PubMed Health⌕ Search

Biomedical subjects

A E Taylor

Publications and source records attributed to A E Taylor.

At least 19 recordsLinked to original sources
PubMed1992

Preliminary results from the self-regulatory treatment of high-medication-consumption headache.

Data are presented from a prospective clinical replication series of ten consecutive high-medication headache patients who presented for nondrug treatment of their headaches. For the first eight, an attempt was made to withdraw the patients from medication, with the assistance of relaxation training, prior to entering a comprehensive self-regulatory treatment program. For the last two, drug withdrawal accompanied the treatment. Six of the ten patients showed clinically significant reductions in headache activity, which held up over follow-ups of up to 12 months. Psychological tests provide some discrimination between success and failures.

Adult↗
PubMed1992

Two controlled evaluations of multicomponent psychological treatment of irritable bowel syndrome.

We report two controlled comparisons of a previously validated multicomponent (relaxation, thermal biofeedback, and cognitive therapy) treatment for irritable bowel syndrome (IBS) to an ostensible attention-placebo control (pseudo-meditation and EEG alpha suppression biofeedback) and to a symptom-monitoring control. In Study 1 (n = 10 per condition) there were nonsignificant trends for the multicomponent treatment to be superior to the attention-placebo condition. In Study 2 (n = 30 per condition), we found no advantage for the multicomponent treatment over the attention-placebo condition. Subjects in both treatment conditions showed significant reductions in GI symptoms, as measured by daily symptom diaries, and significant reductions in trait anxiety and depression. The GI symptom reductions held up over a 6 month follow-up. Possible explanations for the results are explored.

Adult↗
PubMed1992

Pulmonary capillary pressure: a review.

OBJECTIVES: To demonstrate the importance of a) measuring effective pulmonary capillary pressure and b) evaluating the longitudinal distribution of pulmonary vascular resistance relative to pre- and postcapillary resistances. To review the development of methods used to determine pulmonary capillary pressure in experimental animal and clinical studies. DATA SOURCES: Human, animal, and modeling studies published since 1966 identified through MEDLINE and a review of bibliographies of relevant articles. STUDY SELECTION AND DATA EXTRACTION: All studies identified were reviewed with an emphasis on recent studies and those studies identifying various methodologies used to determine capillary pressure. Experimental studies were selected for their historical value and applicability to the clinical setting. DATA SYNTHESIS: Different models of the pulmonary circulation have been proposed. The electrical circuit model, which incorporated capacitance elements and two or four resistive elements, has been the basis for the determination of pulmonary capillary pressure in isolated lungs and in situ lungs in animals and patients. Methods used to determine pulmonary capillary pressure from a pulmonary arterial pressure tracing after balloon occlusion are: a) division of waveform into two components and logarithmic extrapolation of the slow component to occlusion time; b) visual determination of the pressure inflection point of the pulmonary arterial pressure tracing; and c) computer processing of the total arterial pressure transient. Both ease of calculations and difficulties can arise when each method is used. CONCLUSIONS: Pulmonary capillary hydrostatic pressure is an important determinant of pulmonary edema especially in the setting of pulmonary hypertension and adult respiratory distress syndrome. Hypoxia, sepsis, cardiac valvular disease, and inflammatory mediators produce variable changes in the longitudinal distribution of pulmonary vascular resistance so that an increased capillary pressure cannot be predicted by the pulmonary arterial or occlusion pressure. For proper therapy aimed at decreasing pulmonary vascular resistance, it is important to determine whether or not the particular therapy increases capillary pressure. Pulmonary capillary pressure is the most important determinant of lung fluid balance and is the major physiologic parameter that should be measured when various forms of plasma volume expansion and pulmonary vasodilators are used in the critically ill patient.

Animals↗
PubMed1992

Ileal microvascular permeability: a comparison of PS and sigma d using lymphatic and isotopic protein clearances.

