Pulmonary Capillary Volume Research Articles

The Evaluation and Monitoring of Volume Status in Congestive Heart Failure

The increasing prevalence of heart failure dictates that physicians effectively assess and treat congestion. The evaluation of volume status in the complex group of patients with heart failure is very challenging. Physical examination is at best challenging and not always helpful, confounded by body habitus and comorbidities. Weight monitoring has been shown to be helpful, especially in combination with remote monitoring or telephonic checks. Invasive methods such as pulmonary artery catheters provide significant information but have not been proven to be clinically effective. Noninvasive measures such as impedance cardiography and echocardiography provide additional information. The future of heart failure management may reside in implantable monitors, either alone or in combination with other intracardiac devices. These monitors can provide surrogates of pulmonary capillary wedge pressure and volume. They can also be followed remotely and provide information on the patient's status more frequently than office visits. This manuscript will review volume assessment including past, current, and future methods.

Sildenafil improves the alveolar–capillary function in heart failure patients

Background Sildenafil is used for pulmonary hypertension treatment and its use is safe in chronic heart failure (HF) patients. Aims To analyze the effects of sildenafil on lung mechanics, gas diffusion, exhaled nitric oxide (eNO) at rest and during exercise in chronic HF. We did so to evaluate if sildenafil prevents exercise-induced pulmonary edema formation. Methods We studied 22 chronic HF males. We measured after a single dose of placebo, sildenafil (25 mg) and sildenafil (100 mg), lung diffusion (DLCO), molecular diffusion (DM), pulmonary capillary volume (VC), eNO, all at rest and during exercise, standard pulmonary function, and maximal cardiopulmonary exercise. Results At rest sildenafil improved pulmonary mechanics and DLCO from 23.1 ± 6.3 ml/mmHg/min to 23.9 ± 6.4 (25 mg, p < 0.05) and to 25.3 ± 6.7 100 mg, p < 0.02). Sildenafil (100 mg) prevents edema formation (highest DM/VC during exercise). At rest eNO was low and not affected by tested drugs. With light exercise eNO was higher with sildenafil 100 mg. Peak VO 2 increased with sildenafil from 1376 ± 331 ml/min to 1471 ± 375 (25 mg, p < 0.01) and 1524 ± 461 (100 mg, p < 0.02). Peak VO 2 increase was related to DLCO improvement. Conclusion In chronic HF sildenafil increases exercise performance, improves lung mechanics and gas diffusion and prevents exercise-induced pulmonary edema formation probably by restoring NO pathways.

Historical review: the carbon monoxide diffusing capacity (DLCO) and its membrane (DM) and red cell (Theta.Vc) components.

The single breath carbon monoxide diffusing capacity (DLCO sb), also called the transfer factor (TLCO), was introduced by Marie and August Krogh in two papers (Krogh and Krogh, Skand. Arch. Physiol. 23, 236-247, 1909; Krogh, J. Physiol., Lond. 49, 271-296, 1915). Physiologically, their measurements showed that sufficient oxygen (by extrapolation from CO) diffused passively from gas to blood without the need to postulate oxygen secretion, a popular theory at the time. Their DLCO sb technique was neglected until the advent of the infra-red CO meter in the 1950s. Ogilvie et al., J. Clin. Invest. 36, 1-17, 1957 published a standardized technique for a 'modified Krogh' single breath DLCO, which eventually became the method of choice in pulmonary function laboratories. The Roughton-Forster equation (J. Appl. Physiol. 1957, 11, 290-302) was an important step conceptually; it partitioned alveolar-capillary diffusion of oxygen (O2) and carbon monoxide (CO) into a membrane component (DM) and a red cell component (theta.Vc) where theta is the DLCO (or DL(O2)) per ml of blood (measured in vitro), and Vc is the pulmonary capillary volume. This equation was based on the kinetics of O2 and CO with haemoglobin (Hb) in solution and with whole blood Hartridge and Roughton, Nature, 1923, 111, 325-326; Proc. R. Soc. Lond. Ser. A, 1923, 104, 376-394; (Proc. R. Soc. Lond. Ser. B, 1923, 94, 336-367; Proc. R. Soc. Lond. Ser. A 1923, 104, 395-430; J. Physiol., Lond. 1927, 62, 232-242; Roughton, Proc. R. Soc. Lond. Ser. B 1932, 111, 1-36) and on the relationship between alveolar P(O2) and 1/DLCO. Subsequently, the relationship between DL(O2) (Lilienthal et al., Am. J. Physiol. 147, 199-216, 1946) and DL(CO) was defined. More recently, the measurement of the nitric oxide diffusing capacity (DLNO) has been introduced. For DL(O2) and DLNO the membrane component (as 1/DM) is an important part of the overall diffusion (transfer) resistance. For the DLCO, 1/theta.Vc probably plays the greater role as the rate limiting step. A crucial question, the effect of unstirred plasma layers on the 'true' value of thetaCO in vivo, has not been resolved, but this does not detract from the clinical role of the DLCO sb (TLCO) as an essential test of lung function.

