive disease is mediated by improving red cell fluidity in the microcirculation.

Arterial Occlusive Diseases↗

PubMed1992

Secretion of tumor necrosis factor by endotoxin-treated equine mammary exudate macrophages: effect of dexamethasone and pentoxifylline.

Secretion of tumor necrosis factor (TNF) by equine mammary exudate macrophages (MEM phi) exposed to bacterial lipopolysaccharide (LPS) was dose-dependent and was maximal (216.5 +/- 51.9 U/ml) at 100 micrograms LPS/ml, the highest concentration tested. All concentrations of dexamethasone tested (10(-8) to 10(-4) M) significantly (P less than or equal to 0.05) inhibited TNF production by MEM phi when the agent was added 1 hour before LPS. Pretreatment with pentoxifylline at concentrations greater than 3 micrograms/ml also significantly (P less than or equal to 0.05) reduced secretion of TNF by MEM phi. The inhibitory effect of dexamethasone (10(-4) M) was observed when the agent was added to MEM phi from 30 minutes before until 4 hours after LPS. Pentoxifylline (100 micrograms/ml) significantly (P less than or equal to 0.05) suppressed TNF when added from 2 hours before until 2 hours after LPS; however, when pentoxifylline addition was delayed until 8 hours post-LPS, TNF production was enhanced. These apparent inhibitory effects of dexamethasone and pentoxifylline were not due to reduced macrophage viability or to interfering effects of the agents at the level of the TNF bioassay.

Animals↗

PubMed1992

Pentoxifylline modulates deformability, F-actin content, and superoxide anion production of polymorphonuclear leukocytes from diabetic cats.

Capillary occlusion is an early event in the development of diabetic retinopathy, and white blood cells have recently been shown to be involved. We have shown previously that pentoxifylline improves deformability and decreases F-actin content of unstimulated polymorphonuclear leukocytes from normal human subjects. The purpose of this study was to determine if pentoxifylline would improve three properties of unstimulated polymorphonuclear leukocytes from diabetic cats. The measured parameters were mechanical (whole cell deformability), structural (F-actin content) and biochemical (rate of superoxide anion production). Chronic hyperglycemia was induced in three cats by partial pancreatectomy, and they were kept in poor glycemic control for at least 6 months prior to the study. Polymorphonuclear leukocytes were isolated and the entry time of individual passive cells was measured during aspiration into a 4-micron micropipette under constant suction pressure (-15 cmH2O). Deformability was defined as the inverse of the entry time. F-actin content of passive cells was measured by NBD-phallacidin labeling followed by flow cytometry. The rate of superoxide anion production was measured spectrophotometrically by superoxide dismutase-inhibitable cytochrome c reduction. Following incubation for 15 min with 0.1, 1.0 and 10.0 mM pentoxifylline, the average entry time of passive polymorphonuclear leukocytes was reduced from control by 11 +/- 5% (P = 0.045), 17 +/- 6% (P = 0.007), and 36 +/- 5% (P < 0.001), respectively. The F-actin content decreased by 0%, 4 +/- 0.6% (P < 0.001), and 10 +/- 3% (P < 0.001), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Actins↗

PubMed1992

Effects of ibuprofen and pentoxifylline on the cardiovascular response of normal humans to endotoxin.

Endotoxin is a major mediator of the life-threatening cardiovascular dysfunction that characterizes Gram-negative sepsis. In animal models of endotoxemia, pretreatment with ibuprofen or pentoxifylline attenuates some of these cardiovascular changes. To evaluate the effects of these agents on the human cardiovascular response to endotoxemia, hemodynamic variables were measured serially in 24 normal subjects who were given intravenous endotoxin. The subjects were randomized to receive oral ibuprofen (n = 9), pentoxifylline (n = 10), or no medication before endotoxin administration (n = 5). The subjects were volume loaded 3-5 h after endotoxin administration, and hemodynamic measurements were reassessed. Core temperature after endotoxin alone or endotoxin-pentoxifylline approached a maximum at 3 h (greater than or equal to 38.6 degrees C), while the endotoxin-ibuprofen group remained afebrile. At 3 and 5 h, all three groups had significant increases in heart rate, cardiac index, oxygen delivery, and oxygen consumption, while systemic vascular resistance index decreased significantly from baseline. The oxygen extraction ratio remained unchanged. After volume loading, the left ventricular ejection fraction and left ventricular end-diastolic and end-systolic volume indexes did not differ among the groups. The hyperdynamic cardiovascular response to endotoxin in humans occurs in the absence of fever and is not significantly ameliorated by oral cyclooxygenase or phosphodiesterase inhibition.