Lymphatic clearances of total protein, albumin, immunoglobulin (Ig) G, and IgM obtained in autoperfused cat ileum as venous pressure (Pv) was elevated were analyzed using traditional methods as well as the newer maximal diffusion (max,diff) method of Reed et al. [Am. J. Physiol. 261 (Heart Circ. Physiol. 30): H728-H740, 1991; Am. J. Physiol. 257 (Heart Circ. Physiol. 26): H1037-H1041, 1989] to determine capillary osmotic reflection coefficients (sigma d) and unique permeability surface area products (PS). In a control group (n = 6), sigma d max,diff and PSmax,diff for albumin, IgG, and IgM could not be determined due to their transiently high clearance patterns. These patterns were not altered by treatment with vasodilators (n = 6) to prevent redistribution of blood flow from the mucosal-submucosal to muscularis layer of the ileum, which accompanies elevation of ileal Pv. Furthermore, sigma d values for IgG in both groups were lower than those for both albumin and IgM, a finding inconsistent with predictions based on pore theory, together suggesting that lymphatic protein clearances were influenced by washout of interstitial proteins, a conclusion supported by the decrease in tissue content of albumin and IgG after elevation of Pv. Clearances of radiolabeled albumin (n = 10) and IgG (n = 6), measured after an initial 2-h steady-state period at a constant Pv, were markedly reduced at low lymph flow compared with those obtained in the shorter term experiments. In an additional group (n = 5), albumin clearance peaked at 10 times baseline within 15 min after a step increase in Pv to 30 mmHg but fell to only 3 times baseline within 1 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Increased lymphatic flux of hyaluronan from cat intestine during fat absorption.

During fat absorption, chylomicrons with sizes up to 5,000-10,000 A must traverse an interstitium that has estimated pore sizes of 120-200 A to reach the lacteals. The present experiments were performed to study the behavior of the interstitial matrix component hyaluronan during fat absorption from the intestine. Ileal segments were isolated and autoperfused in pentobarbital-anesthetized cats. A postnodal lymphatic was cannulated, and lymph flow, protein, and hyaluronan concentration in lymph were determined. In group 1, a mixture of oleic acid and taurocholate was infused into the ileal lumen, while in group 2 the animals were fed cream overnight. In group 1, control lymph flow and hyaluronan concentration averaged 53.3 +/- 16.0 (SD) microliters.min-1.100 g intestine-1 and 21.4 +/- 16.0 micrograms/ml, respectively. Administration of taurocholate and oleic acid increased lymph flow and lymph hyaluronan concentration by 100 and 50%, respectively, resulting in a nearly three-fold increase in hyaluronan flux. Subsequent increases in venous pressure increased lymph flow and reduced hyaluronan concentration in lymph to less than 3 micrograms/ml. Hyaluronan flux remained approximately 2 micrograms.min-1.100 g intestine-1 independent of lymph flow. In group 2, no lymph sample was available before administration of fat. Hyaluronan concentration at control venous pressure was 19.3 +/- 6.7 micrograms/ml and fell to 10 micrograms/ml at the highest lymph flow. Hyaluronan flux was approximately 10 micrograms.min-1.100 g intestine-1 at the highest lymph flow and venous pressure (P less than 0.05 compared with the same lymph flow in group 1).(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗
PubMed1992

Hyaluronan flux from cat intestine: changes with lymph flow.

Isolated and autoperfused ileal segments from pentobarbital-anesthetized cats were used to study turnover of hyaluronan in the intestine. A postnodal lymphatic was cannulated, and transcapillary and interstitial fluid fluxes were increased by raising venous pressure. Lymph hyaluronan concentration in control averaged 20.2 +/- 18.8 (SD) micrograms/ml (range 4.6-50) and increased with increasing lymph flow in all experiments to peak at concentrations two to three times above control values (at 15-20 mmHg increase in venous pressure). At higher lymph flows, hyaluronan concentration fell to below 5 micrograms/ml to an average of 21.3 +/- 19.5% of control value at the highest venous pressures used (30-40 mmHg). Tissue hyaluronan content fell from 349 +/- 191 micrograms/g dry wt in control to 148 +/- 78 micrograms/g dry wt (P less than 0.05) at the end of the experiment. In a second group, vasodilators were administered before elevation of venous pressure to prevent redistribution of blood flow between mucosal and muscular layers. The results were similar to those obtained above. In a third experimental group, venous pressure was elevated in one step to 30 mmHg and maintained at this level. Again, hyaluronan concentration initially increased and later fell well below control values. We conclude that a major part of the intestinal hyaluronan is easily mobilized by increased interstitial fluid flux.

