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Biomedical subjects

M A Matthay

Publications and source records attributed to M A Matthay.

215 records · Page 12Linked to original sources
PubMed1984

Elevated concentrations of leukotriene D4 in pulmonary edema fluid of patients with the adult respiratory distress syndrome.

The possible contribution of metabolites of arachidonic acid to the increased permeability of the alveolar-capillary barrier in the adult respiratory distress syndrome was examined by quantifying the pulmonary edema fluid concentrations of lipoxygenase and cyclooxygenase products. The concentration of leukotriene D4 in pulmonary edema fluid of 10 patients with the adult respiratory distress syndrome (18.5 +/- 6.8 pmol/ml; mean +/- SD), assessed by specific radioimmunoassay after isolation of the mediator, was significantly higher (P less than 0.001) than that of five patients with cardiogenic pulmonary edema (4.4 +/- 1.1 pmol/ml). The concentrations of leukotrienes B4 and C4, prostaglandin E2, and thromboxane B2 in edema fluid were not significantly different in the adult respiratory distress syndrome patients than in the other subjects with pulmonary edema. The edema fluid concentration of leukotriene D4 correlated with the ratio of edema fluid to plasma concentrations of albumin (r = 0.64). Leukotriene D4 thus may contribute to the permeability defect which allows an accumulation of protein-rich alveolar fluid in the adult respiratory distress syndrome.

Adolescent↗
PubMed1984

Biologically active products of complement and acute lung injury in patients with the sepsis syndrome.

To determine if biologically active products of complement appear during sepsis and to establish the relationship of these components to the respiratory and hemodynamic complications of sepsis, we measured C5a des Arg and C3a des Arg (radioimmunoassay), neutrophil chemotaxis, and neutrophil-aggregating activity in plasma obtained from 40 patients at the time sepsis was suspected clinically. Levels of C3a des Arg and C5a des Arg were elevated in 35 and 38 patients, respectively, and in all 25 with positive blood cultures. Highest C5a des Arg levels occurred in patients with hypotension (less than 90 mmHg) and/or acidemia. The C5a des Arg concentrations were significantly higher in patients with than in those without neutrophil-chemotactic activity. Neutrophil-aggregating activity was less sensitive an index of complement activation, as it was positive in only 8 patients and correlated poorly with C5a des Arg and C3a des Arg values. Using a composite scoring system to quantify sepsis-related pulmonary abnormalities, we found that neither biologic nor immunologic assays of complement activation products correlated with the initial severity nor predicted the development or worsening of associated acute lung injury.

Bacterial Infections↗
PubMed1984

Neurogenic pulmonary edema.

A variety of central nervous system (CNS) insults may be complicated by the acute development of pulmonary edema. This occurrence has been termed neurogenic pulmonary edema (NPE), and experimental models have clearly shown that CNS insults may cause pulmonary edema. Unfortunately, the pathophysiologic aspects of this response are not clearly understood. Basing an approach to the development of pulmonary edema on Starling's equation leads to the conclusion that NPE is caused by changes in pulmonary endothelial permeability and/or microvascular pressures. It was previously suggested (the "blast theory") that CNS insults caused acute systemic arterial and pulmonary venous spasm and increased venous return, which would result in a severe pulmonary vascular hydrostatic insult and a secondary permeability defect. Although such hydrostatic derangements may explain certain cases of NPE, recent clinical and experimental studies have indicated that CNS disorders may cause a permeability defect without a vascular insult. The mediating factor for a permeability defect is not clear. The implications of these findings are that NPE may be caused by either permeability abnormalities or hydrostatic insults, may present clinically in a variety of ways, and may require different approaches to treatment. Our understanding of the CNS sites that might mediate NPE is not sophisticated enough, at present, to define the neural mechanisms involved in the pathogenesis of NPE.

Animals↗
PubMed1984

Cardiovascular-pulmonary monitoring in the intensive care unit (Part 2).

Proliferation of technology in the ICU likely will continue at a rapid pace. This presents a strong challenge to the clinician's task of "above all, do not harm." While invasive techniques carry obvious direct risks, both invasive and noninvasive monitoring present a more subtle threat. Pitfalls in the acquisition and interpretation of data must be recognized before appropriate therapeutic decisions can be made. Advanced monitoring devices and techniques must supplement and not supplant clinical assessment.

