[Pulmonary circulation disorder in patients with chronic obstructive pulmonary disease].
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Humans↗
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Importance of metabolic function of the natural lung evaluated by prolonged exclusion of the pulmonary circulation.
It is generally considered that the natural lung metabolizes various vasoactive substances through the pulmonary circulation. However, the influences of bypassing or eliminating the pulmonary circulation have not been fully elucidated, especially for prolonged periods. In this study, we performed total cardiopulmonary bypass and exclusion of the pulmonary circulation for up to 336 hr in awake goats to clarify the importance of the metabolic function of the lung. In seven adult goats, biventricular bypass with a pulsatile ventricular assist system was first established. After 2 weeks, the biventricular bypass was converted to total cardiopulmonary bypass without anesthesia. Adequate gas exchange and perfusion support were achieved in all animals. However, the institution of total cardiopulmonary bypass led to marked decreases in the mean aortic pressure and systemic vascular resistance, and they remained low thereafter. The arterial levels of prostaglandin E2 and norepinephrine, which are inactivated naturally through the pulmonary circulation, increased remarkably. These results indicate that the natural lung plays an important role in controlling systemic circulation by metabolizing various vasoactive substances. Understanding the non respiratory function of the natural lung is of prime importance for advancement of lung and heart-lung support.
Animals↗
Endothelin production in pulmonary circulation of patients with mitral stenosis.
BACKGROUND: Although plasma endothelin concentrations are elevated in patients with pulmonary hypertension, the precise sites of endothelin production have not been defined. We investigated the endothelin production in the pulmonary circulation of patients with mitral stenosis and its effects on pulmonary vascular tone. METHODS AND RESULTS: We measured plasma concentrations of endothelin-1, angiotensin II, and thrombomodulin in blood samples obtained from the right and left atria of 10 consecutive patients with rheumatic mitral stenosis (mean age, 55 years; range, 39 to 68) who were undergoing percutaneous mitral valvuloplasty. Plasma levels of endothelin-1 were significantly higher in the left atrium than in the right atrium (3.25 +/- 0.45 versus 2.53 +/- 0.36 pg/mL, mean +/- SE, P < .001). The increased plasma endothelin-1 level in the left atrium, which reflected endothelin-1 production in the pulmonary circulation, was correlated with mean pulmonary artery pressure (r = .65, P = .04), mean pulmonary arterial wedge pressure (r = .67, P = .03), total pulmonary resistance (r = .68, P = .03), and 1/mitral valve area (r = .85, P = .002) but not with pulmonary vascular resistance (r = .04, P = .91). There were no significant differences in plasma levels of angiotensin II and thrombomodulin between the right and left atria (angiotensin II, 16.40 +/- 3.08 versus 15.50 +/- 4.85 pg/mL; thrombomodulin, 2.96 +/- 0.34 versus 2.85 +/- 0.37 ng/mL). CONCLUSIONS: Endothelin-1 production is increased in the pulmonary circulation of patients with mitral stenosis in response to increased pulmonary artery pressure but is not directly related to increased pulmonary vascular tone in this disorder.
Angiotensin II↗
Effects of chronic estrogen-receptor blockade on ovine perinatal pulmonary circulation.
Prolonged infusions of 17beta-estradiol reduce fetal pulmonary vascular resistance (PVR), but the effects of endogenous estrogens in the fetal pulmonary circulation are unknown. To test the hypothesis that endogenous estrogen promotes pulmonary vasodilation at birth, we studied the hemodynamic effects of prolonged estrogen-receptor blockade during late gestation and at birth in fetal lambs. We treated chronically prepared fetal lambs with ICI-182,780 (ICI, a specific estrogen-receptor blocker, n = 5) or 1% DMSO (CTRL, n = 5) for 7 days and then measured pulmonary hemodynamic responses to ventilation with low- and high-fraction inspired oxygen (FI(O(2))). Treatment with ICI did not change basal fetal PVR or arterial blood gas tensions. However, treatment with ICI abolished the vasodilator response to ventilation with low FI(O(2)) [change in PVR -30 +/- 6% (CTRL) vs. +10 +/- 13%, (ICI), P < 0.05] without reducing the vasodilator response to ventilation with high FI(O(2)) [change in PVR, -73 +/- 3% (CTRL) vs. -77 +/- 4%, (ICI); P = not significant]. ICI treatment reduced prostacyclin synthase (PGIS) expression by 33% (P < 0.05) without altering expression of endothelial nitric oxide synthase or cyclooxygenase-1 and -2. In situ hybridization and immunohistochemistry revealed that PGIS is predominantly expressed in the airway epithelium of late gestation fetal lambs. We conclude that prolonged estrogen-receptor blockade inhibits the pulmonary vasodilator response at birth and that this effect may be mediated by downregulation of PGIS. We speculate that estrogen exposure during late gestation prepares the pulmonary circulation for postnatal adaptation.