Animals↗
PubMed1992

Role of cAMP-dependent protein kinase in cAMP-mediated vasodilation.

In this study, the role of adenosine 3',5'-cyclic monophosphate (cAMP)-dependent protein kinase A (PKA) in cAMP-dependent relaxation was assessed in the isolated-perfused rat lung using a PKA inhibitor, Rp-cAMPS, 8-bromo-cAMP (8-BrcAMP), and the diterpene activator of adenylate cyclase (AC), forskolin (FSK). A role for K+ channels was also assessed with the nonselective K+ channel blocker, tetraethylammonium (TEA, 10 mM), and an ATP-sensitive K+ channel inhibitor, glibenclamide (GLI, 100 microM). Both 8-BrcAMP (0.1-1.0 mM) and RSK (0.1-10 microM) dose-dependently attenuated the peak pressor response to alveolar hypoxia (HPR). Rp-cAMPS potentiated the HPR and attenuated 8-BrcAMP-mediated vasodilation but had no effect on FSK-mediated vasodilation. FSK-mediated vasodilation was not mimicked by 1,9-dideoxy-FSK, which is biologically inactive on AC but alters K+ channels identically to FSK, nor was it attenuated by the platelet-activating factor antagonist SRI 63-441 or the cyclooxygenase inhibitor indomethacin. TEA, but not GLI, attenuated FSK-mediated vasodilation. Similarly, TEA attenuated 8-BrcAMP-mediated vasodilation. These results support roles for PKA and indirect gating of a non-ATP-sensitive K+ channel in mediating cAMP-dependent pulmonary vasodilation.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1992

Microvascular pressure profile of serosal vessels of rat trachea.

The distribution of intravascular pressures within the pulmonary airway microcirculation is an important determinant of transvascular liquid balance. Intravascular pressures were measured in the serosal vessels of the trachea in anesthetized, ventilated rats. The ventral portion of the trachea was surgically exposed and suffused with warm (37 degrees C) Krebs-Ringer bicarbonate. The serosal microvasculature was observed with a video microscope, and microvessel pressures and diameters were measured using the servo-null technique and video calipers, respectively. Mean arterial pressure (MAP) was monitored from the left femoral artery and averaged 106.1 +/- 5.2 mmHg (n = 14). The highest pressure (77% of MAP) was measured in a large (95-microns diam) transverse arteriole. As arteriolar diameter decreased from 39 to 11 microns, pressures fell from 62 to 18% of MAP. Capillaries drained into venular networks that formed extensive arcades. Pressures in these postcapillary venules (20-75 microns diam) were 7.7 +/- 5.5% of MAP (n = 9). These vessels in turn drained into large venous sinuses (120-425 microns diam) where pressures averaged 5.7 +/- 2.3% of MAP (n = 7). A four-parameter logistical model of these data predicts that capillary pressures range from 27 to 15% of MAP. We conclude that 1) a substantial resistance exists across precapillary arterioles less than 40 microns diam and 2) a small pressure drop occurs between systemic arteries and primary feed arterioles in this tissue.

Animals↗
PubMed1992

Effects of hypertonic saline and dextran 70 resuscitation on microvascular permeability after burn.

Administration of hyperosmolar fluids to burn patients has been proposed as a means of decreasing resuscitative fluid volume and, subsequently, wound edema accumulation. To test this hypothesis, canine hindpaw lymph flow (QL) and lymph (CL) and plasma (CP) total protein concentrations were measured, and capillary filtration coefficient (Kf) was calculated before and for 6 h after a 5-s 100 degrees C footpaw scald. Scald was followed 30 min later by bolus infusion (4 ml/kg) of 7% saline or 6% Dextran 70 or the two in combination. Before scald, venous pressure was elevated until a minimal CL/CP was reached. The reflection coefficient (sigma d) was calculated by the formula: 1-minimal CL/CP. Scald increased QL, CL/CP, and Kf, but sigma d was decreased (P less than 0.05). Compared with burn alone, 7% saline exacerbated burn-induced increases in QL and Kf. In contrast, infusion of Dextran 70 did not exacerbate these changes in QL or Kf. Perhaps more importantly, Dextran 70 may have attenuated the increase in CL/CP and reduced edema formation in the burned hindpaw. However, the addition of 7% saline to the dextran eliminated these beneficial effects.