Increased surface tension decreases pulmonary capillary volume and compliance

Increased surface tension is an important component of several respiratory diseases, but its effects on pulmonary capillary mechanics are incompletely understood. We measured capillary volume and specific compliance before and after increasing surface tension with nebulized siloxane in excised dog lungs. The change in surface tension was sufficient to increase lung recoil 5 cm H(2)O at 50% total lung capacity. Increased surface tension decreased both capillary volume and specific compliance. The changes in capillary volume and compliance were greatest at the lung volumes at which the surface tension change was greatest. Near functional residual capacity, capillary volume postsiloxane was approximately 30% of control. Presiloxane capillary specific compliance was approximately 7%/cm H(2)O near functional residual capacity and approximately 2.5%/cm H(2)O near total lung capacity. Postsiloxane capillary-specific compliance was 3%/cm H(2)O, and was independent of lung volume. We conclude that in addition to their well-known effects on lung mechanics, changes in surface tension also have important effects on capillary mechanics. We speculate that these changes may in turn affect ventilation and perfusion, worsen gas exchange, and alter leukocyte sequestration.

Reference values for alveolar membrane diffusion capacity and pulmonary capillary blood volume.

The reference values for diffusion capacity of the alveolar capillary membrane (Tm,CO) and pulmonary capillary volume (Qc) are scarce, while the standard deviations of the equations are large. New equations and residual standard deviations (RSDs) were determined in a sample of healthy subjects. Tm,CO and Qc values were measured in 117 (72 females, 45 males) nonsmoking healthy subjects. The carbon monoxide transfer factor (TL,CO) was determined when the volunteer was breathing room air and subsequently, when the volunteer was breathing 100% oxygen. From these data, Tm,CO and Qc values were calculated. The females' TL,CO was 3.15 mmol x min(-1) x kPa(-1) lower than the males', apparently caused by lower female lung volume. Tm,CO and Qc were lower in females, but correction for lung volume eliminated this difference. Qc(-1) reference equations for females and males, respectively, are 4.375 x 10(-2) - 1.085 x l0(-2) x height and 4.455 x 10(-2) -1.085 x 10(-2) x height (RSD for both sexes: 2.544 x 10(-3)). Tm,CO(-1) reference equations for females and males, respectively, are 0.111+3.304 x 10(-4) x age-4.753 x 10(-2) x height and 0.127+3.304 x 10(-4) x age-4.753 x 10(-2) x height (RSD for both sexes: 1.085 x 10(-2)). The general character of these equations complies with earlier publications, the only difference being that the RSDs are 1.18-2.76 times lower. New reference equations for diffusion capacity of the alveolar capillary membrane and pulmonary capillary volume are available with considerably smaller residual standard deviations.

Pulmonary diffusion abnormalities in relation to cytomegalovirus antigenemia and cytomegalic endothelial cells in blood.