Animals↗
Extrinsic allergic alveolitis caused by pigeon breeding at a high altitude (2,240 meters). Hemodynamic behavior of pulmonary circulation.
The hemodynamic characteristics of the pulmonary circulation were examined in 10 patients with proved extrinsic allergic alveolitis caused by pigeons (EAA-P) raised at a high altitude. All patients had lung biopsies that showed an interstitial inflammatory response with vascular lesions. At rest, all patients had mean pulmonary pressures (PAP) greater than 16 mmHg; the average PAP was 22 +/- 12 mmHg for the whole group. Pulmonary vascular resistance was high and the mean for the whole group was 225 +/- 25 d.s.cm-5. The pulmonary artery diastolic-pulmonary wedge pressure (PAd-PWP) difference was elevated and averaged 8.5 +/- 2 mmHg. All patients were hypoxemic with elevated AaDO2. With exercise, both PAP and PAd-PWP increased abnormally. While breathing oxygen (FIO2, 99.6%) PAP decreased an average of 7 mmHg (p less than 0.05) and PAd-PWP decreased an average of 5 mmHg (p less than 0.05) without a significant change in PWP. The calculated compliance of the elastic pulmonary arteries in EAA-P was not different from that in normal subjects. Alveolar hypoxia produced mainly by EAA-P and presumably enhanced by living at a high altitude appeared to be the factors in the genesis of pulmonary hypertension, because pulmonary artery diastolic pressure and PAd-PWP difference were correlated with arterial oxygen saturation.
Adult↗
Molecular identification of O2 sensors and O2-sensitive potassium channels in the pulmonary circulation.
Small, muscular pulmonary arteries (PAs) constrict within seconds of the onset of alveolar hypoxia, diverting blood flow to better-ventilated lobes, thereby matching ventilation to perfusion and optimizing systemic PO2. This hypoxic pulmonary vasoconstriction (HPV) is enhanced by endothelial derived vasoconstrictors, such as endothelin, and inhibited by endothelial derived nitric oxide. However, the essence of the response is intrinsic to PA smooth muscle cells in resistance arteries (PASMCs). HPV is initiated by inhibition of the Kv channels in PASMCs which set the membrane potential (EM). It is currently uncertain whether this reflects an initial inhibitory effect of hypoxia on the K+ channels or an initial release of intracellular Ca2+, which then inhibits K+ channels. In either scenario, the resulting depolarization activates L-type, voltage gated Ca2+ channels, which raises cytosolic calcium levels [Ca2+]i and causes vasoconstriction. Nine families of Kv channels are recognized from cloning studies (Kv1-Kv9), each with subtypes (i.e. Kv1.1-1.6). The contribution of an individual Kv channel to the whole-cell current (IK) is difficult to determine pharmacologically because Kv channel inhibitors are nonspecific. Furthermore, the PASMC's IK is an ensemble, reflecting activity of several channels. The K+ channels which set EM, and inhibition of which initiates HPV, conduct an outward current which is slowly inactivating, and which is blocked by the Kv inhibitor 4-aminopyridine (4-AP) but not by inhibitors of Ca(2+)- or ATP-sensitive K+ channels. Using anti-Kv antibodies to immunolocalize and inhibit Kv channels, we showed that the PASMC contains numerous types of Kv channels from the Kv1 and Kv2 families., Furthermore Kv1.5 and Kv2.1 may be important in determining the EM and play a role as effectors of HPV in PASMCs. While the Kv channels in PASMCs are the "effectors" of HPV, it is uncertain whether they are intrinsically O2-sensitive or are under the control of an "O2 sensor". Certain Kv channels are rich in cysteine, and respond to the local redox environment, tending to open when oxidized and close when reduced. Candidate sensors vary the PASMC redox potential in proportion to O2. These include Nicotinamide Adenine Dinucleotide Phosphate Oxidase, (NADPH oxidase) and the cytosolic ratio of reduced/oxidized redox couples (i.e. glutathione GSH/GSSG), as controlled by electron flux in the mitochondrial electron transport chain (ETC). Using a mouse that lacks the gp91phox component of NADPH oxidase, we have recently shown that loss of the gp91phox-containing NADPH oxidase as a source of activated oxygen species does not impair HPV. However, inhibition of complex 1 of the mitochondrial electron transport chain mimics hypoxia in that it inhibits IK, reduces the production of activated O2 species and causes vasoconstriction. We hypothesize that a redox O2 sensor, perhaps in the mitochondrion, senses O2 through changes in the accumulation of freely diffusible electron donors. Changes in the ratio of reduced/oxidized redox couples, such as NADH/NAD+ and glutathione (GSH/GSSG) can reduce or oxidize the K+ channels, resulting in alterations of PA tone.
