[Effect of Deseril on respiration and the pulmonary circulation with regard to the mechanism of development of "capillary" pulmonary hypertension].
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Capillaries↗
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Increasing oxygen tension dilates fetal pulmonary circulation via endothelium-derived relaxing factor.
We examined the role of endothelium-derived relaxing factor (EDRF) in the increase in pulmonary blood flow caused by increasing oxygen tension in the lungs of the fetus. Fetal lambs at 133 days of gestation were instrumented for intrauterine measurement of pulmonary arterial, left atrial, and amniotic fluid pressure and pulmonary blood flow. Three days later oxygen tension in the pulmonary arterial blood of the fetus was doubled by having the ewe breathe 100% oxygen at 3 atm absolute pressure. In the control fetuses (n = 5), hyperbaric oxygenation increased pulmonary blood flow eightfold. Blocking EDRF production by infusing 45 mg of NG-monomethyl-L-arginine into the superior vena cava of the fetus over 5 min starting 30 min after the beginning of hyperbaric oxygen reversed the increase in pulmonary blood flow (n = 5). Blocking EDRF production by infusing NG-nitro-L-arginine at 1 mg/min for 60 min starting 30 min before hyperbaric oxygen blunted the initial increase in pulmonary blood flow and eliminated it by the end of the experiment (n = 5). As hyperbaric oxygen did not significantly alter pulmonary arterial or left atrial pressure, changes in pulmonary vascular conductance paralleled those in pulmonary blood flow. We conclude that the majority of the vasodilation of the fetal pulmonary circulation caused by increasing oxygen tension is mediated by EDRF. We speculate that EDRF is involved in maintaining low vascular tone at the relatively high oxygen tension of the postnatal lung.
Animals↗
Inhibition of cyclic 3'-5'-guanosine monophosphate-specific phosphodiesterase selectively vasodilates the pulmonary circulation in chronically hypoxic rats.
While it is known that nitric oxide (NO) is an important modulator of tone in the hypertensive pulmonary circulation, the roles of cyclic 3'-5'-guanosine monophosphate (cGMP) and cGMP-phosphodiesterase (PDE) are uncertain. We found that isolated lung perfusate levels of cGMP were over ninefold elevated in hypertensive vs. normotensive control rats. 98-100% of lung cGMP hydrolytic activity was cGMP-specific PDE5, with no significant decrease in PDE activity in hypertensive lungs, suggesting that the elevation in cGMP was due to accelerated production rather than reduced degradation. In pulmonary hypertensive rat lungs, in vitro, cGMP-PDE inhibition by E4021[1-(6-chloro-4-(3,4-methylbenzyl) amino-quinazolin-2-yl)piperdine-4-carboxylate], increased perfusate cGMP threefold, reduced hypoxic vasoconstriction by 58 +/- 2%, and reduced baseline pulmonary artery pressure by 37 +/- 5%. In conscious, pulmonary hypertensive rats, intravenous administration of E4021 reduced hypoxic vasoconstriction by 68 +/- 8%, pulmonary artery pressure by 12.6 +/- 3.7% and total pulmonary resistance by 13.1 +/- 6.4%, with no significant effect on cardiac output, systemic pressure, and resistance. Comparison of E4021 to inhaled nitric oxide demonstrated that cGMP-PDE inhibition was as selective and as effective as inhaled NO.
3',5'-Cyclic-GMP Phosphodiesterases↗
Multi-detector row CT angiography of pulmonary circulation with gadolinium-based contrast agents: prospective evaluation in 60 patients.