The pathophysiology of HCMV infection may involve many different organs including the lungs. In this study we investigated HCMV antigenemia levels and cytomegalic endothelial cells (CEC) in blood in relation to the pulmonary diffusion capacity. Patients with high HCMV antigenemia (> or = 100 pp65+ PMNs/50.000) (n = 8) showed a more extensive decrease in the membrane factor (Dm) than patients with lower levels of HCMV antigenemia (n = 7). The decline of the diffusion capacity of the alveolar capillary membrane (KCOc) and of the pulmonary capillary volume (Vcap) was the same in both groups. Four out of nine patients had CEC in the range of 0.22 CEC/ml to 30.26 CEC/ml. All the HCMV patients showed a decreased KCOc together with a decrease of Dm and Vcap but no difference was observed between patients with and without CEC. We conclude that a higher viral load is associated with a more extensive decrease in the membrane factor and therefore with more subclinical pneumonitis. No relation was observed between CEC and pulmonary dysfunction. Therefore, we postulate that CEC levels are related indirectly to subclinical pneumonitis mediated via the viral load.

Estudio de la difusión pulmonar de monóxido decarbono en dos situaciones clínicas: asma bronquial y diabetes mellitus

The aim of our work has been the study and comparison of diffusion capacity of CO (DLCO) in two different clinical situations: bronchial asthma and diabetes mellitus. We have studied 16 control subjects, 38 patients with bronchial asthma and 65 patients with diabetes mellitus. We performed CO pulmonary diffusion tests by single breath method to determine two components: membrane diffusion factor (Dm) and pulmonary capillary blood volume (Vc). We have found a positive correlation of FEV1 with Dm. The bronchial asthma group had a lower FEV1 and FEF25-75% and an increase in DLCO, Dm and Vc, with respect to the control group. The diabetes mellitus group presented a decrease in CVF, FEV1, DLCO and Vc, with respect to the control group. The bronchial asthma group showed a lower ratio of Dm/Vc than the control and diabetes groups. The bronchial asthma patients have an increase in CO pulmonary diffusion, membrane diffusion factor and pulmonary capillary volume. However, the diabetes mellitus patients present a decrease in CO pulmonary diffusion mainly due to pulmonary capillary volume.

The lung diffusing capacity for nitric oxide in rats is increased during endotoxemia.

Rats, when injected with endotoxin, begin to exhale nitric oxide (NO) within 1 h. This study measured the diffusing capacity for NO in the lungs of rats (DL(NO)) under both control and endotoxemic conditions, and it also estimated the rate at which endogenous NO (VP(NO)) enters the distal compartment of the lung, both in control rats and during endotoxemia. DL(NO) increased from 0.68 +/- 0.12 (SE) ml. min(-1). mmHg(-1) in control rats to 1.17 +/- 0.25 ml. min(-1). mmHg(-1) in endotoxemic rats. VP(NO) was 2.6 +/- 0.5 nl/min in control rats and attained a value of 218.6 +/- 50.1 nl/min at the height of NO exhalation 3 h after the endotoxin. We suggest that increased DL(NO) reflects an increase in pulmonary membrane diffusing capacity, caused by a pulmonary hypertension that is due to neutrophil aggregation in the lung capillaries. DL(NO) may also be increased by an enlarged pulmonary capillary volume because of the vasodilatory effects of the endogenous NO that is produced by the lung in response to the endotoxin. NO production by the lungs in response to endotoxin is unique in that it is the only situation reported to date in which pathologically induced increases in NO exhalation originate from the alveolar compartment of the lung, as opposed to the small conducting airways.

