Disease relevance of Vital Capacity

• Not the presence of cough, dyspnea, or constitutional symptoms or pulmonary function as measured by forced vital capacity and carbon monoxide diffusing capacity served to predict a positive transbronchial biopsy finding any more accurately than did the roentgenographic staging of the disease itself [1].
• In subjects free of overt coronary heart disease, the risk of sudden death varies widely in relation to risk factors, including systolic pressure, serum cholesterol, vital capacity, cigarette smoking, relative weight, heart rate and electrocardiographic abnormality [2].
• Three of the patients with cryptogenic fibrosing alveolitis and all five patients with lymphocytic infiltration responded with a reduction in dyspnoea or an increase in vital capacity, or both; cyclosporin A appeared to be effective, or at least to have a corticosteroid potentiating effect [3].
• Despite these high plasma concentrations of the peptide and the substantial tachycardia and increase in skin blood flow, there was no change in partial expiratory flow at 40% of vital capacity (Vp40) or in the airway response to inhaled histamine (geometric PD40 9.37 and 9.73 mumol during saline and peptide histidine valine infusion respectively) [4].
• When systolic blood pressure, serum cholesterol, cigarette smoking, and vital capacity were also taken into account, the ratio chest circumference/biacromial diameter remained significantly associated with coronary heart disease mortality [5].

Psychiatry related information on Vital Capacity

• To study this, PCR was measured in ten children and adolescents with MMC and ACM with normal alveolar ventilation during wakefulness, and in ten sex- and age-matched controls by measuring the ventilatory responses induced by 100% O2 breathing, five tidal breaths of 100% N2, and vital capacity breaths of 15% CO2 in O2 [6].

High impact information on Vital Capacity

• When the subjects were 34 or 35 years old, their forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) were measured before and after they inhaled albuterol [7].
• Measurement of forced vital capacity and forced expiratory volume in one second showed that there was no deterioration in the condition of patients in whom the dosage of prednisone was reduced [8].
• The expiratory and inspiratory pressures, forced vital capacity, and ability to cough, speak, and swallow also improved after edrophonium [9].
• The point of identical flow was increased by methacholine to 43.5 per cent of vital capacity in the patients, as compared to 6 per cent in normal controls (P less than 0.001), and the alveolar plateau was 4.8 deltaN2 per liter, as compared to 1.4 in normal controls (P less than 0.01) [10].
• Within one week of the initiation of daily high-dose steroid therapy, the patient's symptoms dramatically improved; chest roentgenogram and forced vital capacity (60%) improved at a slower rate [11].

Chemical compound and disease context of Vital Capacity

• In addition, the interaction between weight change and age was significant for fasting glucose, uric acid, and forced vital capacity, indicating that the effect of weight gain on uric acid and forced vital capacity was greater in younger men whereas the effect of weight gain on fasting glucose was greater in older men [12].
• Seventy-six unpremedicated ASA physical status I or II patients were anesthetized with either a single vital capacity breath of sevoflurane 8% or i.v. propofol 3 mg/kg, which produced equally rapid loss of consciousness (40.5 +/- 13.9 vs 37.7 +/- 9.9 s; P > 0.05) [13].
• The earliest manifestations of pulmonary normobaric O2 toxicity in normal adults include diminished vital capacity and the onset of respiratory symptoms, but early O2 toxicity does not produce altered responsiveness to inhaled methacholine [14].
• Bradykinin (1 mug/kg body weight) was rapidly injected intravenously and respiratory system resistance (Rrs), closing volume (CV), forced vital capacity (FVC), expiratory volume in the first second (FEV1) maximal midexpiratory flow (MMF), and peak flow (PF) were measured [15].
• No significant changes occurred in forced expiratory volume in one second, forced vital capacity, oxygen saturation, body weight, sputum volume, culture and rheology, serum urea, and electrolytes, white cell count and erythrocyte sedimentation rate during either treatment period [16].

Biological context of Vital Capacity

• All patients with ILD underwent testing for total lung capacity (TLC), forced vital capacity (FVC), and diffusing capacity for carbon monoxide [17].
• METHOD: Sixty-two subjects who had completed a study examining fearful responses to a single vital capacity inhalation of 35% CO2 were reevaluated 1 year following the challenge test [18].
• RESULTS: Peak oxygen uptake (Vo(2)) (p < 0.001), peak oxygen pulse (p = 0.0027), and vital capacity (p = 0.0086) improved after ASD closure, although peak heart rate did not [19].
• Six months after LVRS, however, vital capacity, percentage vital capacity showed no significant change, and forced expiratory volume in 1 second, percentage of forced expiratory volume in 1 second, diffusing capacity for carbon monoxide, and maximal voluntary ventilation showed marked improvement [20].
• RESULTS: Cetirizine with or without albuterol significantly increased FEV1, peak expiratory flow rate, and forced expiratory flow rate between 25% and 75% of vital capacity relative to baseline and placebo but did not have a significant effect on forced vital capacity [21].