Arrhythmias, Cardiac↗
PubMed1983

Overperfusion, hypoxia, and increased pressure cause only hydrostatic pulmonary edema in anesthetized sheep.

Overperfusion (high pressure and flow through a restricted microvascular bed) has been suggested as the mechanism for both microembolic and high altitude pulmonary edema. In eighteen anesthetized, ventilated sheep, we measured pulmonary hemodynamics, lung lymph flow, and lymph:plasma protein concentration ratio. After a 2-hour stable baseline, we resected 65% of lung mass (right lung and left upper lobe) and gave whole blood transfusions to maintain cardiac output. During overperfusion of the left lower lobe, lymph flow increased moderately (5.8 +/- 2.3 to 7.7 +/- 3.8 ml/hr) and lymph:plasma protein concentration decreased (0.73 +/- 0.08 to 0.64 +/- 0.08). After a 2-hour stable period, we decreased inspired oxygen in 10 sheep (Pao2 = 40 +/- 3 mm Hg). With added alveolar hypoxia, pulmonary artery pressure increased modestly, but lymph flow and the lymph:plasma protein concentration ratio did not change. In eight sheep (four hypoxic, four normoxic), we raised left atrial pressure approximately 12 cm H2O for 2 hours. Lymph flow rose (10.8 +/- 3.8 ml/h) and lymph:plasma protein concentration decreased further (0.52 +/- 0.07). At each step, lymph:plasma protein concentration decreased, as predicted for the calculated rise in microvascular pressure. There was no evidence that overperfusion, with or without alveolar hypoxia, increased lung endothelial barrier protein permeability.

Animals↗
PubMed1982

Differential liquid and protein clearance from the alveoli of anesthetized sheep.

We determined the clearance rates of 50 ml of isosmotic fluids from the lungs of anesthetized, ventilated sheep with lung lymph fistulas. The removal of the liquid volume followed a monoexponential process over 4 h for both Ringer lactate [half time (t 1/2) = 3 h] and autologous serum (t 1/2 = 6 h). Lymph flow did not increase with Ringer lactate, indicating that the alveolar fluid was cleared via the circulation. With serum, however, lymph flow increased 40%. In both groups the lymph-to-plasma protein concentration ratio fell slightly. Using protein tracers in the alveolar instillate, we found that less than 2% of the protein entered the lymph and plasma. Almost all of the protein remained in the air spaces and was concentrated in proportion to the amount of liquid volume that was cleared. Clearance of liquid volume from alveoli to interstitium could be due to subatmospheric interstitial fluid pressure or to active metabolic processes that cause small molecules to leave the alveolar fluid, or both. The results of the serum experiments tend to favor a metabolic process, but passive mechanisms are possible. The difference in lymph flow response between the two fluids must be due to the protein in the alveolar fluid. We believe Ringer lactate dilutes the alveolar wall interstitial protein concentration thereby decreasing local filtration, whereas serum concentrates alveolar wall interstitial fluids proteins thereby increasing local filtration.

Anesthesia↗
PubMed1981

Anatomic variations of efferent duct from caudal mediastinal lymph node in sheep.

Collection of lymph from the efferent duct of the caudal mediastinal node in sheep is accepted as a reliable method for following lung microvascular fluid and protein filtration. There are significant variations in the efferent duct anatomy, which can complicate the cannulation procedure and, therefore, the success of the preparations. We analyzed the major variations in the efferent duct in 75 consecutive sheep. The majority (59%) had a single efferent duct varying in length, course, and origin fom the caudal mediastinal node; 41% had multiple ducts, often with confluences or bifurcations, making successful cannulation more difficult. It is important to recognize the potential variations in the efferent duct to facilitate useful cannulation.

Animals↗
PubMed1976

Grand mal seizure induced by oral theophylline.

A grand mal convulsion occurred in a patient with decompensated cor pulmonale. Although only modest doses of oral theophylline were being administered at the time of the convulsion the serum theophylline level was markedly raised and the theophylline clearance was very low. After treatment for cor pulmonale theophylline clearance improved; however, with the subsequent onset of fever and pneumonia the clearance decreased again, illustrating the potential lability of theophylline clearance.

