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Query: UMLS:C0027947 (
neutropenia
)
17,527
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Invasive aspergillosis continues to be a significant cause of morbidity and mortality in patients with prolonged
neutropenia
. We performed a phase I trial of escalating doses of aerosolized amphotericin B given by a face mask nebulizer system with a disposable bacterial exhale filter. Five, 10, 15, and 20 mg of drug were dissolved in sterile water and inhaled over 10 to 15 minutes twice daily. Tolerance was studied in 26 patients (18 transplant recipients, and 8 leukemia patients). No side effects were observed at any dose level. Prophylactic treatment ended for 14 patients (54%) when intravenous (IV) amphotericin B was begun empirically for antifungal coverage following fevers. Eleven patients (43%) continued inhaled amphotericin B until blood counts recovered. One patient was taken off study when she developed cardiogenic
pulmonary edema
. No patient developed clinically suspicious or pathologically documented infection with invasive aspergillosis. Prophylactic aerosolized amphotericin B is well tolerated at 5, 10, 15, and 20 mg twice daily dosing. In addition, prophylactic aerosolized amphotericin B does not appear to sensitize patients to the subsequent use of IV amphotericin B. Although this study suggests that prophylactic inhaled amphotericin B is well tolerated and effective, a large scale controlled trial is needed.
...
PMID:A pilot study of prophylactic aerosolized amphotericin B in patients at risk for prolonged neutropenia. 149 Jan 49
Thromboxane-mediated pulmonary hypertension,
pulmonary edema
, arterial hypoxia and pulmonary leukostasis occur in response to the infusion of plasma containing zymosan-activated complement (ZAP) in sheep. Platelet-activating factor (PAF) is a potential mediator of some of these effects. We investigated the effects of PAF infusions in unanesthetized sheep and the effects of the PAF receptor antagonist L-652,731 [trans-2,5-bis(3,4,5-trimethoxyphenyl)tetrahydrofuran] on the hematologic, hemodynamic and biochemical alterations produced by infusions of both ZAP and PAF. Infusions of 2 to 20 micrograms of PAF in 0.25% ovine serum albumin-saline produced pulmonary hypertension, hypoxia and dose-dependent thrombocytopenia,
neutropenia
and thromboxane synthesis. The effects of a 2 micrograms of PAF infusion were both qualitatively and quantitatively similar to those produced by a ZAP infusion. Pretreatment with aspirin (10 mg/kg) protected the sheep against the pulmonary vascular response to 20 micrograms of PAF and blocked completely the thromboxane synthesis. L-652,731 at a dose of 8 mg/kg blocked completely the
neutropenia
, thrombocytopenia, thromboxane synthesis, pulmonary hypertension and hypoxia induced by 5 micrograms of PAF, but this protective effect was not observed in animals infused with ZAP. These results indicate that PAF is probably not a mediator of the
neutropenia
, thromboxane-mediated pulmonary hypertension and hypoxia which result from the infusion of ZAP into sheep.
...
PMID:Effects of L-652,731, a platelet-activating factor (PAF) receptor antagonist, on PAF- and complement-induced pulmonary hypertension in sheep. 282 Dec 22
This study investigated the possible contribution of neutrophils to development of reexpansion
pulmonary edema
(RPE) in rabbits. Rabbits' right lungs were collapsed for 7 days and then reexpanded with negative intrathoracic pressure for 2 h before study, a model that creates unilateral edema in the reexpanded lungs but not in contralateral left lungs. Two hours after lung reexpansion, significant increases in lavage albumin concentration (17-fold), percent neutrophils (14-fold), and total number of neutrophils (7-fold) recovered occurred in the reexpanded lung but not in the left. After 2 h of reexpansion increased leukotriene B4 was detected in lavage supernatant from right lungs (335 +/- 33 pg/ml) compared with the left (110 +/- 12 pg/mg, P less than 0.01), and right lung lavage acid phosphatase activity similarly increased (6.67 +/- 0.35 U/l) compared with left (4.73 +/- 0.60 U/l, P less than 0.05).
Neutropenia
induced by nitrogen mustard (17 +/- 14 greater than neutrophils/microliters) did not prevent RPE, because reexpanded lungs from six neutropenic rabbits were edematous (wet-to-dry lung weight ratio 6.34 +/- 0.43) compared with their contralateral lungs (4.97 +/- 0.04, P less than 0.01). An elevated albumin concentration in reexpanded lung lavage from neutropenic rabbits (8-fold) confirmed an increase in permeability. Neutrophil depletion before reexpansion did not prevent unilateral edema, although neutrophils were absent from lung sections and alveolar lavage fluid from neutropenic rabbits.