Anatomical context of Vital Capacity

• After 4 years, the prednisone-treated group had significant advantages over the placebo group for height, weight, vital capacity, forced expiratory volume in 1 s, peak flow rate, erythrocyte sedimentation rate, and serum IgG [22].
• Ortho-tyrosine showed an inverse relationship with forced vital capacity (p = .01) but was not related to inflammation of the upper airways as assessed by cell counts of polymorphonuclear neutrophils [23].
• A repeat study of the patients when their radiograph had cleared maximally showed that the levels of lavage lymphocytes, SACE, and gallium tended to fall, but frequently remained raised even in the presence of a normal radiograph or vital capacity or both [24].
• TLCO, carbon monoxide transfer coefficient (KCO), FEV1, and vital capacity (VC) values were lower 6 and 12 months after bone marrow transplant than initially [25].
• There was a strong correlation between the levels of eosinophil proteins and variables of pulmonary function, like between ECP and forced vital capacity (r = -0.764, P < 0.0001) [26].

Associations of Vital Capacity with chemical compounds

• Forced expiratory volume at 1 s (FEV1) and forced vital capacity (FVC) did not change significantly following sublingual nitroglycerin, but both FEV1 and FVC improved significantly after epinephrine administration [27].
• Expired vital capacity was also greater on the summit in the acetazolamide group (6.9 +/- 0.4 L compared with 5.8 +/- 0.4 L) [28].
• The improvements with prednisolone in general wellbeing, 12 min walk distance, peak expiratory flow, FEV1, and relaxed vital capacity were significantly greater than those with placebo [29].
• Diary-card and clinic morning peak expiratory flows improved significantly in the fluticasone propionate group (p<0.001, p=0.048, respectively), as did clinic FEV1 (p<0.001), forced vital capacity (p<0.001), and mid-expiratory flow (p=0.01) [30].
• Patients with the severest pulmonary calcification had abnormalities of vital capacity, carbon monoxide diffusion, and Po2 [31].

Gene context of Vital Capacity

• BACKGROUND: Conventional measures of the severity of alveolar proteinosis (AP) include alveolar-arterial oxygen gradient ([A - a]DO(2)), vital capacity (VC), and carbon monoxide transfer factor (TLCO), but alternative serological measures have been sought [32].
• Eotaxin level in EBC had a significant negative correlation with the FEV(1)/forced vital capacity ratio (r=-0.43, P=0.03) in steroid-naïve asthmatics [33].
• An elevated serum VEGF level was correlated with the frequency of lung fibrosis and reduced vital capacity in the patients with SSc [34].
• In addition, serum IL-6 was detected more frequently in patients with pulmonary fibrosis, and these values were inversely correlated with the percentage of vital capacity of individual patients [35].
• The circulating TIMP-1 concentration was significantly higher in stable COPD patients than in control and asthmatic subjects, and was significantly negatively correlated with forced expiratory volume in one second/forced vital capacity in COPD patients [36].

Analytical, diagnostic and therapeutic context of Vital Capacity

• MEASUREMENTS: Esophageal manometry, dual-probe (distal and proximal) esophageal 24-hour pH measurements, and pulmonary function studies (forced vital capacity, forced expiratory volume at 1 second, total lung capacity, and single-breath carbon monoxide diffusing capacity [DLco]) [37].
• Following chemotherapy, there was a significant decline in median forced vital capacity (FVC) and diffusing capacity of carbon monoxide (DLCO) [38].
• DESIGN: Total lung capacity (TLC), the ratio of forced expiratory volume in one second to vital capacity (FEV1/VC), the carbon monoxide transfer factor (TLCO) and the alveolar-arterial oxygen gradient [delta (A-a)O2] were determined in this retrospective study [39].
• Gastrostomy insertion in ALS patients with low vital capacity: respiratory support and survival [40].
• In a double blind, random, cross-over design, 10 patients and seven controls inhaled one vital capacity of 35% CO2-65% O2 during their early-follicular and midluteal phases [41].

References