Administration, Oral↗
PubMed1976

Hypertrophic osteoarthropathy in adults with cystic fibrosis.

Three adult patients with cystic fibrosis presented with arthralgia, and investigation for the usual causes of arthritis proved negative. Radiographs of long bones revealed periostitis and new bone fromation characteristic of hypertrophic osteoarthropathy. Symptomatic improvement occurred after analgesic and anti-inflammatory therapy. In patients with cystic fibrosis and bone or joint pain, the diagnosis of hypertrophic osteoarthropathy should be considered and long bone radiographs obtained.

Adult↗
PubMedDate not supplied

Beta1-adrenoceptor stimulation by high-dose terbutaline downregulates terbutaline-stimulated alveolar fluid clearance in ex vivo rat lung.

Because high-dose terbutaline and isoproterenol (10(-3) M), beta2-adrenergic agonists, failed to increase alveolar fluid clearance, the mechanisms responsible for this effect were examined in ex vivo rat lungs. An isosmolar 5% albumin solution with Evans blue dye was instilled into the distal airspaces in isolated rat lungs that were then inflated with 100% oxygen at an airway pressure of 8 cm H2O in a 37 degrees C incubator. Alveolar fluid clearance was measured by the progressive increase in dye concentrations over 1 hour. The results indicated that: (1) although 10(-5) M terbutaline or isoproterenol increased alveolar fluid clearance, 10(-3) M terbutaline or isoproterenol did not; (2) both concentrations of terbutaline (10(-5), 10(-3) M) increased intracellular adenosine 3',5'-cyclic monophosphate in cultured type II alveolar epithelial cells; (3) instillation of atenolol, a selective beta1-adrenergic antagonist, in the presence of either 10(-3) M terbutaline or isoproterenol was associated with an increase in alveolar fluid clearance. These results suggested that beta1-adrenoceptor stimulation prevented the normal response to a beta2-adrenergic agonist. To further test this hypothesis, a selective beta1-adrenergic agonist, denopamine, was administered; these results showed that (4) 10(-3) M denopamine, a selective beta1-adrenergic agonist, inhibited the increase in alveolar fluid clearance in the presence of 10(-5) M terbutaline; (5) hypoxia for 2 hours did not alter the effects of terbutaline on alveolar fluid clearance. The mechanism for the inability of the alveolar epithelium to respond to high-dose terbutaline or isoproterenol with the normal upregulation of alveolar fluid clearance in ex vivo rats lungs appears to be mediated by beta1-adrenoceptor stimulation that subsequently suppresses the beta2-adrenergic response.

Adrenergic beta-Agonists↗
PubMedDate not supplied

The adult respiratory distress syndrome.

The adult respiratory distress syndrome (ARDS) represents a common denominator of acute lung injury leading to alveolar flooding, decreased lung compliance, and altered gas transport. In the absence of specific etiology and therapy, the management of ARDS remains largely supportive. Ubiquitous use of intermittent positive-pressure ventilation with positive end-expiratory pressure (PEEP) improves arterial oxygenation but with some risk of pulmonary barotrauma and decreased cardiac output. The recent understanding of lung inflation as a modulator of right heart afterload and the effect of the right ventricle on global cardiac performance continues to redefine optimal patterns of ventilatory and hemodynamic intervention in ARDS.

Capillary Permeability↗
PubMedDate not supplied

Alveolar epithelial fluid transport: basic mechanisms and clinical relevance.

New evidence indicates that alveolar fluid clearance is driven by active sodium transport across the alveolar epithelium. Several in vivo as well as some in vitro studies indicate that vectorial sodium transport drives fluid clearance across the alveolar epithelium. This transport process can be upregulated by both catecholamine-dependent and catecholamine-independent mechanisms. Water transport appears to move across the alveolar epithelium primarily via transcellular water channels, recently termed aquaporins. Under some conditions, net alveolar fluid clearance continues even in the presence of acute lung injury. It is now possible to study the rate and mechanisms of alveolar fluid clearance in patients with either hydrostatic or increased permeability pulmonary edema. In addition, it may be possible to increase the rate of alveolar fluid clearance and hence the resolution of pulmonary edema in some patients, using aerosolized beta-adrenergic agonist therapy.

Animals↗