Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0034069 (pulmonary fibrosis)
 7,050 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study the effects of coronary artery bypass surgery on ventricular function were evaluated at rest by quantitative analysis of segmental wall motion on cineventriculography, and during maximal treadmill exercise by measurement of serial cardiac outputs (Fick method) with the use of indwelling pulmonary artery and radial artery catheters. The patient had single vessel coronary disease and exertional angina. Following placement of a bypass graft to the proximally occluded left anterior descenting coronary artery, and despite the presence of arterial hypoxemia secondary to interstitial pulmonary fibrosis, a striking increase in maximal cardiac output occurred, mediated by a rise in both maximal heart rate and stroke volume. In this patient, resting ventricular volumes and ejection fraction were normal both before and after surgery, but preoperative abnormalities in extent of segmental wall motion, identified quantitatively, were restored to normal after bypass grafting. These investigations indicate that bypass surgery can provide substantial physiologic benefits in addition to providing subjective relief of anginal symptoms.
 ...
PMID:Physiologic improvement following coronary artery bypass surgery. 30 22

Pulmonary precapillary hypertension present only during exercise is the first stage of corpulmonale. Examination of the reaction of central haemodynamics to exercise is the only way to detect it. In a model situation like unilateral pulmonary artery occlusion (UPAO) in healthy subjects, an increase in pulmonary artery pressure (Ppa) during exercise is a linear function of restriction of the pulmonary vascular bed and blood flow increase. Central haemodynamics during exercise in younger subjects after pneumonectomy (PNE) resemble the situation with UPAO provided the remaining lung is intact. In older patients after PNE the same rise of blood flow is associated with a considerably greater rise of Ppa. PNE patients compared to healthy individuals increase their cardiac output during exercise more by increasing stroke volume. Patients with pulmonary fibrosis show a disproportionate rise in Ppa in relation to flow. This is due to reduced distensibility of the pulmonary system. Hypoxia also seems to be involved in pulmonary hypertension during exercise. Pulmonary wedge pressure rises at work but remains within the normal range, even in patients having marked hypoxaemia at rest and during exercise. In idiopathic intersitial pulmonary fibrosis (IIPF), pulmonary hypertension during exercise is greater than in other forms of pulmonary fibrosis. Inhalation of oxygen during exercise in patients IIPF leads to a reversal of hypoxaemia but the decrease of Ppa is small and due to a passive decrease of cardiac output. Finally right ventricular function in restrictive pneumopathies is discussed.
 ...
PMID:Central haemodynamics during exercise in patients with restrictive pulmonary disease. 88 Mar 98

A 58-year-old man experienced paradoxic air embolism with passage of air from the systemic venous to the systemic arterial circulation with subsequent stroke and death. No intracardiac shunt was present. Pulmonary fibrosis concomitant with severe pulmonary arterial hypertension appears to have been responsible for the air traversing the pulmonary capillary bed. This unusual outcome of a complicated central venous catheterization must be borne in mind and guarded against in similar patients.
 ...
PMID:Paradoxic air embolism in the absence of an intracardiac defect. 199 38

A total of 636 episodes of peritonitis occurred in 440 patients who entered our continuous ambulatory peritoneal dialysis (CAPD) program from September 1977 to February 1988. Sixteen patients (8 male and 8 female, aged 37-77 years) died during an episode of peritonitis (fatality rate 2.5%). They had been on CAPD for 3 to 105 (average 39) months. Six of them were diabetics. The peritonitis rate among these 16 patients were 1 episode per 12 patient months, while the corresponding figure for the whole (440) CAPD population was 14 patient months. Risk factors present in the 16 patients were: cardiovascular disease (12), cerebrovascular accident (2) peripheral artery disease (1) and pulmonary fibrosis (1). Fever and leukocytosis were present on admission in 11 patients, while total serum proteins and albumin were significantly lower (p less than 0.001) than the corresponding values before peritonitis (56 +/- 8 vs. 65 +/- 5). Staph. aureus was isolated in 8 patients (50%), multiple organisms in 6, Pseudomonas and Candida albicans in 1 each. An abdominal abscess was found in 4 (25%) patients. The peritoneal catheter was removed between the 5th and 10th day in 6 and after the 10th day in 7 patients. Peritonitis with sepsis was the cause of death in 13 patients. Contributing factors were cardiovascular accident in 9, uremic coma in 2, extensive GI bleeding in 2, GI perforation in 2, intestinal infarction in 1, and pneumonia in 2 patients. We conclude that the risk of peritonitis-related death in CAPD patients is increased with Staph. aureus or multibacterial peritonitis. Contributing factors are concomitant cardiovascular disease and delayed (greater than 5 days) catheter removal.
 ...
PMID:Peritonitis-related deaths in continuous ambulatory peritoneal dialysis (CAPD) patients. 208 82