Animals↗
PubMed1992

Compounds that increase cAMP prevent ischemia-reperfusion pulmonary capillary injury.

This study evaluated the physiological effects of compounds that increase adenosine 3',5'-cyclic monophosphate (cAMP) on changes in pulmonary capillary permeability and vascular resistance induced by ischemia-reperfusion (I-R) in isolated blood-perfused rabbit lungs. cAMP was elevated by 1) beta-adrenergic stimulation with isoproterenol (ISO, 10(-5) M), 2) post-beta-receptor stimulation of adenylate cyclase with forskolin (FSK, 10(-5) M), 3) and dibutyryl cAMP (DBcAMP, 1 mM), a cAMP analogue. Vascular permeability was assessed by determining the capillary filtration coefficient (Kf,c), and capillary pressure was measured using the double occlusion technique. The total, arterial, and venous vascular resistances were calculated from measured pulmonary arterial, venous, and capillary pressures and blood flow. Reperfusion after 2 h of ischemia significantly (P less than 0.05) increased Kf,c (from 0.115 +/- 0.028 to 0.224 +/- 0.040 ml.min-1.cmH2O-1.100 g-1). These I-R-induced changes in capillary permeability were prevented when ISO, FSK, or DBcAMP was added to the perfusate at reperfusion (0.110 +/- 0.022 and 0.103 +/- 0.021, 0.123 +/- 0.029 and 0.164 +/- 0.024, and 0.153 +/- 0.030 and 0.170 +/- 0.027 ml.min-1.cmH2O-1.100 g-1, respectively). I-R significantly increased total, arterial, and venous vascular resistances. These increases in vascular resistance were also blocked by ISO, FSK, and DBcAMP. These data suggest that beta-adrenergic stimulation, post-beta-receptor activation of adenylate cyclase, and DBcAMP prevent the changes in pulmonary vascular permeability and vascular resistances caused by I-R in isolated rabbit lungs through a mechanism involving an increase in intracellular levels of cAMP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Lung protection against paraquat is calcium dependent.

Isolated, perfused, and ventilated rat lungs were challenged by paraquat (0.01 M) in the presence of 2.5 mM Ca2+, 2.5 mM Ca2+ with trifluoperazine (100 microM), 0.025 mM Ca2+, or 0.025 mM Ca2+ with sodium metavanadate (10 microM) to establish the effect of varying calcium concentration or calcium-dependent enzyme activities on injury induced by paraquat. Segmental vascular resistances, microvascular permeability (as assessed by the capillary filtration coefficient), lung tissue oxidized glutathione, and lung paraquat accumulation were measured. Exposure to paraquat for 2.5 h did not increase microvascular permeability or pulmonary vascular resistance in the presence of either normal extracellular calcium or low extracellular calcium and sodium metavanadate. Lungs exposed to paraquat were injured (as assessed by increased filtration coefficient) only in the presence of low extracellular calcium or after trifluoperazine was added. This injury was associated with decreased levels of oxidized glutathione and increased paraquat accumulation, suggesting that calcium's protective effect was both by inhibition of paraquat accumulation and maintenance of NADPH. Pulmonary vascular resistance was not increased with paraquat challenge.

Animals↗
PubMed1992

Characterization of thromboxane and prostacyclin effects on pulmonary vascular resistance.

Although thromboxane and prostacyclin (PGI2) have long been described as major controllers of pulmonary vascular resistance, little has been reported on the characteristics of the interactions between the two arachidonic acid products. The current study uses segmental vascular resistance and compliance measurements to evaluate the actions of thromboxane and PGI2 in isolated blood-perfused rat lung. The thromboxane analogue U-46619 increases pulmonary vascular resistance by increasing only small artery resistance and decreases pulmonary vascular compliance in the middle compartment. Among the vascular effects of U-46619 are a maximum increase in resistance (RmaxU-46619) of 60.3 +/- 15.6 cmH2O.l-1.min.100 g-1 and a concentration required for 50% of maximum increase (K0.5,U-46619) of 1.60 +/- 0.85 nM for small artery resistance, a minimum vascular compliance (CminU-46619) of -0.93 +/- 0.58 cmH2O, and a K0.5,U-46619 of 1.10 +/- 1.60 nM for middle compartment compliance. Similar results were obtained for total resistance and total compliance. The effects of PGI2 on thromboxane-induced resistance and compliance changes were evaluated using K0.5,PGI2, RmaxPGI2, and CmaxPGI2 at each dose of thromboxane. PGI2 was more effective in reversing the thromboxane constriction at higher concentrations of thromboxane. These data show that the absolute concentration of PGI2 and thromboxane and not a simple ratio of thromboxane to PGI2 determines vascular tone.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1992

