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Query: UMLS:C0027947 (neutropenia)
 17,527 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The physiologic responses during prolonged exposure to platelet activating factor (PAF) are largely unexplored. Thus, the cardiopulmonary and intravascular effects of a sustained infusion of 1-O-hexadecyl-2-acetyl-sn-glycero-3- phosphocholine (C16:0-AGEPC; 0.159 nmole/kg/min for 120 min) were characterized in anesthetized rabbits. Within minutes, a transient period of tachypnea developed and was followed by 30 min of stable ventilation. Subsequently, both respiratory rate and tidal volume irreversibly increased. The latter pulmonary ventilatory alterations were preceded by lung mechanical changes, i.e., dynamic lung compliance (CLdyn) decreased 21.6 +/- 3.4% (mean +/- SE) and total pulmonary resistance (Rpulm) increased 25.1 +/- 8.5%. In contrast to CLdyn which partially recovered during infusion, Rpulm remained elevated throughout the study, Concurrent with these pulmonary alterations, significant cardiovascular changes also occurred. Right ventricular hypertension developed immediately and was maximal within 7.9 +/- 0.9 min; this hypertension persisted throughout the infusion period but rapidly reversed thereafter. Mean arterial pressure (MAP) decreased 37.1 +/- 5.8% within 31.4 +/- 2.5 min and then remained at this level. The patterns and extent of alterations in left ventricular pressure, +dP/dtmax, and -dP/dtmax paralleled the changes in MAP and were accompanied by a progressive decrease in left ventricular end-diastolic pressure. These cardiopulmonary effects of C16:0-AGEPC developed in association with prolonged thrombocytopenia and intravascular platelet activation. In contrast, C16:0-AGEPC-induced neutropenia at 5 min was reversed within 60 min and was followed by sustained neutrophilia. In combination, these data suggest that the continuous biosynthesis and release of PAF in vivo could modulate significant, persistent pathophysiological alterations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiopulmonary and intravascular alterations during the sustained infusion of PAF. 195 34

Respiratory decompression sickness (RDCS, "the chokes") is a potentially lethal consequence of ambient pressure reduction. Lack of a clearly suitable animal model has impeded understanding of this condition. RDCS, unaccompanied by central nervous system signs, occurred in 17 of 18 unanesthetized sheep exposed to compressed air at 230 kPa (2.27 ATA) for 22 h, returned to normal pressure for approximately 40 min, and taken to simulated altitude (0.75 ATA, 570 Torr). Respiratory signs, including tachypnea, sporadic apnea, and labored breathing, were accompanied by precordial Doppler ultrasound evidence of marked venous bubble loading. Pulmonary arterial pressures exceeded 30 Torr in five catheterized sheep that died or became moribund. Hypoxemia (arterial Po2 less than 40 Torr), neutropenia, and thrombocytopenia were observed. Peribronchovascular edema was the most prominent necropsy finding. Chest radiography indicated interstitial edema in most affected sheep. High body weight and catheterization predisposed the sheep to severe RDCS. It appears that this protocol reliably provides a useful animal model for studies of RDCS and obstructive pulmonary hypertension, that the precipitating event is massive pulmonary embolization by bubbles, and that venous bubbles, detected by Doppler ultrasound, can signal impending RDCS.
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PMID:Experimental respiratory decompression sickness in sheep. 318 87

