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To determine if ammonium ion plays a role in the lactate and ventilatory thresholds of incremental exercise, we investigated the effects on blood lactate and ventilation of NH(4+)-buffering by monosodium glutamate. Six normal volunteers underwent intravenous loading with MSG, 9 g, in a randomized, double-blind, saline placebo controlled crossover study. Four of the six subjects had a greater than 10 percent fall in peak (NH4+) following MSG (37 +/- 2.0 vs 25 +/- 4.3 micrograms/dl p = 0.003, PLB vs MSG). When MSG blunted the rise in venous (NH4+) during exercise, uncoupling of the LT and VT was observed. Specifically, with suppression of peak exercise (NH4+) by MSG, the LT was delayed (r = -0.84, p = 0.03), the VT was earlier (r = 0.86, p = 0.02), and the VO2 difference between the LT and VT widened (r = -0.90, p = 0.02). We conclude that NH4+ plays a role in determining the LT and VT of incremental exercise and that the VT may not be exclusively dependent on blood lactate.

Three patients with severe progressive interstitial lung disease refractory to steroid therapy were treated with immunosuppressive drugs. Biopsy material of one showed mainly fibrosis, while that of the second showed interstitial pneumonitis as well; both patients received azathioprine. Cyclophosphamide was employed in the third patient with systemic vasculitis and massive hemoptysis. All patients had reduced lung volumes and abnormal gas exchange, which continued to worsen on high doses of steroids. In patients 1 and 2, there was long-term stabilization of lung function, while pulmonary physiologic abnormalities in the patient with vasculitis reverted to normal on five months of cyclophosphamide. Although the etiology of most forms of interstitial lung disease is unknown, several reports suggest at least a partial immunologic basis. Abatement in progression of disease in this small series would suggest that a trial of immunosuppressive drugs be considered in interstitial lung disease when steroid therapy fails.

Mixed pneumoconiosis is pulmonary disease due to two or more inhaled mineral irritants. Chronic disease due to beryllium has not been a component of any described mixed pneumoconiosis. A man with occupational exposure to a combination of dusts developed severe pulmonary disease. Silicosis, talcosis, asbestosis, and berylliosis were all documented by an open biopsy of the lung. The varieties of mixed pneumoconiosis are summarized.

We carried out a medical and environmental survey to evaluate respiratory disease at two tungsten carbide (TC) production plants. The study population of 290 subjects (19.2 percent of the total work force) was chosen to focus on those with the greatest potential exposures to cobalt, a binding agent which is probably the cause of interstitial fibrosis and airways disease in TC workers. We found peak air concentrations of cobalt exceeding 500 micrograms/m3 during many major steps in TC production. Nine subjects at plant A and two at plant B had interstitial infiltrates. Two of these nine from plant A had restriction (total lung capacity less than 80 percent of predicted). A lung biopsy specimen in one showed interstitial fibrosis. Two nonsmokers at plant A and one nonsmoker at plant B had obstructive defects. These results suggest that interstitial and obstructive lung disease occur in TC workers in association with elevated peak air concentrations of cobalt.

Derangement of pulmonary function following myocardial infarction is related to the severity of hemodynamic dysfunction. Abnormalities of pulmonary function appear even in patients without clinical or radiologic evidence of congestive failure. There is a reduction in vital capacity and rates of air flow. There is evidence for dysfunction of "small airways" and diminished ventilation to dependent parts of the lung. Total lung capacity may be normal or reduced, and residual volume may be increased slightly in uncomplicated myocardial infarction. Residual volume falls with more pronounced pulmonary congestion and edema. Distribution of pulmonary perfusion is altered after myocardial infarction, with a shift of perfusion away from the dependent parts of the lung (bases) towards the apices. Pulmonary gas exchange is impaired, with hypoxemia (due to both ventilation-perfusion inequality and increased shunting); and the diffusing capacity for carbon monoxide is diminished. Dead space is increased. The basic pathophysiologic mechanism responsible for abnormalities of pulmonary function is increased pulmonary water, which may be very minimal with uncomplicated myocardial infarction and stay primarily in the pulmonary interstitial space, but becomes progressively more severe with eventual alveolar flooding and marked impairment of pulmonary function.

Although hyperventilation is a well-known compensatory mechanism in metabolic acidosis, compensatory hypoventilation has been inconsistent and controversial in metabolic alkalosis. Six healthy subjects were studied under baseline conditions and during steady-state metabolic acidosis (seven episodes) and alkalosis (14 episodes). Minute ventilation (VE) fell in metabolic alkalosis and rose in metabolic acidosis. These changes in ventilation were entirely due to reduction and elevation of tidal volume (VT) respectively, while respiratory frequency (f) remained unchanged. Alveolar ventilation fell during metabolic alkalosis and resulted in elevation of arterial PCO2 in all subjects. The ventilatory response to arterial PCO2 in all subjects. The ventilatory response to CO2 breathing was also diminished. There was a linear relationship between PaCO2 and plasma [HCO-3] in metabolic acidosis and alkalosis which was defined as PaCO2 (mm Hg = 0.7 [HCO-a] + 20 (+/- SEM), r = 0.95. Although arterial PO2 and plasma [K+] fell during metabolic alkalosis, minute ventilation did not change upon breathing oxygen and there was no correlation between changes in plasma [K+] and plasma H+ regulation.