We previously reported that hypoxia-mediated reductions in α-adrenoceptor sensitivity do not explain the augmented vasodilatation during hypoxic exercise, suggesting an enhanced vasodilator signal. We hypothesized that β-adrenoceptor activation contributes to augmented hypoxic exercise vasodilatation. Fourteen subjects (age: 29 ± 2 years) breathed hypoxic gas to titrate arterial O 2 saturation (pulse oximetry) to 80%, while remaining normocapnic via a rebreath system. Brachial artery and antecubital vein catheters were placed in the exercising arm. Under normoxic and hypoxic conditions, baseline and incremental forearm exercise (10% and 20% of maximum) was performed during control (saline), α-adrenoceptor inhibition (phentolamine), and combined α-and β-adrenoceptor inhibition (phentolomine/propranolol). Forearm blood flow (FBF), heart rate, blood pressure, minute ventilation, and end-tidal CO 2 were determined. Hypoxia increased heart rate (P < 0.05) and minute ventilation (P < 0.05) at rest and exercise under all drug infusions, whereas mean arterial pressure was unchanged. Arterial adrenaline (P < 0.05) and venous noradrenaline (P < 0.05) were higher with hypoxia during all drug infusions. The change (Δ) in FBF during 10% hypoxic exercise was greater with phentolamine (Δ306 ± 43 ml min −1 ) vs. saline (Δ169 ± 30 ml min −1 ) or combined phentolamine/propranolol (Δ213 ± 25 ml min −1 ; P < 0.05 for both). During 20% hypoxic exercise, ΔFBF was greater with phentalomine (Δ466 ± 57 ml min −1 ; P < 0.05) vs. saline (Δ346 ± 40 ml min −1 ) but was similar to combined phentolamine/propranolol (Δ450 ± 43 ml min −1 ). Thus, in the absence of overlying vasoconstriction, the contribution of β-adrenergic mechanisms to the augmented hypoxic vasodilatation is dependent on exercise intensity.

Key elements for determining alveolar-capillary membrane conductance (Dm) and pulmonary capillary blood volume (Vc) from the lung diffusing capacity (Dl) for carbon monoxide (DlCO) or for nitric oxide (DlNO) are the reaction rate of carbon monoxide with hemoglobin (thetaCO) and the DmCO/DlNO relationship (alpha-ratio). Although a range of values have been reported, currently there is no consensus regarding these parameters. The study purpose was to define optimal parameters (thetaCO, alpha-ratio) that would experimentally substantiate calculations of Dm and Vc from the single-inspired O2 tension [inspired fraction of O2 (FiO2)] method relative to the multiple-FiO2 method. Eight healthy men were studied at rest and during moderate exercise (80-W cycle). Dm and Vc were determined by the multiple-FiO2 and single-FiO2 methods (rebreathe technique) and were tabulated by applying previously reported thetaCO equations (both methods) and by varying the alpha-ratio (single-FiO2 method) from 1.90 to 2.50. Values were then compared between methods throughout the examined alpha-ratios. Dm and Vc were critically dependent on the applied thetaCO equation. For the multiple-FiO2 method, Dm was highly variable between thetaCO equations (rest and exercise); the range of Vc was less widespread. For the single-FiO2 method, the thetaCO equation by Reeves and Park (1992) combined with an alpha-ratio between 2.08 and 2.26 gave values for Dm and Vc that most closely matched those from the multiple-FiO2 method and were also physiologically plausible compared with predicted values. We conclude that the parameters used to calculate Dm and Vc values from the single-FiO2 method (using DlCO and DlNO) can significantly influence results and should be evaluated within individual laboratories to obtain optimal values.