Effect of simvastatin on micropulmonary red cell mass in patients with hyperlipoproteinemia

The purpose of this study was to compare the macrocirculatory and microcirculatory effects of simvastatin in hyperlipemic patients. In vitro measurements of lipoprotein levels and macrocirculatory hemorheology were complemented by in vivo measurements of the pulmonary capillary red cell volume (RCVpc) before and after 6 weeks of treatment with 40 mg of simvastatin daily in 30 male patients with hyperlipoproteinemia type IIa. RCVpc was assessed from the vascular component of the lung diffusing capacity for carbon monoxide, using the modification of the Roughton–Forster's method. RCVpc was increased in patients (60.9±9 versus 40±9 ml in healthy controls) and it decreased to 47±6 ml after treatment ( P=5×10 −11). The decreases in RCVpc correlated to concomitant decreases in peripheral hematocrit ( R=0.68) and serum total cholesterol (−34% on average; R=0.59). Membrane diffusing capacity was normal in patients and not affected by the therapy; suggesting that increased RCVpc was due to increased micropulmonary hematocrit. Thus, it appears that viscosity in microcirculation is greatly increased in hyperlipemic patients and that simvastatin is able to normalize it. Since microcirculatory conditions can only partly be inferred from in vitro measurements the use of lung diffusional parameters was advocated, which enable in vivo assessment of hemorheology in microcirculation.

Changes in transfer factor of the lung in response to bronchodilatation

Measurement of the transfer factor for carbon monoxide (TLCO) is a widely used clinical lung function test. Although it is frequently applied in patients with bronchial obstruction, there is little information on the effects of bronchodilatation on the test. We therefore measured TLCO in 40 patients before and after inhalation of terbutaline. TLCO was measured with the single-breath technique in 20 patients and with the intra-breath technique in 20 patients. TLCO was also measured in 20 healthy subjects with the single-breath technique. Forced expiratory volume (FEV1) increased from 2.9 +/- 1. 1 to 3.2 +/- 1.2 l in patients with bronchial obstruction in response to terbutaline inhalation. TLCO increased from 8.2 +/- 2.6 to 8.6 +/- 2.7 mmol min-1 kPa-1 (P< 0.001) and alveolar volume (VA) from 5.74 +/- 1.21 to 5.90 +/- 1.21 l (P<0.001). There was no difference between the single-breath and the intra-breath techniques. There was little change in FEV1 in the healthy subjects in response to terbutaline. TLCO increased from 10.2 +/- 2.1 to 10.5 +/- 2.2 mmol min-1 kPa-1 (P< 0.01), but there was no change in VA. The increase in TLCO in patients may partly be explained by improved distribution of the inhaled gas. In healthy subjects, terbutaline may increase pulmonary capillary volume. We conclude that bronchodilatation results in a small increase in TLCO in patients with light to moderate bronchoconstriction as well as in healthy subjects. The effect is small and should in most cases be simple to account for in the interpretation of pulmonary function tests, provided the patient's treatment is known.

The effect of repeat exercise on pulmonary diffusing capacity and EIH in trained athletes.

The purpose of this study was to determine the effects of repeated heavy exercise on postexercise pulmonary diffusing capacity (DL) and the development of exercise induced arterial hypoxemia (EIH). 13 endurance-trained, male athletes (age = 27+/-3 yr, height = 179.6+/-5.0 cm, weight = 71.8+/-6.9 kg, VO2max = 67.0+/-3.6 mL x kg(-1) x min(-1) performed two consecutive, continuous exercise tests on a cycle ergometer to VO2max, separated by 60 min of recovery. Arterial oxygen saturation (%SaO2) was measured via ear oximetry, and resting DL was measured and partitioned by the single-breath method, before exercise and 60 min after each exercise bout. No significant differences resulted in VO2max, VE, peak heart rate (HR), or breathing frequency between exercise bouts (P > 0.05). There was a small but significant decrease (454-446 W; P < 0.05) in peak power output in the second test. %SaO2 decreased from resting values during both exercise tasks, but there was no difference between the minimum saturation achieved in test 1 (91.4) or test 2 (91.6; P > 0.05). After the initial exercise bout, significant decreases (P < 0.05) occurred in DL (11%), membrane diffusing capacity (DM) (11%) and pulmonary capillary volume (VC) (10%). Further decreases occurred in DL (6%; P < 0.05), DM (2%; P > 0.05), and VC (10%; P < 0.05) after the second exercise bout. These observations question the meaning of post exercise measurements of pulmonary diffusion capacity, and its components, relative to pulmonary gas exchange and pulmonary fluid accumulation during exercise. The fact that there was no further change in %SaO2 after the second test suggests that if any interstitial edema developed, it was of no clinical significance; alternatively, the changes in DL(CO) may be related more to redistribution of blood than the development of pulmonary edema.