PURPOSE: To prospectively evaluate gadolinium dose safety and effectiveness for 16-detector pulmonary computed tomographic (CT) angiography. MATERIALS AND METHODS: Ethics committee approval and informed consent were obtained. Sixty patients with contraindications to iodine underwent CT of the pulmonary circulation with 0.5 mmol/L gadolinium chelate given at either 0.3 (n = 29, group A) or 0.4 (n = 31, group B) mmol/kg; clinical and biologic tolerances were evaluated. Enhancement of central and segmental pulmonary arteries was measured (poor enhancement, <100 HU; good, 100-150 HU; excellent, >150 HU). Subsegmental artery enhancement was assessed as similar or inferior to that of segmental arteries. Confidence in analysis of the pulmonary arterial bed was graded according to arterial enhancement: Grades 1-3, diagnostic images; grade 4, nondiagnostic. The main effectiveness parameter for comparison between groups A and B was diagnostic value of CT angiograms. Nonparametric statistics were used to analyze results. RESULTS: The mean (+/- standard deviation) contrast material volume was 50.09 mL +/- 8.45 (all patients: range, 30-64 mL; group A: 46.54 mL +/- 8.59; group B: 53.42 mL +/- 6.92). Diagnostic images were obtained in 55 (92%) patients, and confident analysis of pulmonary arteries to the subsegmental level was achieved in 26 (grade 1, 44%) and to the segmental level, in 21 (grade 2, 35%). Mean attenuation was higher in group B than in group A in central (180.61 HU +/- 53.85 vs 148.14 HU +/- 52.61; P = .04) and segmental (201.59 HU +/- 54.70 vs 164.73 HU +/- 59.26; P = .03) arteries. Number of diagnostic CT angiograms was higher (P = .02) in group B (n = 31 [100%]) than in group A (n = 24 [83%]). In both groups, mean enhancement of pulmonary arteries was significantly higher at 80 or 100 kV than at 120 kV. Renal function was impaired in two group A patients. CONCLUSION: Gadolinium chelates may be used as an alternative CT contrast agent in patients who cannot receive iodine.
Adult↗
Left ventricular performance and pulmonary circulation following addition of nitrous oxide to morphine during coronary-artery surgery.
The effects of nitrous oxide on ventricular performance and pulmonary circulation were studied in 12 patients with angiographically demonstrated coronary-artery disease and normal ventricular contractility who had received 2 mg/kg morphine intravenously. Seventeen studies were performed intraoperatively, five before and 12 after cardiopulmonary bypass and myocardial revascularization. Recordings were obtained during oxygen breathing and during nitrous oxide administration. Fifty per cent nitrous oxide significantly decreased mean arterial pressure (P less than 0.05), cardiac index (P less than 0.01), stroke index (P less than 0.01), left ventricular stroke work index (P less than 0.01), peak left ventricular dP/dt (P less than 0.05) and dP/dt/P (P less than 0.01), and heart rate-systolic arterial pressure product (P less than 0.01). Mean pulmonary arterial pressure (P less than 0.05), pulmonary artery occluded pressure (P less than 0.01), left ventricular end-diastolic pressure (P less than 0.01) and pulmonary vascular resistance (P less than 0.05) increased. Heart rate, right atrial pressure and systemic vascular resistance remained unchanged. When nitrous oxide was discontinued, all variables returned to control except mean pulmonary arterial pressure and pulmonary vascular resistance. Responses were similar before and after cardiopulmonary bypass and myocardial revascularization. These findings suggest that nitrous oxide depresses left ventricular performance when administered intraoperatively to patients who have received large doses of morphine for coronary-artery surgery. Nitrous oxide also increases pulmonary vascular resistance, possibly via alpha-adrenergic stimulation.
Anesthesia, Inhalation↗
The effects of dopamine and isoproterenol on the pulmonary circulation.
Dopamine and isoproterenol, although used primarily for their inotropic effects, are also potent vasoactive substances. To determine their effects on the pulmonary circulation, we cannulated the left lower lobe bronchus in 20 dogs to permit ventilation with either air or a mixture of 95% nitrogen and 5% carbon dioxide; systemic oxygenation was maintained by venitlating the right lung with 95% oxygen. The lobe was perfused at a controlled flow rate and left atrial pressure was held constant. Hypoxic ventilation increased the lobar vascular resistance by 52% (p less than 0.001). Dopamine infusion (20 mcg. per kilogram per minute) during air ventilation also increased lobar vascular resistance by 50% (p less than 0.001). During hypoxic ventilation, dopamine increased the resistance by an additional 19% (p less than 0.001). In contrast, isoproterenol (0.2 mcg. per kilogram per minute) abolished the hypoxic pressor response (p less than 0.001). Combined alpha- and beta-adrenergic blockade did not alter hypoxia-induced vasoconstriction, whereas phentolamine blocked the dopamine response and propranolol abolished the isoproterenol-induced vasodilation. These results indicate the following: (1) The hypoxic pressor response is independent of sympathetic innervation; (2) dopamine in dogs is a pulmonary vasoconstrictor; and (3) isoproterenol is a pulmonary vasodilator. If these findings can be extrapolated to man, isoproterenol may be the preferred inotropic agent in patients with an elevated pulmonary vascular resistance.