Reactive oxygen species have been proposed as pathophysiological factors responsible for the hypodynamic circulatory response to gram-negative endotoxin. To test this hypothesis, we examined the cardiorespiratory effects of mechanistically different oxygen free radical scavenging agents during Escherichia coli endotoxemia in beagle dogs. Pentobarbital-anesthetized dogs were instrumented for repeated sampling of cardiorespiratory, hematologic, and tissue blood flow (radiolabeled 15-micron microspheres) indexes. Four groups were studied: 1) time-matched control dogs (n = 6); 2) dogs receiving only endotoxin (1.5 mg/kg; n = 6); 3) dogs receiving endotoxin and combination therapy with allopurinol (150 mg/kg) plus superoxide dismutase (5 mg/kg) and catalase (5 mg/kg; n = 6); and 4) dogs receiving endotoxin and deferoxamine (30 mg/kg; n = 5). Measured variables in control dogs were constant during the 4-h study, whereas endotoxin-injected dogs consistently demonstrated the following: 1) maintained reductions in blood pressure (greater than 45%), left ventricular systolic pressure (greater than 43%), left ventricular maximum rate of pressure development (+/- dP/dtmax) (greater than 41%), cardiac index (greater than 33%), and blood flow in all sampled tissues except liver and skeletal muscle; 2) transient tachypnea, bradycardia, and arterial acidosis; and 3) persistent neutropenia and hemoconcentration. Neither of the free radical scavenging protocols significantly improved measured variables during endotoxemia (P greater than 0.05). This lack of efficacy suggests that superoxide anion, hydrogen peroxide, and hydroxyl radical may lack primary pathophysiological importance during the development of E. coli endotoxicosis in intact dogs.
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PMID:Evidence for lack of importance of oxygen free radicals in Escherichia coli endotoxemia in dogs. 328 94

Two controversial issues of neonatal transfusion practices, erythrocyte 'booster' transfusions and granulocyte transfusions, are critically reviewed, and current recommendations for transfusion practices are made. Infants should receive erythrocyte transfusions to treat congestive heart failure caused primarily by anemia. It is customary to maintain the hematocrit at greater than 40% in neonates with severe respiratory disease, although the efficacy of this practice has not been firmly established. Erythrocyte transfusions seem to be indicated for infants with anemia plus recurrent apnea, poor weight gain or the syndrome of tachycardia, tachypnea, dyspnea and poor feeding for which no other cause can be found. Granulocyte transfusions are likely to benefit seriously ill neonates exhibiting all three of the following: strong evidence of bacterial sepsis, neutropenia (compared to age-related normal values) and a diminished marrow neutrophil storage pool. Granulocyte transfusions for septic infants expressing only one or two of these features should be considered to be experimental therapy.
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PMID:Current issues in neonatal transfusions. 352 25

Acute lung injury was induced in 24 calves by intratracheal inoculation with Pasteurella haemolytica. Calves in groups 1 and 2 were neutrophil depleted, using hydroxyurea given IV. Group 1 calves (n = 7) were inoculated intratracheally with saline solution, and group 2 calves (n = 7) were inoculated with P haemolytica. Group 3 calves (n = 7) had normal numbers of neutrophils and were inoculated with P haemolytica. Group 4 calves (n = 3) were treated acutely with hydroxyurea IV, had normal numbers of neutrophils, and were inoculated with P haemolytica. After inoculation, calves with normal numbers of neutrophils (groups 3 and 4) became hypoxemic 2 hours after inoculation, and hypoxemia persisted until necropsy (6 hours after inoculation). These calves also developed tachypnea, bradycardia, neutropenia, and lymphopenia. Lung lesions consisted of necrosis of the alveolar walls, intra-alveolar hemorrhage, and a severe exudative and necrotizing bronchopneumonia, with accumulation of proteinaceous fluid in alveoli and lymphatics. In neutrophil-depleted calves (groups 1 and 2), blood gas values, heart and respiratory rates, and numbers of circulating leukocytes did not change after inoculation with saline solution or with P haemolytica. At necropsy, the lungs of neutrophil-depleted calves were grossly normal. Therefore, neutrophils were required for the acute lung injury induced by P haemolytica. The protective effect of neutrophil depletion was a specific effect of hydroxyurea because calves with high circulating concentrations of hydroxyurea and calves with normal numbers of neutrophils (group 4) developed lung injury.
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PMID:Importance of neutrophils in the pathogenesis of acute pneumonic pasteurellosis in calves. 407 35