...
PMID:Neutrophils in reexpansion pulmonary edema. 284 Dec 77
A patient with acquired immunodeficiency syndrome (AIDS) developed rash, fever,
neutropenia
, and elevated liver function tests during an initial course of trimethoprim-sulfamethoxazole (TMP-SMX) therapy. Upon reexposure to the drug, the patient experienced a severe anaphylactoid reaction associated with
pulmonary edema
and rhabdomyolysis. Reactions associated with TMP-SMX rechallenge in this patient population have been previously reported but have not been associated with this degree of severity. TMP-SMX therapy should be instituted with extreme caution in patients with AIDS who have demonstrated a prior hypersensitivity reaction to the drug.
...
PMID:Severe hypersensitivity reaction upon rechallenge with trimethoprim-sulfamethoxazole in a patient with AIDS. 296 2
We developed a new model of acute lung injury caused by live Escherichia coli peritonitis in guinea pigs. Arterial blood gas determinations, arterial blood pressure, and white blood cell counts were monitored serially for 12 h after the injection of either 2 x 10(9) E. coli J96 or saline. Lung water, albumin concentration in bronchoalveolar lavage fluid (BALF) and in lung tissue, WBC counts in BALF, and thiobarbituric-acid-reactive materials (TBARM) in plasma, lung tissue, and BALF were examined. Increased TBARM might be associated with pulmonary injury and are produced either by the generation of lipoperoxides secondary to oxygen-free radicals or as metabolic byproducts of prostanoid metabolism. Lung tissue sections were studied by light microscopy. E. coli peritonitis, as compared with control animals, caused significant peripheral
neutropenia
, histopathologic evidence of lung inflammation, acidosis, and hypotension. The wet-to-dry lung ratio was increased in the peritonitis group when compared with that in the control group (p less than 0.01).
Pulmonary edema
in the peritonitis group was associated with significantly increased albumin concentrations in BALF and lung tissue. We report the new finding of increased TBARM concentrations in BALF after E. coli peritonitis (p less than 0.01 and p less than 0.05, respectively). In contrast, plasma TBARM concentrations were unchanged. The levels of TBARM in the BALF correlated significantly with both lung water (p less than 0.01) and lung tissue albumin concentration (p less than 0.01). The measurement of elevated TBARM in BALF may allow acute lung injury to be detected. We conclude that this model may be useful for further studies of acute lung injury caused by E. coli peritonitis.
...
PMID:Pulmonary edema after Escherichia coli peritonitis correlates with thiobarbituric-acid-reactive materials in bronchoalveolar lavage fluid. 328 28
Neutrophils have been implicated in the pathogenesis of acute lung injury associated with clinical and experimental sepsis. Data from in vitro systems and experimental animals have suggested that neutrophil-derived oxidants, particularly H2O2, may be primarily responsible for endothelial damage, vasoconstriction, and
lung edema
. With the use of endotoxin infusion as an in vivo model of sepsis we tested the hypothesis that pretreatment with catalase, a peroxide scavenger, would ameliorate the resultant changes in pulmonary vasoconstriction and lung fluid balance. Paired experiments were performed in 16 goats with chronic lung lymph fistulas. One group of animals (n = 7) received endotoxin first alone and then again, several days later, after pretreatment with Ficoll-linked catalase. As a control, identical experiments were performed in a separate group (n = 6) with Ficoll-linked albumin substituted for Ficoll-catalase. A third group (n = 3) was given endotoxin alone and then again during a continuous infusion of catalase. Plasma and lymph levels of catalase were comparable to or exceeded those previously shown to be completely protective in isolated perfused lung preparations and in vitro systems. Endotoxin caused
neutropenia
, pulmonary arterial hypertension, decreased cardiac output, and increases in lymph flow to approximately three times base line, with a return of all variables toward control values by 6 h. Catalase pretreatment produced no significant differences in any of these variables. These experiments do not support a role for H2O2 as a mediator of acute lung injury due to endotoxemia.
...
