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Introduction: Pulmonary congestion is a common finding of heart failure (HF), but it remains unclear how pulmonary and heart blood volumes (V p and V h , respectively) and extravascular lung water (EVLW) change in stable HF and affect lung function., Methods: Fourteen patients with HF (age 68 ± 11 y, LVEF 33 ± 8%) and 12 control subjects (age 65 ± 9 y) were recruited. A pulmonary function test, thoracic computerized tomographic (CT) scan, and contrast perfusion scan were performed. From the thoracic scan, a histogram of CT attenuation of lung tissue was generated and skew, kurtosis, and full-width half-max (FWHM) calculated as surrogates of EVLW. Blood volumes were calculated from the transit time of the contrast through the great vessels of the heart., Results: Patients with HF had greater V p and V h (V p 0.55 ± 0.21 L vs 0.41 ± 0.13 L; V h 0.53 ± 0.33 L vs 0.40 ± 0.15 L) and EVLW (skew 3.2 ± 0.5 vs 3.7 ± 0.7; kurtosis 19.4 ± 6.6 vs 25.9 ± 9.4; FWHM 73 ± 13 HU vs 59 ± 9 HU). Spirometric measures were decreased in HF (percentage of predicted: forced vital capacity 86 ± 17% vs 104 ± 9%; forced expiratory volume in 1 second 83 ± 20% vs 105 ± 11%; maximal mid-expiratory flow 82 ± 42% vs 115 ± 43%). V p was associated with decreased expiratory flows, and EVLW was associated with decreased lung volumes., Conclusions: Congestion in stable patients with HF includes expanded V p and V h and increased EVLW associated with reductions in lung volumes and expiratory flows., (Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.)

Purpose: We determined whether well-acclimatized humans have a reserve to recruit pulmonary capillaries in response to exercise at high altitude., Methods: At sea level, lung diffusing capacity for carbon monoxide (DLCO), alveolar-capillary membrane conductance (DmCO), and pulmonary capillary blood volume (V c) were measured at rest before maximal oxygen consumption ([Formula: see text]) was determined in seven adults. Then, DLCO, DmCO and V c were measured pre- and post-exhaustive incremental exercise at 5150 m after ~40 days of acclimatization., Results: Immediately after exercise at high altitude, there was an increase in group mean DmCO (14 ± 10%, P = 0.040) with no pre- to post-exercise change in group mean DLCO (46.9 ± 5.8 vs. 50.6 ± 9.6 ml/min/mmHg, P = 0.213) or V c (151 ± 28 vs. 158 ± 37 ml, P = 0.693). There was, however, a ~20% increase in DLCO from pre- to post-exercise at high altitude (51.2 ± 0.2 vs. 61.1 ± 0.2 ml/min/mmHg) with a concomitant increase in DmCO (123 ± 2 vs. 156 ± 4 ml/min/mmHg) and V c (157 ± 3 vs. 180 ± 8 ml) in 2 of the 7 participants. There was a significant positive relationship between the decrease in [Formula: see text] from sea level to high altitude and the change in DLCO and lung diffusing capacity for nitric oxide (DLNO) from rest to end-exercise at high altitude., Conclusion: These data suggest that recruitment of the pulmonary capillaries in response to exercise at high altitude is limited in most well-acclimatized humans but that any such a reserve may be associated with better exercise capacity.

Alveolar-capillary membrane conductance (D(M,CO)) and pulmonary-capillary blood volume (V(C)) are calculated via lung diffusing capacity for carbon monoxide (DL(CO)) and nitric oxide (DL(NO)) using the single breath, single oxygen tension (single-FiO2) method. However, two calculation parameters, the reaction rate of carbon monoxide with blood (θ(CO)) and the D(M,NO)/D(M,CO) ratio (α-ratio), are controversial. This study systematically determined optimal θ(CO) and α-ratio values to be used in the single-FiO2 method that yielded the most similar D(M,CO) and V(C) values compared to the 'gold-standard' multiple-FiO2 method. Eleven healthy subjects performed single breath DL(CO)/DL(NO) maneuvers at rest and during exercise. D(M,CO) and V(C) were calculated via the single-FiO2 and multiple-FiO2 methods by implementing seven θ(CO) equations and a range of previously reported α-ratios. The RP θ(CO) equation (Reeves, R.B., Park, H.K., 1992. Respiration Physiology 88 1-21) and an α-ratio of 4.0-4.4 yielded DM,CO and VC values that were most similar between methods. The RP θ(CO) equation and an experimental α-ratio should be used in future studies., (Copyright © 2015 Elsevier B.V. All rights reserved.)

Background The purpose of this study was to determine: (1) whether stable heart failure patients with reduced ejection fraction (HFrEF) have elevated extravascular lung water (EVLW) when compared with healthy control subjects; and (2) the effect of acute β 2 -adrenergic receptor (β 2 AR) agonist inhalation on lung fluid balance. Methods Twenty-two stable HFrEF patients and 18 age- and gender-matched healthy subjects were studied. Lung diffusing capacity for carbon monoxide (DLCO), alveolar–capillary membrane conductance (Dm CO ), pulmonary capillary blood volume (V c ) (via re-breathe) and lung tissue volume (V tis ) (via computed tomography) were assessed before and within 30 minutes after administration of nebulized albuterol. EVLW was derived as V tis – V c . Results Before administration of albuterol, V tis and EVLW were higher in HFrEF vs control (998 ± 200 vs 884 ± 123 ml, p = 0.041; and 943 ± 202 vs 802 ± 133 ml, p = 0.015, respectively). Albuterol decreased V tis and EVLW in HFrEF patients (–4.6 ± 7.8%, p = 0.010; –4.6 ± 8.8%, p = 0.018) and control subjects (–2.8 ± 4.9%, p = 0.029; –3.0 ± 5.7%, p = 0.045). There was an inverse relationship between pre-albuterol values and pre- to post-albuterol change for EVLW ( r 2 = –0.264, p = 0.015) and Dm CO ( r 2 = −0.343, p = 0.004) in HFrEF only. Conclusion Lung fluid is elevated in stable HFrEF patients relative to healthy subjects. Stimulation of β 2 ARs may cause fluid removal in HFrEF, especially in patients with greater evidence of increased lung water at baseline. [ABSTRACT FROM AUTHOR]