Cattle with Pasteurella bronchopneumonia usually have a fever, abnormal respiratory sounds in the cranioventral lung fields, consolidation, pleuritis and abscesses. Lungworms primarily affect 4- to 6-month-old calves, which become febrile and dyspneic, with moist rales. Diagnosis is by fecal examination using the Baermann technic. Proliferative pneumonia usually affects stabled adults, which develop severe dyspnea and tachypnea. Diagnosis is by the history, clinical signs and lung biopsy. Acute bovine pulmonary emphysema is caused by ingestion of large amounts of L-tryptophan in lush pasture. Affected cattle have severe, acute dyspnea, an expiratory grunt and froth around the muzzle. Diagnosis is by the history and clinical signs. Bronchiolitis obliterans narrows the airways of older animals to cause dyspnea. A positive response to corticosteroids aids diagnosis. Anaphylaxis occurs in cattle of all types and ages and is precipitated by various antigens in a type-I hypersensitivity reaction. Use of atropine aids diagnosis. Allergic or hypersensitivity pneumonia is caused by an allergy to insecticides, dead ascarid larvae or the mold, Micropolyspora faeni. Diagnosis is by a history of insect fogger use, finding M faeni in the forage, and typical histologic lesions in lung samples. Cattle with caudal vena caval thrombosis have dyspnea, a fever, froth around the muzzle, an expiratory groan and hypergammaglobulinemia. Malignant catarrhal fever is diagnosed by a history of previous exposure to sheep and finding swollen lymph nodes, fever, neutropenia and arteritis.
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PMID:Diagnosis of causes of respiratory diseases in cattle. 623 84

Phorbol myristate acetate is a potent aggregator of platelets. It was found that it was similarly potent in aggregating neutrophils and in producing striking thrombocytopenia and neutropenia when infused intravenously into rabbits. Aggregation and cytopenia were further correlated in that both types of responses developed abruptly and persisted for more than 90 minutes. Animals infused with 40 microgram/kg of the phorbol ester exhibited moderately severe respiratory distress. Their respiratory rate doubled shortly after the infusion, and this tachypnea persisted for more than 2 hours. At necroscopic examination, the lungs of these rabbits contained two outstanding abnormalities: numerous foci of alveolar hemorrhage and extensive intravascular accumulations of platelets and neutrophils. Thus, these animals had evidence of increased permeability and potential occlusion of the pulmonary microvasculature. Increased permeability, occlusion of lung blood vessels, or the occurrence of both processes was further indicated in studies on animals pre-infused with the plasma protein marker 125I-albumin: animals infused with the phorbol ester had a significantly increased amount of this label in their lungs in spite of thorough postmortem perfusion of their pulmonary vasculature with saline and fixative. We conclude that phorbol myristate acetate has actions in vivo that resemble those of a variety of other platelet (eg, arachidonic acid) and neutrophil (eg, chemotactic factors) aggregating agents that cause cytopenia and lung dysfunction. However, compared with these other agents, the phorbol ester produces respiratory distress of intermediate severity and greater duration. The drug, therefore, induces a syndrome that more closely resembles that seen in a variety of clinical and experimental conditions that associate shocklike states with cytopenia and lung dysfunction. It may serve as a useful tool in the study of the pathophysiology of these states as well as in those produced by other aggregating agents.
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PMID:Phorbol myristate acetate: in vivo effects upon neutrophils, platelets, and lung. 744 4

We reviewed the experience over 20 years with primary Candida pneumonia among fatal cancer cases at our hospital. Unequivocal evidence of primary Candida pneumonia has been reported in only 55 cases. We report here 31 such cases. Unlike patients with disseminated candidiasis, and contrary to previous studies concentrating on cancer patients, only 9 of our 31 patients had severe neutropenia. In this report, the lack of organ involvement other than the lungs at complete autopsy examination, the exclusion of patients with candidemia, the very high percentage of intrabronchial and intra-alveolar fungal involvement without vascular invasion, and the concomitant presence of candidal esophagitis in some patients suggest that the mechanism of entry of the infectious particles may have been aspiration of oropharyngeal contents. The major clinical manifestations of primary Candida pneumonia are fever and tachypnea. Radiologically, nonspecific patchy infiltrates can be seen. Histopathologically, there is prevalence of bronchopneumonia, hemorrhage, and necrosis. The only accepted criterion for the definitive diagnosis of Candida pneumonia is histologic demonstration of the fungus in lung tissue. In contrast to previous reports, we demonstrated that primary Candida pneumonia can be life-threatening in patients with cancer since it directly contributed to the death of 84% of the patients in the present series. Very little data are available on the therapy and outcome of patients with Candida pneumonia. However, primary Candida pneumonia in the compromised host should be treated as a life-threatening infection with systemic antifungal therapy.
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PMID:Primary Candida pneumonia. Experience at a large cancer center and review of the literature. 850 66