PMID:Effect of intravenous catalase on the pulmonary vascular response to endotoxemia in goats. 328 99
Neutropenia
was produced in goats by injection of either nitrogen mustard, (1.5 mg/kg) or hydroxyurea (200 mg X kg-1 X day-1). A nitrogen mustard (M + E) group (n = 6), a hydroxyurea (H + E) group (n = 5), and a control (E) group (n = 7) were given 1-h infusions of endotoxin (5 micrograms/kg total dose), then monitored for up to 5 h. Postmortem extravascular lung water (EVLW) was significantly higher in the M + E group (14.2 +/- 4.4 ml/kg) and the E group (11.9 +/- 3.9 ml/kg) when compared with a normal control (6.6 +/- 1.3 ml/kg) group that did not receive endotoxin. EVLW in a group made neutropenic with nitrogen mustard (6.7 +/- 1.3 ml/kg) and the H + E (7.9 +/- 1.5 ml/kg) groups were not statistically different from each other or from normal controls. Circulating neutrophil counts averaged 32 +/- 42 cells/microliter in the M + E group and 180 +/- 210 cells/microliter in the H + E group. Only minimal histological changes were seen in the H + E group, but the E and M + E lungs had severe
pulmonary edema
. We conclude that neutrophils are not required for increased EVLW and decreased arterial O2 partial pressure after endotoxin infusion, and hydroxyurea prevents at least part of the
pulmonary edema
after endotoxin by a mechanism that is not neutrophil dependent.
...
PMID:Neutrophil depletion does not prevent lung edema after endotoxin infusion in goats. 354 69
Ritodrine hydrochloride, a beta-sympathomimetic treatment for premature labor, has been associated with the development of
pulmonary edema
, various metabolic derangements, myocardial ischemia, and infarction. We present the first reported case of absolute
neutropenia
after prolonged intravenous administration of ritodrine with rapid, spontaneous reversal once the medication was discontinued.
...
PMID:Ritodrine-induced neutropenia. 396 86
We did two studies to see if severe
neutropenia
might reduce the severity or delay development of O2-induced lung microvascular injury. First, we treated 11 rabbits with nitrogen mustard until their circulating neurophil count decreased to less than 50/microliters of blood, after which the rabbits breathed pure O2 until death; nine other rabbits received no nitrogen mustard and had normal numbers of circulating neutrophils during O2 breathing. All rabbits died of respiratory failure with
pulmonary edema
, and although chemotherapy decreased the number of neutrophils in the lungs by greater than 90%, it did not influence survival time or extravascular lung water content. To see if severe
neutropenia
might slow the development of O2-induced lung microvascular injury, we assessed the effects of sustained hyperoxia on lung fluid balance in unanesthetized lambs treated with hydroxyurea, so that their absolute neutrophil count was less than 50/microliters of blood. We measured pulmonary arterial and left atrial pressures, cardiac output, lung lymph flow, and concentrations of protein in lymph and plasma during a 2- to 4-h control period and then daily for 2 to 4 h as the lambs continuously breathed pure O2. After 3 days of hyperoxia, lymph flow doubled and the concentration of protein in lymph increased from 3.3 +/- 0.5 to 4.2 +/- 0.3 g/dl. Tracer studies with 125I-albumin before and 3 days after the start of O2 breathing confirmed the development of increased lung vascular permeability to protein. All lambs died of respiratory failure with
pulmonary edema
after 3-5 days in O2.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Oxygen-induced lung microvascular injury in neutropenic rabbits and lambs. 398 Mar 93
Calves were sensitized to horse serum in Freund's complete adjuvant and were subjected to acute systemic anaphylactic shock. Increased packed cell volume and potassium ion concentration together with severe
neutropenia
were observed to accompany the systemic hypotension. The hemoconcentration and hyperkalemia were not inhibited by antihistaminic or antiserotonin drugs, but were strongly inhibited by pretreatment of the calves with sodium meclofenamate and by disodium cromoglycate (DSCG) given simultaneously with diethylcarbamazine (DECC). In contrast there was no measurable diminution of the leukopenia by any inhibitor drug tested.
Pulmonary edema
and congestion of the liver, intestine, spleen, and kidney accompanied anaphylaxis. Atelectasis and edema with thickening of alveolar septa, together with polymorphonuclear cell infiltration were recorded histologically in the lungs of calves subjected to anaphylaxis. Calves premedicated with sodium meclofenamate sustained slight
pulmonary edema
only, with no other obvious pathological changes. Pretreatment with DSGG and DECC reduced the edema, congestion, and histopathological damage, but offered less protection than sodium meclofenamate. Antihistaminic or antiserotonin drugs were ineffective in protecting against anaphylactic changes in calves.
...
PMID:Hematological and pathological changes in acute systemic anaphylaxis in calves: effects of pharmacological agents. 426 91
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