Evaluation of prostaglandin F2 alpha and prostacyclin interactions in the isolated perfused rat lung.

To characterize the interactions between prostaglandin F2 alpha and prostacyclin in controlling tone in the pulmonary circulation, isolated rat lungs were ventilated, perfused with blood, and subjected to challenge by prostaglandin F2 alpha in increasing doses. The pulmonary resistance was evaluated using occlusion techniques that separate the resistance into segments of large and small arteries and veins. The total vascular compliance was evaluated using outflow occlusion. Resistance increased after prostaglandin F2 alpha, and this resistance change was primarily in the small artery segment. The maximum resistance increase by prostaglandin F2 alpha (Rmax,PGF2 alpha), calculated from the Michaelis-Menton equation, was 16.6 +/- 3.6 cmH2O.l-1.min.100 g-1 for total vascular resistance with a concentration required to produce 50% Rmax (K0.5) of 5.26 +/- 3.57 nM. The Rmax,PGF2 alpha for small artery resistance was 13.5 +/- 2.4 cmH2O.l-1.min.100 g-1 with a K0.5 of 2.35 +/- 1.57 nM. The vascular compliance decreased during vasoconstriction by prostaglandin F2 alpha, and the maximum decrease in compliance (Cmin,PGF2 alpha) was -0.43 +/- 0.12 ml/cmH2O with a K0.5 of 2.84 +/- 2.99 nM. At each dose of prostaglandin F2 alpha, prostacyclin was administered in increasing doses to reverse the vasoconstriction caused by prostaglandin F2 alpha. For each concentration of prostaglandin F2 alpha, prostacyclin almost completely reversed the resistance increases and approximately one-half the compliance decrease. The maximum change in vascular resistance or compliance produced by prostacyclin was dependent on the dose of prostaglandin F2 alpha; yet the K0.5 for prostacyclin was within the picomolar range for all doses of prostaglandin F2 alpha.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Bronchial collateral vessel micropuncture pressure in postobstructive pulmonary vasculopathy.

Postobstructive pulmonary vasculopathy, produced by chronic ligation of one pulmonary artery, markedly increases bronchial blood flow. Previously, using arterial and venous occlusion, we determined that bronchial collaterals enter the pulmonary circuit at the distal end of the arterial segment. In this study, we tested the hypothesis that pressure in bronchial collaterals (Pbr) closely approximates that at the downstream end of the arterial segment (Pao). We pump perfused [111 +/- 10 (SE) ml/min] left lower lobes of seven open-chest live dogs 3-15 mo after ligation of the left main pulmonary artery. Bronchial blood flow was 122 +/- 16 ml/min. We measured pulmonary arterial and venous pressures and, by arterial and venous occlusion, respectively, Pao and the pressure at the upstream end of the venous segment (Pvo). Pbr was obtained by micropuncture of 34 pleural surface bronchial vessels 201 +/- 16 microns in diameter. We found that Pbr (14.4 +/- 1.0 mmHg) was similar to Pao (15.0 +/- 0.8 mmHg) but differed significantly (P < 0.01) from Pvo (11.3 +/- 0.5 mmHg). In addition, Pbr was independent of systemic arterial pressure and bronchial vessel diameter. Light and electron microscopy revealed that, in the lobes with the ligated pulmonary artery, the new bronchial collaterals entered the thickened pleura from the parenchyma via either bronchovascular bundles or interlobular septa and had sparsely muscularized walls. We conclude that, in postobstructive pulmonary vasculopathy, bronchial collateral pressure measured by micropuncture is very close to the pressure in precapillary pulmonary arteries and that most of the pressure drop in the bronchial collaterals occurs in vessels > 350 microns in diameter.