Pulmonary capillary blood volume in patients with probable pulmonary Kaposi's sarcoma.

An increase in pulmonary capillary blood volume secondary to angiogenesis has been described in Kaposi's sarcoma. The value of the pulmonary capillary blood volume as an early marker of pulmonary Kaposi's sarcoma was evaluated. In a prospective study 45 HIV positive patients (nine asymptomatic for Kaposi's sarcoma, 29 with cutaneous or mucocutaneous Kaposi's sarcoma, and seven with pulmonary Kaposi's sarcoma), underwent pulmonary function tests and determination of transfer capacity for carbon monoxide (TLCO) with its components, pulmonary capillary volume and membrane factor. Total lung capacity (TLC), TLCO, and its components were similar in the three groups. TLCO was normal in patients with pulmonary Kaposi's sarcoma and no changes in membrane factor or pulmonary capillary volume were observed. Pulmonary function tests and pulmonary capillary volume alone are not useful for identifying patients with pulmonary Kaposi's sarcoma.

High-resolution computed tomography and pulmonary capillary volume in patients with probable pulmonary Kaposi's sarcoma

Summary Objective : pulmonary Kaposi's sarcoma (KS) remains difficult to diagnose because of the poor specificity of clinical and radiological signs and the low yield of biopsies. Computed tomography (CT) has been used to describe characteristic aspects of pulmonary KS, and high-resolution CT (HRCT) may be able to depict more precise features. An increase in pulmonary capillary volume has been reported in patients with cutaneous KS. Design and patients : in a prospective study, we determined the specificity of HRCT for pulmonary KS and divided 51 HIV patients into four groups, as follows : 10 asymptomatic patients without KS (control group 1), 14 patients with cutaneous KS (control group 2), 15 patients with mucocutaneous KS (control group 3) and 12 patients with probable pulmonary KS (group 4) documented by HRCT and/or bronchoscopy. Major patterns of probable pulmonary KS i.e spiculated nodules and peribronchovascular thickenings were precisely described. Pulmonary function tests (PFT) were done in every case. Results : total lung capacity (TLC), transfer lung capacity ( DLco ) and its components: pulmonary capillary volume Vc and membrane factor Dm were not different in the 4 groups. Forced expiratory volume for one second over vital capacity (FEV1/VC) was significantly lower in control group 2 and in group 4 than in control groups 1 and 3. DLco was normal in patients with pulmonary KS (group 4); no significant change in Dm (mean = 71.5 ± 17.5 % of predicted values) or Vc (mean = 83.6 ± 14.1 % of predicted values) was observed. Conclusions : these results show that Vc alone is unsuitable for the early diagnosis of pulmonary KS, but that HRCT combined with bronchoscopy can yield findings strongly suggestive of pulmonary KS and obviate the need for more invasive investigations.

Resistive Loading and Pulmonary Capillary Volume in Asthma

We recently observed that an inspiratory flow-resistive load can worsen airflow obstruction in supine asthmatic patients. As such loads reportedly augment intrapulmonary blood volume, we examined the effect of a prolonged inspiratory resistive load on pulmonary capillary volume (corrected for alveolar volume—Vc/Va) in 15 asthmatic and 4 normal subjects. Subjects inspired continuously while supine through increasing resistances (hour 1, 9.0; hour 2, 17.0, and hours 3 and 4, 21.5 cm H2O/L/s).