Abstract: We examined mechanisms by which hypoxia may elicit pulmonary capillary recruitment in humans. On separate occasions, twenty-five healthy adults underwent exposure to intravenous saline infusion (30ml/kg ∼15min) or 17-h normobaric hypoxia (). Cardiac output and pulmonary capillary blood volume (Vc) were measured before and after saline infusion and hypoxic-exposure by a rebreathing method. Pulmonary artery systolic pressure (sPpa) and left ventricular (LV) diastolic function were assessed before and after hypoxic-exposure via echocardiography. Saline infusion increased and Vc (P <0.05) with no change in (P =0.97). Hypoxic-exposure increased Vc (P <0.01) despite no change in (P =0.25), increased sPpa (P <0.01), and impaired LV relaxation. Multiple regression suggested that ∼37% of the hypoxia-mediated increase in Vc was attributable to alterations in , sPpa and LV diastolic function. In conclusion, hypoxia-induced pulmonary capillary recruitment in humans is only partly accounted for by changes in , sPpa and LV diastolic function. We speculate that hypoxic pulmonary venoconstriction may play a role in such recruitment. [Copyright &y& Elsevier]

Whether the specific blood transfer conductance for nitric oxide (NO) with hemoglobin (θ NO ) is finite or infinite is controversial but important in the calculation of alveolar capillary membrane conductance (Dm CO ) and pulmonary capillary blood volume (V C ) from values of lung diffusing capacity for carbon monoxide (DLCO) and nitric oxide (DLNO). In this review, we discuss the background associated with θ NO , explore the resulting values of Dm CO and V C when applying either assumption, and investigate the mathematical underpinnings of Dm CO and V C calculations. In general, both assumptions yield reasonable rest and exercise Dm CO and V C values. However, the finite θ NO assumption demonstrates increasing V C , but not Dm CO , with submaximal exercise. At relatively high, but physiologic, DLNO/DLCO ratios both assumptions can result in asymptotic behavior for V C values, and under the finite θ NO assumption, Dm CO values. In conclusion, we feel that the assumptions associated with a finite θ NO require further in vivo validation against an established method before widespread research and clinical use. [ABSTRACT FROM AUTHOR]

Purpose: Despite a growing body of literature on the physiological responses to ultramarathon, there is a paucity of data in females. This study assessed the female physiological response to ultramarathon and compared the frequency of perturbations to a group of race- and time-matched males. Methods: Data were collected from 53 contestants of an ultramarathon trail race at the Ultra-Trail du Mont-Blanc (UTMB®) in 2018/19. Before and within 2 h of the finish, participants underwent physiological assessments, including blood sampling for biomarkers (creatine kinase–MB isoenzyme [CK-MB], cardiac troponin I [cTnI], brain natriuretic peptide [BNP], and creatinine [Cr]), pulmonary function testing (spirometry, exhaled NO, diffusing capacities, and mouth pressures), and transthoracic ultrasound (lung comet tails, cardiac function). Data from eight female finishers (age = 36.6 ± 6.9 yr; finish time = 30:57 ± 11:36 h:min) were compared with a group of eight time-matched males (age = 40.3 ± 8.3 yr; finish time = 30:46 ± 10:32 h:min). Results: Females exhibited significant pre- to postrace increases in BNP (25.8 ± 14.6 vs 140.9 ± 102.7 pg·mL−1; P = 0.007) and CK-MB (3.3 ± 2.4 vs 74.6 ± 49.6 IU·L−1; P = 0.005), whereas males exhibited significant pre- to postrace increases in BNP (26.6 ± 17.5 vs 96.4 ± 51.9 pg·mL−1; P = 0.002), CK-MB (7.2 ± 3.9 vs 108.8 ± 37.4 IU·L−1; P = 0.002), and Cr (1.06 ± 0.19 vs 1.23 ± 0.24 mg·dL−1; P = 0.028). Lung function declined in both groups, but males exhibited additional reductions in lung diffusing capacities (DLCO = 34.4 ± 5.7 vs 29.2 ± 6.9 mL⋅min−1⋅mm Hg−1, P = 0.004; DLNO = 179.1 ± 26.2 vs 152.8 ± 33.4 mL⋅min−1⋅mm Hg−1, P = 0.002) and pulmonary capillary blood volumes (77.4 ± 16.7 vs 57.3 ± 16.1 mL; P = 0.002). Males, but not females, exhibited evidence of mild postrace pulmonary edema. Pooled effect sizes for within-group pre- to postrace changes, for all variables, were generally larger in males versus females (d = 0.86 vs 0.63). Conclusions: Ultramarathon negatively affects a range of physiological functions but generally evokes more frequent perturbations, with larger effect sizes, in males compared to females with similar race performances. [ABSTRACT FROM AUTHOR]