Adult↗

PubMed1976

Statistical evaluation of polygraphic investigations of pentoxifylline.

Changes in the electro-encephalogram, and in the electro-oculogram electromyogram, ECG, blood supply, blood pressure, electrical skin activity and neurological/psychiatric findings, were investigated in 100 patients given single administrations of 200 mg of pentoxifylline (BL 191). It is concluded from the changes in the EEG wave patterns that pentoxifylline produces a beneficial effect on the cerebral processes contributing to bio-electrical brain activity. Pentoxifylline can be classed as a substance with microcirculatory/metabolic effects on the brain, which lead to stimulation of psychomotor behaviour.

Adult↗

PubMed1979

Influence of pentoxifylline on erythrocyte deformability in peripheral occlusive arterial disease.

Impaired red cell deformability has been found in patients suffering from chronic peripheral vascular disorders, the implication being that microcirculatory blood flow is hindered and tissue hypoxaemia is aggravated. Measurement of erythrocyte deformability by a standard filtration technique for whole blood was carried out in 40 young healthy persons, in 25 untreated patients with peripheral occlusive arterial disease and in 25 patients with matching vascular disease, before and after a 6-weeks' oral treatment with 400 mg pentoxifylline 4-times daily. The filtration rates were significantly lower in the patient groups compared to those of healthy volunteers. After the oral administration of pentoxifylline, a significant increase in filtration rates was observed pointing to an improvement in erythrocyte deformability. The findings suggest that by improving erythrocyte deformability pentoxifylline positively influences the microcirculatory blood fluidity, an important factor for efficient therapy in peripheral arterial occlusive disease.

Adult↗

PubMed1992

[Evaluation of the antithrombotic effects of pentoxifylline, acetylsalicylic acid and low molecular weight heparin in the laser model of thrombosis].

Antithrombotic effects of different agents including acetylsalicylic acid (Asprocol/Polfa PL/), pentoxifylline (Agapurin/Spofa CS/) and low molecular weight heparin (Antixarin B. Braun, Melsungen, FRG) were studied in the laser-induced rat thrombosis model. The investigations were carried out on male Wistar rats weighing 200-300 g. Thrombus formation was induced in small mesenteric arteries 25-30 microns; using argon laser. An interference contrast system based on a Leitz Orthoplan microscope for the evaluation of thrombus formation was used. The number of laser injuries needed to induce a defined thrombus proved to be a useful way to quantitate the results in this thrombosis mode. All agents showed dose dependent antithrombotic effect in our laser model. Acetylsalicylic acid (ASA) 2 hours after oral administration markedly inhibited thrombus formation in minimal dose 50 mg/kg, pentoxifylline in dose 10 mg/kg 30 min after i.v. injection and low molecular weight heparin (Antixarin) in dose 0.1 mg/kg, 2 hours, after s.c. injection. Antithrombotic effect of administration of minimal effective doses of ASA (orally) and pentoxifylline (i.v.) lasted longer than 4 hours but less then 6 hours. LMW heparin (Antixarin) in minimal effective dose 0.1 mg/kg after s.c. injection inhibited thrombus formation in small mesenteric vessels for more than 12 hours but less than 24 hours.

Animals↗

PubMed1992

Pentoxifylline in vitro reverses neutrophil chemotactic deficiency induced by interleukin-2 treatment.