Estimation of the pulmonary capillary transport function in isolated rabbit lungs.

Recently, we presented a method for estimating the pulmonary capillary volume and transport function based on the use of a reference indicator and two or more indicators that rapidly equilibrate (radially) with the tissue (i.e., the concentrations in the vascular and extravascular spaces at a given axial location are in equilibrium) during transit through the capillaries in a bolus-injection indicator dilution method (S. H. Audi, G. S. Krenz, J. H. Linehan, D. A. Rickaby, and C. A. Dawson. J. Appl. Physiol. 77:332-351, 1994). The objectives of the present study were 1) to determine whether [14C]diazepam and [3H]alfentanil equilibrate sufficiently rapidly between the vascular space and tissue and with sufficiently different pulmonary extra-vascular mean residence times to be used in a single bolus to estimate the pulmonary capillary volume and transport function using this method and 2) to estimate the pulmonary capillary volume and transit time distribution in isolated perfused rabbit lungs. Both [14C]diazepam and [3H]alfentanil were found to be rapidly equilibrating indicators by the criteria that, over a wide range of flow rates, their respective venous effluent concentration curves were nearly congruent on a time scale normalized to the lung mean transit time for the reference indicator (fluorescein isothiocyanate dextran). In addition, at a given plasma albumin concentration, [14C]diazepam had a significantly longer extravascular mean residence time than [3H]alfentanil, e.g., at 6% plasma albumin concentration, the extravascular mean residence time of [14C]diazepam was more than twice that of [3H]alfentanil. On average, the estimated pulmonary capillary volume for a 2.7-kg was approximately 4.2 ml or approximately 44% of the total pulmonary vascular volume (9.5 ml). The relative dispersion of the pulmonary capillary transport function of the rabbit was approximately 90%.

994-97 Quantitating Pulmonary Capillary Volume Using Digital Parametric Angiographic Analysis

Assessment of the distal pulmonary vasculature in patients with pulmonary hypertension has been limited to qualitative description of pulmonary arteriograms. Digital parametric imaging, using contrast density and transit time, has been used to qualitative blood volume and flow in the coronary and renal vascular beds. This study was performed to determine whether digital parametric imaging can quantitate vascular volume in the distal pulmonary capillary bed with pulmonary flow intact. Two digital angiograms of the pulmonary vasculature were acquired in 11 patients with varying degrees of pulmonary hypertension. A balloon flotation catheter was advanced distally into the pulmonary artery. The first angiogram (static image) was performed with blood flow occluded by inflation of the catheter balloon. Non-ionic contrast was then hand injected to completely fill the vasculature beyond the balloon occlusion. The second angiogram (flow image) was performed with the balloon deflated and blood flow preserved. A hand injection of a rapid bolus of contrast, 1–2 cc, was given. Digital subtraction image data were obtained at 15 frames/sec at end expiration for both angiograms. Contrast density measurements of the distal pulmonary vasculature were determined from the static images in various 2 × 2 mm areas using digital parametric imaging. The maximum density in these same areas was similarly determined from the flow images. The correlation of the density measurements between the static and the flow images in 64 regions of interest was excellent (R = 0.92, regression slope = 0.98). This correlation was similar to that observed for repeated injections using the same technique (flow image) (R = 0.97, regression slope = 0.97). Digital parametric measurements of pulmonary capillary volume obtained with blood flow preserved are the same as those obtained with flow occluded and the entire bed replaced by contrast. This method allows quantitation of pulmonary vascular volume and flow using a simple, single contrast injection in the distal pulmonary artery.