Animals↗
Chronic airway infection leads to angiogenesis in the pulmonary circulation.
In both pulmonary and systemic hypertension, the walls of the arteriolar vessels are thickened and the lumen size is reduced, leading to increased total vascular resistance. It has been reported previously that chronic airway infection and inflammation lead to increased wall thickness in the pulmonary vasculature, without the development of pulmonary hypertension. The aim of the present study was to examine quantitatively the remodeling of intra-acinar blood vessels in chronically infected rat lungs. Adult rats were anesthetized and inoculated intratracheally with Pseudomonas aeruginosa (n = 10) incorporated into agar beads to induce chronic airway infection. Control groups included rats inoculated with sterile agar beads (n = 8) and rats that were not inoculated (n = 6). Chronic infection caused vascular wall thickening without reduction in mean lumen radius. Furthermore, chronic infection led to increased total length of intra-acinar vessels and increased numbers of branch points, demonstrating that angiogenesis had occurred. Preservation of lumen size and formation of new parallel pathways in the vasculature of chronically infected lungs account for the maintenance of normal PVR despite vessel wall remodeling.
Animals↗
Aorta-pulmonary shunts in growing pigs. Functional and structural assessment of the changes in the pulmonary circulation.
Aorta-pulmonary shunts were produced in growing pigs, 4 to 12 weeks of age, by anastomosing the thoracic descending aorta to the pulmonary trunk, and the animals were followed for periods of 1 to 3 months. Correlation between the hemodynamic findings and the lung structure, analyzed by quantitative methods, showed that the young group (operated upon at 4 weeks of age) developed more severe pulmonary hypertension with increased muscularization of arteries of all sizes and reduction in the size of those running with respiratory bronchioli and beyond. Since this response is similar to that seen in cases of left-to-right shunt associated with congenital heart defects and pulmonary hypertension early in life, it seems that the present experiments reproduce the early response of the growing lung to such hemodynamic disturbance.
Animals↗
Chronic bronchitis: reflex on the pulmonary circulation.
Chronic obstructive pulmonary disease (COPD) is characterized by lower alveolar oxygen content and hypoxia. Hypoxia itself is able to evoke a vascular reflex in a pulmonary vasoconstriction, the explanation of which is, in part, unknown. Pulmonary vasoconstriction leads to different degrees of pulmonary artery pressure (PAP) increase which statistically suggests that the higher the PAP, the poorer the survival rate. Many substances are involved in the vascular homeostasis. An important role is played by cyclooxygenase as well as lipoxygenase pathways metabolites, the antagonists of which have been extensively used in the treatment of pulmonary hypertension in subjects suffering from COPD. An even more important role is played by the endothelium. It is able to modify its metabolism towards the production of substances (e.g., endothelin, EDRF, etc.) which are able to negatively influence the vascular tone. Complete identification of such substances, when possible, would allow us to have a better understanding of the complexity of the mechanism which controls the pulmonary vascular district. In this direction we could hopefully look forward to the detection of specific new drugs able to improve the management of the disease by preventing it from worsening to that extent which statistically and drastically correlates with the worst prognosis.
Bronchitis↗
The pulmonary circulation in acute lung injury: a review of some recent advances.
1. According to the Starling resistor model of the pulmonary circulation, the pulmonary hypertension of oleic acid lung injury, an experimental model close to the early stage of clinical ARDS, primarily results from an increased vascular closing pressure which exceeds Pla and becomes the effective outflow pressure of the pulmonary circulation. Therefore, calculated pulmonary vascular resistance should be interpreted cautiously during haemodynamic investigations in patients with ARDS. 2. Part of this increased vascular closing pressure is functional. During acute lung injury pulmonary vasomotor tone can be reduced by vasodilators, or increased by cyclooxygenase inhibitors and almitrine. 3. Pulmonary vasodilation due to infused vasodilators usually impairs gas exchange in ARDS. 4. There is evidence that HPV is altered during ARDS. Drugs capable of enhancing the efficacy of HPV could improve gas exchange. If proven safe in the future, cyclooxygenase inhibitors and almitrine are interesting compounds to be tested in ARDS.
Acute Disease↗
Imaging of the pulmonary circulation in the closed-chest rat using synchrotron radiation microangiography.