Introduction:Each year, the US Antarctic Program rapidly transports scientists and support personnel from sea level (SL) to the South Pole (SP, 2835 m) providing a unique natural laboratory to quantify the incidence of acute mountain sickness (AMS), patterns of altitude related symptoms and the field effectiveness of acetazolamide in a highly controlled setting. We hypothesized that the combination of rapid ascent (3 hr), accentuated hypobarism (relative to altitude), cold, and immediate exertion would increase altitude illness risk.Methods:Medically screened adults (N = 246, age = 37 ± 11 yr, 30% female, BMI = 26 ± 4 kg/m2) were recruited. All underwent SL and SP physiological evaluation, completed Lake Louise symptom questionnaires (LLSQ, to define AMS), and answered additional symptom related questions (eg, exertional dyspnea, mental status, cough, edema and general health), during the 1st week at altitude. Acetazolamide, while not mandatory, was used by 40% of participants.Results:At SP, the barometric pressure resulted in physiological altitudes that approached 3400 m, while T °C averaged −42, humidity 0.03%. Arterial oxygen saturation averaged 89% ± 3%. Overall, 52% developed LLSQ defined AMS. The most common symptoms reported were exertional dyspnea-(87%), sleeping difficulty-(74%), headache-(66%), fatigue-(65%), and dizziness/lightheadedness-(46%). Symptom severity peaked on days 1–2, yet in >20% exertional dyspnea, fatigue and sleep problems persisted through day 7. AMS incidence was similar between those using acetazolamide and those abstaining (51 vs. 52%, P = 0.87). Those who used acetazolamide tended to be older, have less altitude experience, worse symptoms on previous exposures, and less SP experience.Conclusion:The incidence of AMS at SP tended to be higher than previously reports in other geographic locations at similar altitudes. Thus, the SP constitutes a more intense altitude exposure than might be expected considering physical altitude alone. Many symptoms persist, possibly due to extremely cold, arid conditions and the benefits of acetazolamide appeared negligible, though it may have prevented more severe symptoms in higher risk subjects.

Summary Pulmonary congestion is a hallmark feature of heart failure and is a major reason for hospital admissions in this patient population. Heart failure patients often demonstrate restrictive and obstructive pulmonary function abnormalities; however, the mechanisms of these functional declines remain controversial. It has been suggested that the bronchial circulation may play an important role in the development of these pulmonary abnormalities and in the symptoms associated with pulmonary congestion. Congestion may occur in the bronchial circulation from either a marked increase in flow or an increase in blood volume but with a reduction in flow due to high cardiac filling pressures and/or high pulmonary vascular pressures (a stasis like condition). Either may lead to thickened bronchial mucosal and submucosal tissues and reduced airway compliance resulting in airway obstruction and restriction and a lack of airway distensibility. These structural changes may contribute to “cardiac asthma” and dyspnea, characteristic features common in HF patients. Thus the bronchial circulation may be a potential target for therapeutic interventions. The aim of this paper is to review factors governing the control of the bronchial circulation, how bronchial vascular conductance may change with HF and to pose arguments, both supporting and in opposition to the bronchial circulation contributing to congestion and altered pulmonary function in HF. We ultimately hypothesize that the engorgement of the bronchial circulatory bed may play a role in pulmonary function abnormalities that occur in HF patients and contribute to symptoms such as orthopnea and exertional dyspnea.

Background The aim of this study was to determine the relationship between body position, pulmonary function (PF) and bronchial blood flow (Qaw) in a group of heart failure (HF) and control subjects. Methods Thirty-six subjects were studied: 24 stable, ambulatory HF patients (HF: LVEF=27±6%, age=65±9yr) and 12 age- and sex-matched controls (CTRL: LVEF=60±7%, age=62±8yr). Measures of Q̇aw (soluble gas method) and PF were collected upright and following 30 min in the supine position. Results Q̇aw was similar between groups and remained unchanged with body position. Declines in forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV1) with the supine position were observed in both groups; declines in forced expiratory flow 25–75% (FEF25–75) and FEF 75% (FEF75) with the supine position were observed in the HF group only. Changes in Q̇aw were related to changes in PF only in the HF patient groups (ΔFVC, %predicted, r=−0.45, p<0.04, ΔFEV1 r=−0.61, p<0.01, ΔFEV1 %predicted, r=−0.45, p<0.04). Conclusion These data demonstrate that relationships between postural changes in Q̇aw and PF exist only in the HF population and that the bronchial circulation may contribute to postural PF decline in HF.