Effects of balloon mitral commissurotomy on the diffusing capacity of the alveolar capillary membrane and pulmonary capillary volume in patients with mitral stenosis

Effects of balloon mitral commissurotomy on the diffusing capacity of the alveolar capillary membrane and pulmonary capillary volume in patients with mitral stenosis

Hemodynamic Performance During Exercise in Patients with Severe Chronic Congestive Heart Failure Before and After a Single Dose of Pimobendan

Duration of symptom-limited exercise on a bicycle ergometer (constant workload of 25 W) was determined in 12 patients with severe chronic congestive heart failure (CHF) due to dilated cardiomyopathy (CMP, 4 patients) or ischemic heart disease (IHD, 8 patients) undergoing hemodynamic monitoring. Mean exercise duration was 214 +/- 124 s and produced severe dyspnea lasting > 5 min in all patients. The next morning, each patient exercised again to the same level; pimobendan (10 mg orally) was then administered, and exercise to the same workload was repeated 4 and 10 h later. Mean +/- SD exercise-induced changes in heart rate (HR, min-1), pulmonary capillary wedge pressure (PCW, mm Hg), cardiac output (CO, L/min-1), and stroke volume index (SVI, ml.min-1) were as follows. At baseline, HR was 85 +/- 17-110 +/- 21 beats/min (p < 0.001), PCW 21 +/- 10-31 +/- 10 mm Hg (p < 0.05), CO 3.7 +/- 1.0-3.9 +/- 1.0 L.min-1 (NS), and SVI, 25 +/- 7-20 +/- 7 ml.m-2 (NS). Four hours after pimobendan administration, HR was 90 +/- 14-113 +/- 21 beats/min (p < 0.001), PCW 11 +/- 7-20 +/- 10 mm Hg (p < 0.05), CO 5.3 +/- 0.7-5.8 +/- 1.0 L.min-1 (NS), and SVI 33 +/- 3-29 +/- 7 ml.m-2 (NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of varying alveolar oxygen partial pressure on diffusing capacity for nitric oxide and carbon monoxide, membrane diffusing capacity and lung capillary blood volume.

1. To examine the effect of varying oxygen partial pressure (PAO2) on nitric oxide (DLNO) and carbon monoxide (DLCO) diffusing capacity (transfer factor), 10 subjects performed combined DLCO/DLNO measurements with the inspired mixture made up with three different oxygen concentrations (25%, 18% and 15%) to give PAO2 values of 12-20 kPa. 2. A novel method is described for calculating membrane diffusing capacity (DM) and pulmonary capillary volume (Qc) from DLNO and DLCO. 3. The mean DMCO was 52.89 mmol min-1 kPa-1 and Qc was 0.056 litre. Reducing PAO2 from 20 to 12 kPa resulted in an increase in DLCO = -0.124 (O2%) + 11.67 (P less than 0.001) and a fall in DLNO = 0.538 (O2%) + 32.01 (P less than 0.001) and a fall in DLNO/DLCO = 0.107 (O2%) + 2.52 (P less than 0.001). DM (P = 0.59) and Qc (P = 0.64) also tended to fall with falling PAO2. 4. It appears more likely that the minor reduction in DLNO that we have observed with falling PAO2 is due to diffusion rather than reaction limitation.

Early Radiation Response of the Canine Heart and Lung

In this study three groups of four adult beagle dogs were irradiated with a 12-Gy single dose to the thorax. The fields used were the entire thorax, the entire thorax with a heart block in place, and the heart with one-third of the lung volume. The response of the lung was evaluated by cellular and biochemical analysis of sequential bronchoalveolar lavage fluids, blood gas analysis, physical examination, and histopathology. Sparing a small volume of lung improved survival. Cardiac function was evaluated by right heart catheterization, echocardiography, physical exam, and histopathology. Pulmonary artery pressure was increased in all dogs, mean systemic artery pressure was decreased in all dogs, and no difference could be shown among the groups. These effects are likely secondary to a reduced pulmonary capillary volume. Stroke volume was significantly deceased in dogs that had their hearts included in the field but not in dogs with their hearts shielded. This effect was not thought to be secondary to lung injury. The influence of lung irradiation on cardiac function was limited to pulmonary hypertension. Pulmonary hypertension may be enhanced by the release of vasoactive compounds. Pulmonary hypertension may contribute to radiation-induced heart failure.