To detect whether pulmonary vascular responsiveness is a factor which can aggravate the pulmonary hypertension induced by irreversible pulmonary fibrosis, we examined the acute hemodynamic effects of low-flow oxygen and of nifedipine both at rest and during exercise in 8 patients with idiopathic pulmonary fibrosis (IPF). During exercise, the increments in pulmonary artery pressure, pulmonary vascular resistance (PVR), and right ventricular stroke work index relative to resting values were blunted by both treatments. During exercise, both systemic vascular resistance and PVR decreased more significantly after nifedipine than on oxygen (p less than 0.001). At exercise, nifedipine administration induced a greater increment in oxygen delivery (CaO2 X CI) than that produced by oxygen breathing (p less than 0.01). Our results in patients with IPF seem to confirm that active vasoconstriction of pulmonary vessels may contribute to the pulmonary hypertension during exercise. The evaluation of reversibility of pulmonary hypertension by nifedipine in IPF deserves further long-term studies.
 ...
PMID:Pulmonary vascular responsiveness at rest and during exercise in idiopathic pulmonary fibrosis: effects of oxygen and nifedipine. 374 13

The hemodynamic effects of nifedipine s.l. (20 mg) on pulmonary hypertension following chronic obstructive pulmonary disease (COPD) and advanced pulmonary fibrosis (PF) have been studied in 6 patients under stable conditions (3 patients with COPD and 3 patients with PF). Nifedipine induced a significant reduction in mean arterial pressure, right atrial pressure and systemic vascular resistances, with a significant increase in heart rate, right ventricular stroke work index and cardiac index. There was no significant change in mean pulmonary artery pressure, pulmonary arteriolar resistances and oxygen delivery. Individual analysis showed that in 2 patients with COPD there was a real direct vasodilating effect of nifedipine on the pulmonary circulation. In 2 patients with PF, the drug induced an increase in mean pulmonary artery pressure and pulmonary arteriolar resistances. In the last 2 patients, the effect of the drug on the pulmonary circulation was associated with an increase in driving pressure concomitantly with a rise in cardiac output, suggesting recruitment of the pulmonary vessels. In conclusion, nifedipine can dilate pulmonary vessels constricted by hypoxia in patients with COPD, but deleterious effects are observed in patients with pulmonary hypertension following PF.
 ...
PMID:[Variable hemodynamic response to nifedipine in pulmonary hypertension secondary to chronic obstructive bronchopathy and pulmonary fibrosis]. 407 Oct 9

Idiopathic hypereosinophilic syndrome (HES) is a poorly understood disorder characterized by a markedly elevated peripheral blood eosinophil count in the absence of known associated causes of hypereosinophilia. Idiopathic hypereosinophilic syndrome is associated with eosinophil-induced organ damage, including endomyocardial and pulmonary fibrosis, stroke, and gastrointestinal disease. Treatment of idiopathic HES is centered on the reduction of peripheral circulating eosinophils in an effort to diminish tissue infiltration and destruction. Multiple cytotoxic agents have been tried, with variable results. Prednisone and hydroxyurea have remained the therapies of choice in long term treatment of idiopathic HES. We report here the successful 2 year treatment of aggressive idiopathic HES, refractory to hydroxyurea and prednisone, with alpha-interferon.
 ...
PMID:alpha-Interferon treatment for idiopathic hypereosinophilic syndrome. 784 74