Patients undergoing immunotherapy with Interleukin-2 experience multiple side effects and are highly susceptible to bacteremia. In a previous study, we confirmed the profound neutrophil chemotactic deficiency induced by Interleukin-2 therapy. Peripheral blood cells exposed to Interleukin-2 in vitro secrete secondary cytokines. The release of tumor necrosis factor into the circulation after Interleukin-2 injection has been proposed as an important mechanism underlying cell function alterations. We tested chemotaxis of neutrophils from normal subjects after incubation with the serum from treated patients. Serums induced a defective chemotaxis of normal neutrophils similar to the one observed with neutrophils from Interleukin-2 treated patients. We have previously demonstrated a dose-dependent reversion of neutrophil chemotaxis after incubation with anti-Tumor Necrosis Factor-alpha antibody. Pentoxifylline is known for counteracting the inflammatory action of tumor necrosis factor. We tested its capability to reverse the chemotactic deficiency of neutrophils induced by treated patient serums. Pentoxifylline was added after incubation of normal cells with patient serum, and the directed chemotaxis was restored. Pentoxifylline may have a significant therapeutic potential for the prevention or treatment of complications related to inappropriately activated neutrophils.

Bacteremia↗

PubMed1979

Amelioration of blood viscosity in sickle cell anemia by pentoxifylline. A case report.

An 18 year old female patient with homozygous sickle cell anemia (HbSS: HbS 65% and HbF 4.9%) has been suffering from painful hemolytic crises about once a week since her childhood. Under treatment with pentoxifylline (2.4 gm daily in three divided doses), the blood viscosity decreased from 6.7 to 4.9 cP (normal: 4.3 to 5.3 cP at shear rate 46/sec) and the erythrocyte filtration accelerated from 127 to 77 sec (normal: 30 to 49 sec). Though hemolysis could not be prevented by pentoxifylline, there was no further demand for analgesic medication even in the hemolytic state. By decreasing blood viscosity and improving microcirculation, pentoxifylline may prevent the vasoocclusive complications of sickle cell anemia.

Adolescent↗

PubMed1979

On the influence of pentoxifylline on the permeability of rat erythrocytes for methyl-O-glucose.

In a series of experiments it was established that in the presence of pentoxifylline (Trental), methyl-O-glucose permeates rat erythrocyte membrane significantly more than in untreated control experiments. Pentoxifylline itself, apparently does not permeate erythrocyte membrane. It is possible that some of the therapeutic effects of pentoxifylline can be related to the facilitation of red blood cell membrane permeability for glucose.

Adenosine Triphosphate↗

PubMed1977

[Investigations on the pharmacokinetics of pentoxifylline in chronic renal failure (authors transl)].

The pharmacokinetical behaviour of 14C-labelled pentoxifylline was investigated in normal volunteers and in patients with different stages of impaired renal function. It was shown that in patients, having a creatinine-clearance of less than 10,0 ml/min., occurs an accumulation of pentoxifylline. This finding leads to the conclusion that in patients with advanced renal failure the daily dose of pentoxifylline should be adjusted to the diminished renal elimination.

Administration, Oral↗

PubMed1978

Effect of pentoxifylline and aminophylline on biogenic amine metabolism of the rat brain.

In the brain of rats injected with pentoxifylline [3,7-dimethyl-1(5-oxo-hexyl)-xanthine] or aminophylline the following was observed: (i) dose-dependent increases of tryptophan and 5-hydroxyindoleacetic acid levels and of 5-hydroxytryptophan and dihydroxyphenylalanine accumulation after treatment with the decarboxylase inhibitor benserazide HCl; (ii) acceleration of norepinephrine turnover following alpha-methyl-p-tyrosine; (iii) increase of 3-methoxytyramine accumulation following pargyline. On a molar basis pentoxifylline was more potent than aminophylline in affecting brain biogenic amine metabolism.

Aminophylline↗