[Round table discussion of the treatment of respiratory insufficiency. Madrid, 22 October 1965].
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A case of functional upper airway obstruction is presented. The case is unusual because even though no identifiable organic cause could be found for dyspnea and stridor, the patient developed respiratory failure from respiratory muscle fatigue.
The cortical collecting duct (CCD) mediates net secretion or reabsorption of protons according to systemic acid/base status. Using indirect immunofluorescence, we examined the localization and abundance of the vacuolar H(+)-ATPase and the AE1 anion exchanger in intercalated cells (IC) of rat kidney connecting segment (CNT) and CCD during acute (6 hr) metabolic (NH4Cl) acidosis and respiratory (NaHCO3) alkalosis. AE1 immunostaining intensity quantified by confocal microscopy was elevated in metabolic acidosis and substantially reduced in metabolic alkalosis. AE1 immunostaining was restricted to Type A IC in all conditions, and the fraction of AE1+IC was unchanged in CNT and CCd. Metabolic acidosis was accompanied by redistribution of H(+)-ATPase immunostaining towards the apical surface of IC, and metabolic alkalosis was accompanied by H(+)-ATPase redistribution towards the basal surface of IC. Therefore, acute metabolic acidosis produced changes consistent with increased activity of Type A IC and decreased activity of Type B IC, whereas acute metabolic alkalosis produced changes corresponding to increased activity of Type B IC and decreased activity of Type A IC. These data demonstrate that acute systemic acidosis and alkalosis modulate the cellular distribution of two key transporters involved in proton secretion in the distal nephron.
While exercise training appears to have no effect on resting respiratory function, and its effect on ventilation/perfusion relationships is uncertain, it can significantly reduce the rate of lactic acid production, carbon dioxide generated from buffering of acid and the hydrogen ion stimulus to breathe during exercise. We had two objectives in this study: 1) to determine if patients who might benefit from exercise training could be selected based on resting respiratory function measurements; 2) to determine if the work rate at which the metabolic acidosis starts to develop could be reliably determined, non-invasively, by a simple modification of the recently described V-slope method of Beaver et al. Patients with severe obstructive lung disease, all of whom experienced exertional dyspnoea, underwent incremental exercise testing to determine if they could exercise to a level causing metabolic acidosis. About two thirds of the patients with severe airflow obstruction developed a significant metabolic acidosis (arterial standard HCO3- decrease of more than 2 mEq.l-1 after two minutes recovery following an incremental exercise test to maximum). The oxygen uptake (VO2) at which the metabolic acidosis (directly measured) and that of which the increase in CO2 in the expired air attributable to buffering (V-slope method), were in close agreement. There was no significant correlation between the magnitude of the exercise metabolic acidosis and the forced expiratory volume in one second (FEV1) or the diffusing capacity for carbon monoxide (DLCO). Thus, it is necessary to perform exercise testing in order to select patients for exercise training, based on the benefits accrued from reducing the exercise metabolic acidosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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