Cyclophosphamide-induced neutropenia exacerbates septic shock and multiple organ injury in conscious rats during Escherichia coli (EC) bacteremia despite antibiotics and fluid administration. We hypothesized that such shock and inflammatory organ injury would be mitigated by rBPI23's microbicidal activity and/or binding of EC endotoxins. Four days after 100 mg cyclophosphamide/kg, catheterized rats with < 300 PMNs/microL were pretreated with rBPI23 or the irrelevant 22 kDa protein thaumatin [3.3-6.6 mg/kg, i.v. in 0.9% NaCl (NS)] 5 min before graded i.v. infection with 5 x 10(9) or 1 x 10(10) cfu of EC serotype 055:B5 ending at t = 0. Posttreatment with each protein continued (3.3-6.6 mg/kg in 1 mL NS/h) through 8 h, in addition to penicillin plus amikacin sulfate at t = 1.5 and 8 h. Arterial samples were obtained before pretreatment and at t = 1.5, 4.5, 8, and 24 h when animals were necropsied. One of eight thaumatin + 5 x 10(9) EC rats and none of six thaumatin + 10(10) EC rats survived 24 h. In contrast, rBPI23 significantly reduced mortality after either inoculum, improved bacterial clearance, and led to renormalization of early EC-induced hypotension, hypothermia, tachypnea, hyperoxemia, and hypocarbia. Compared with thaumatin, however, rBPI23 did not reduce circulating endotoxin or bioactive and antigenic tumor necrosis factor-alpha. Sepsis-induced severe neutropenia (< 50 PMNs/microL) evident in all EC rats by t = 1.5 h was reversed with rBPI23 by t = 8 h, but thrombocytopenia (< 5 x 10(4) platelets/microL) evident in all groups by t = 4.5 h was not altered.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The recombinant 23-kDa N-terminal fragment of bactericidal/permeability-increasing protein (rBPI23) decreases Escherichia coli-induced mortality and organ injury during immunosuppression-related neutropenia. 856 60

A total of 207 thoracic radiographs obtained from 128 foals were evaluated to assess the impact of pulmonary radiographic pattern, distribution, and severity of pulmonary changes on short-term survival of neonatal foals. The association between selected clinical variables and the radiographic manifestation of neonatal respiratory disease was also investigated. The evaluation of interstitial and alveolar-interstitial radiographic patterns within the caudodorsal, caudoventral, and cranioventral lung regions proved to be highly reliable between viewers in the study. A diagnosis of systemic inflammatory response syndrome was related to increased pulmonary infiltrates within the caudodorsal lung region. Dyspneic foals had more extensive pulmonary infiltrates within the cranioventral lung, advanced respiratory disease, and lower survival rates. A fibrinogen concentration >400 mg/dL was associated with increased cranioventral radiographic abnormalities. In addition, tachypnea most consistently related to diffuse (caudodorsal, caudoventral, and cranioventral) pulmonary changes. Neutropenia, milk reflux from the nares, upper airway pathology, abnormal respiratory sounds, failure of transfer of passive immunity (IgG concentration <400 mg/dL), immaturity, or fever, however, were not related to radiographic pattern, distribution, or severity of radiographic changes. Sixty-five percent of foals with radiographic pulmonary disease were discharged alive from our referral hospital. Concurrent caudodorsal and caudoventral radiographic disease was most frequently observed in this foal population. Increased caudodorsal radiographic scores retained statistical significance as a prognostic indicator for nonsurvival in a multiple stepwise logistic regression analysis.
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PMID:Clinical and prognostic significance of radiographic pattern, distribution, and severity of thoracic radiographic changes in neonatal foals. 1465 26


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