Airway Obstruction↗
PubMed1992

Regional bioelectric properties of porcine airway epithelium.

Ion transport properties of pulmonary small airway epithelia are poorly understood. To characterize these properties, airways were excised from anesthetized pigs. Transepithelial potential difference (PD) and conductance were measured in five airway regions: trachea (T, 7.9 +/- 0.2 mm diam), mainstem bronchi (MB, 5.5 +/- 0.2 mm diam), large bronchi (LB, 1.69 +/- 0.12 mm diam), small bronchi (SB, 0.70 +/- 0.06 mm diam), and bronchioles (BR, 0.25 +/- 0.05 mm diam). T and MB were mounted in Ussing-type chambers, and LB, SB, and BR were cannulated with pipettes and perfused. PDs of control tissues were -9.7 +/- 0.8 mV (T), -4.0 +/- 0.5 mV (MB), -4.3 +/- 1.0 mV (LB), -4.5 +/- 0.4 mV (SB), and -1.5 +/- 0.4 mV (BR), lumen negative. Amiloride significantly (P < 0.05) inhibited PDs by 25-70% in all airway regions and decreased conductance 17-33% in all regions except LB where a 10% increase was observed. Bumetanide significantly reduced the amiloride-insensitive PD 54-62% in all regions except BR. Bumetanide had little effect on conductance in T, SB, and BR, but conductance was increased in MB and LB. All airways except the smallest BR significantly hyperpolarized when the solution that bathed the lumen was replaced with Cl(-)-free solution. In bronchioles, hyperpolarization by luminal Cl(-)-free solution was inversely related to fractional inhibition of PD with amiloride but directly related to lumen diameter. These results suggest that 1) porcine tracheas, bronchi, and bronchioles actively absorb Na+, and 2) secretion of Cl- may occur in all airway regions except small bronchioles.

Amiloride↗
PubMed1992

Environmental tobacco smoke and cardiovascular disease. A position paper from the Council on Cardiopulmonary and Critical Care, American Heart Association.

Although the number of cardiovascular deaths associated with environmental tobacco smoke cannot be predicted with absolute certainty, the available evidence indicates that environmental tobacco smoke increases the risk of heart disease. The effects of environmental tobacco smoke on cardiovascular function, platelet function, neutrophil function, and plaque formation are the probable mechanisms leading to heart disease. The risk of death due to heart disease is increased by about 30% among those exposed to environmental tobacco smoke at home and could be much higher in those exposed at the workplace, where higher levels of environmental tobacco smoke may be present. Even though considerable uncertainty is a part of any analysis on the health affects of environmental tobacco smoke because of the difficulty of conducting long-term studies and selecting sample populations, an estimated 35,000-40,000 cardiovascular disease-related deaths and 3,000-5,000 lung cancer deaths due to environmental tobacco smoke exposure have been predicted to occur each year. The AHA's Council on Cardiopulmonary and Critical Care has concluded that environmental tobacco smoke is a major preventable cause of cardiovascular disease and death. The council strongly supports efforts to eliminate all exposure of nonsmokers to environmental tobacco smoke. This requires that environmental tobacco smoke be treated as an environmental toxin, and ways to protect workers and the public from this health hazard should be developed. According to a 1989 Gallup survey commissioned by the American Lung Association, 86% of nonsmokers think that environmental tobacco smoke is harmful and 77% believe that smokers should abstain in the presence of nonsmokers.(ABSTRACT TRUNCATED AT 250 WORDS)

American Heart Association↗
PubMed1992

Microvascular function. Transvascular exchange of fluid in the airways.

Fluid exchange in the airway microcirculation is presented relative to whether the airway epithelium is in an absorbing or a secreting state. The effects of increasing microvascular pressures and damaging the endothelial barrier are also examined relative to fluid dynamics and lymph flow, especially with regard to "filtration secretion." The microvessel pressure profile of the tracheal circulation is discussed relative to our recent data and to the published literature. These micropuncture data indicate that the major resistance to tracheal blood flow resides in arterioles with diameters less than 50 microns. It is hoped that this review will stimulate research on the airway microcirculation since the available data on the physiology and biophysics of circulation in the large and small airways are insufficient to define the microcirculatory exchange characteristics in this capillary bed.

Absorption↗