Structural changes of the pulmonary circulation during the pathogenesis of pulmonary arterial hypertension remain to be fully elucidated. Although angiography has been used for visualizing the pulmonary circulation, conventional angiography systems have considerable limitations for visualizing small microvessels (diameters < 200 microm), particularly within a closed-chest animal model. In this study we assess the effectiveness of monochromatic synchrotron radiation (SR) for microangiography of the pulmonary circulation in the intact-chest rat. Male adult Sprague-Dawley rats were anesthetized, and a catheter was positioned within the right ventricle, for administering iodinated contrast agent (Iomeron 350). Subsequently, microangiography of pulmonary arterial branches within the left lung was performed using monochromatic SR. Additionally, we assessed dynamic changes in vessel diameter during acute hypoxic (10% and 8% O2 for 4 min each) pulmonary vasoconstriction (HPV). Using SR we were able to visualize pulmonary microvessels with a diameter of <100 microm (the 4th generation of branching from the left axial artery). Acute hypoxia caused a significant decrease in the diameter of all vessels less than 500 microm. The greatest degree of pulmonary vasoconstriction was observed in vessels with a diameter between 200 and 300 microm. These results demonstrate the effectiveness of SR for visualizing pulmonary vessels in a closed-chest rat model and for assessing dynamic changes associated with HPV. More importantly, these observations implicate SR as an effective tool in future research for assessing gross structural changes associated with the pathogenesis of pulmonary arterial hypertension.
Angiography↗
Pressor effects of circulating endothelin are limited by its removal in the pulmonary circulation and by the release of prostacyclin and endothelium-derived relaxing factor.
Endothelin releases prostacyclin and thromboxane A2 from guinea pig or rat isolated lungs and endothelium-derived relaxing factor in the perfused mesentery of the rat. Endothelin is also substantially removed by the pulmonary circulation of the rat in vitro and in vivo and by guinea pig lungs in vitro. In the rat, the effects of endothelin on the blood pressure vary from pressor (in pithed rats) to purely depressor in anesthetized rats where the resting blood pressure is high. It therefore has the characteristics of a local pressor hormone, rather than a circulating one.
Animals↗
Maximal oxygen consumption and pulmonary circulation in patients with chronic bronchitis.
In order to study the relations between maximal oxygen consumption during exercise (VO2max) and the pulmonary circulation when pulmonary artery pressure (PPA) and pulmonary vascular resistance (PVR) are normal or close to normal, we evaluated twenty-three patients with chronic bronchitis, in stable clinical condition. All these patients performed a progressive exercise test on a bicycle ergometer until exhaustion (VO2max); they were also subjected to right heart catheterization at rest and during light exercise at constant load. In these patients with moderate functional impairment, we observed on average a significant, although weak, correlation (r = -0.52, P less than 0.01) between pulmonary vascular resistance at rest and VO2max. When VO2max exceeded 2 1 min-1, PVR was below 210 dyn s cm-5. From the heart rate during maximal exercise we computed the oxygen pulse (O2Pmax). In eight patients O2Pmax was reduced (less than or equal to 11 ml) with maximal heart rate close to its predicted value; in seven of these subjects PVR was abnormal and Ppa at rest was at least 20 mmHg. Thus it seems that in chronic obstructive bronchitis mild disturbances in pulmonary circulation may be a contributory factor in the limitation of exercise performance, and a maximal exercise test may help to detect pulmonary hypertension in these patients.
Adult↗
Hyperventilation, alkalosis, prostaglandins, and pulmonary circulation of the newborn.
This study was designed to determine whether the effects of hyperventilation on the pulmonary circulation of the newborn lamb were 1) due to mechanical factors or to respiratory alkalosis; and 2) mediated by prostaglandins. Six control lambs were studied during normal ventilation and during hyperventilation with, and without, decreased carbon dioxide (CO2). Five lambs were given indomethacin and studied similarly. In control lambs, hyperventilation with decreased CO2 decreased pulmonary arterial pressure from 26 +/- 2.2 to 18 +/- 1.0 (SE) Torr (P less than or equal to 0.005) and pulmonary vascular resistance from 0.099 +/- 0.035 to 0.070 +/- 0.011 Torr X kg-1 X min-1 (P less than or equal to 0.015). Hyperventilation with normal CO2 did not affect the pulmonary circulation. Hyperventilation with decreased CO2 increased pulmonary arterial concentrations of 6-ketoprostaglandin F1 alpha, a major metabolite of prostacyclin, in control lambs but not in the indomethacin-treated lambs. However, it affected the pulmonary circulation of the control- and indomethacin-treated lambs similarly. In conclusion, hyperventilation affected the pulmonary circulation by respiratory alkalosis not by mechanical factors and prostaglandins did not mediate its effects.
6-Ketoprostaglandin F1 alpha↗
[STUDY OF THE PULMONARY CIRCULATION USING THE ELECTROKYMOGRAPHIC METHOD IN THROMBOSIS AND EMBOLISM OF THE PULMONARY ARTERY].
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Electrokymography↗
[A new dilution method for the investigation of the pulmonary circulation and the relationship between pulmonary and bronchial arteries (author's transl)].
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Bronchial Arteries↗
[Cardiohemodynamics and pulmonary circulation in patients with recurrent infiltrative pulmonary tuberculosis].
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Adult↗
Leukocyte changes in the pulmonary circulation. A mechanism of acute pulmonary injury by various stimuli.
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Animals↗