Various molecules expressed on the surface of platelets have been shown to mediate the protective or deleterious role of these cells in immuno-inflammatory mechanisms. Increasing evidence points to the involvement of the cell adhesion molecules, gpIIb-IIIa, P-selectin, CD31, LFA-1, and CD36 in the interaction between platelets and endothelial cells as well as other cell types. The possible role of these molecules in the ability of platelets to support endothelium and to protect against tumour necrosis factor mediated cytolysis or parasitic invasion are reviewed. The involvement of platelets as effectors of tissue damage in cerebral malaria, lipopolysaccharide induced pathology, and pulmonary fibrosis is also discussed. This has then been extended to include the intercellular mechanisms underpinning their pathogenic role in metastasis, transplant rejection, stroke, brain hypoxia, and related conditions. A better understanding of the complex regulation and hierarchical organisation of these various platelet adhesion molecules may prove useful in the development of new approaches to the treatment of such diseases.
 ...
PMID:Role of platelet adhesion in homeostasis and immunopathology. 935 Mar

Pirfenidone is an antifibrotic drug that we have shown attenuates the increase in collagen buildup in hamsters exposed to bleomycin, in turn reducing pulmonary function and blood gas decrements seen in this model of interstitial pulmonary fibrosis. The systemic effects of pirfenidone ingestion, however, are unknown. We examined the effect of diet-ingested pirfenidone on pulmonary function, systemic and pulmonary cardiovasculature and blood gas measurements, breathing pattern and lung hydroxyproline content in rats fed either a control diet or a diet containing 0.5% pirfenidone. Residual volume was higher and expiratory reserve volume lower in the pirfenidone group, with no change in functional residual capacity. Tidal volume was also lower in the pirfenidone group, with no change in the overall level of ventilation. There was a trend toward a reduced hydroxyproline content and an increased lung compliance in the pirfenidone group. There were no differences in systemic or pulmonary pressures, cardiac output, stroke volume, heart rate, pH or blood gases between the two groups. These data indicate that pirfenidone has few systemic side-effects but may have a mild effect on the basal level of lung collagen content with resulting clinical changes in some pulmonary function measurements and changes in breathing pattern.
 ...
PMID:Effect of diet-ingested pirfenidone on pulmonary function, cardiovasculature and blood gas measurements in rats. 1050 37

The members of the NOX/DUOX family of NADPH oxidases mediate such physiologic functions as host defense, cell signaling, and thyroid hormone biosynthesis through the generation of reactive oxygen species (ROS), including superoxide anion and hydrogen peroxide. Moreover, ROS are involved in a broad range of fundamental biochemical and cellular processes, and data accumulated in recent years indicate that the NOX enzymes comprise one of the most important biological sources of ROS. Given the high biochemical reactivity of ROS, it is not surprising that they have been implicated in a wide variety of pathologies and diseases. Prominent among the settings that feature ROS-mediated tissue injury are disorders associated with inflammation, aging, and progressive degenerative changes in cells and organ systems, and it appears that essentially no organ system is exempt. Among the disorders currently believed to be mediated at least in part by NOX-derived ROS are hypertension, aortic aneurysm, myocardial infarction (and other ischemia-reperfusion disorders), pulmonary fibrosis and hypertension, amyotropic lateral sclerosis, Alzheimer's disease, Parkinson's disease, ischemic stroke, diabetic nephropathy, and renal cell carcinoma. Several small-molecule and peptide inhibitors of the NOX enzymes have been useful in experimental studies, but issues of specificity, potency, and toxicity militate against any of the existing published compounds as candidates for drug development. Given the broad array of disease targets documented in recent work, the time is here for vigorous efforts to develop clinically useful inhibitors of the NOX enzymes. As most (though not all) NOX-related diseases appear to be mediated by a single member of the NOX family, agents with isoform specificity will be preferred, although broadly active NOX inhibitors may prove to be useful in some settings.
 ...
PMID:NOX enzymes as novel targets for drug development. 1850 46


1 2 Next >>