Adrenergic alpha-Antagonists↗
Targeted delivery of therapeutic oligonucleotides to pulmonary circulation.
Functional oligodeoxynucleotides (ODN) such as antisense ODN (AS-ODN) show promise as new therapeutics for the treatment of a number of pulmonary diseases. They also hold potential to serve as a research tool for the study of gene function related to lung physiology. The success of their application is largely dependent on the development of an efficient delivery vehicle. This chapter summarizes work toward the development of lipidic vectors for targeted ODN delivery to pulmonary circulation. Recent advancements in the development of novel ODN are also discussed briefly.
Animals↗
A single skeletal muscle powered ventricle that assists both systemic and pulmonary circulations.
Extraaortic counterpulsation using skeletal muscle powered ventricles (SMPVs) has been studied mainly for the purpose of assisting the systemic circulation. The purpose of this study was to investigate the possibility of assisting both the systemic and pulmonary circulations using a single SMPV. An SMPV that counterpulses the systemic circulation is placed beside the right atrium (RA) or the right ventricle (RV), the former after procedures such as a Fontan operation, and the latter in cases of biventricular failure. Because the SMPV dilates passively during cardiac systole, it is designed to press the RA or the RV directly from outside. This study is a preliminary report, and only the ability of a specially constructed SMPV to dilate was assessed. Using seven dogs with heart failure, the SMPV dilated with an internal pressure of 88 mmHg and 1.0 cm, while the volume inside increased by 10.8 ml. From these results, it is suggested that the SMPV has enough dilating power to press the RA or to assist the RV while counterpulsing the systemic circulation.
Animals↗
The pulmonary circulation: the radiology of adaptation.
In this George Simon Lecture, I have tried to present a simplistic yet philosophical approach to the physiological processes of adaptation of circulatory and respiratory function in response to pathophysiological challenge. The objective of the body is to achieve a normal ventilation-perfusion ratio of 1 in order to optimise blood-gas exchange in a wide variety of pathological conditions. It is all a question of the right ingredients (oxygen in atmospheric air and reduced haemoglobin in desaturated blood), in the right copious amounts (100 ml/s), in the right proportion (1:1) and in the right place (alveolar capillary membrane). In order to demonstrate the above concepts, a variety of well known conditions, congenital and acquired, have been discussed in the developing infant lung and the adult mature lung; some primarily cardiovascular, others primarily respiratory; some conditions resulting in permanent and others resulting in temporary and reversible major readjustments of the blood supply to the lung. The emphasis has been to illustrate that simple, unsophisticated radiological techniques may provide a substantial amount of valuable information concerning the remarkable capacity of the pulmonary circulation to adapt to varying physiological or pathological demands in order to conserve our precious respiratory resources. George Simon, like all good doctors, had a tremendous respect for the ability of the body to respond to these challenges. He always emphasised the important basic principles rather than fine minutiae. It is hoped that this lecture in his honour follows these principles which he preached so well.
Adaptation, Physiological↗
Effects of protamine on nitric oxide level in the pulmonary circulation.
Protamine reversal of heparin anticoagulation often causes systemic hypotension by releasing nitric oxide (NO) from vascular endothelium. We investigated the hypothesis that protamine prevents severe pulmonary vasoconstriction by increasing NO. Twenty patients undergoing elective coronary artery bypass graft surgery were included in the study. Nitrite and nitrate levels--as end-metabolites of NO--were measured in blood samples obtained before and after protamine administration. Mean arterial pressure, heart rate, mean pulmonary artery pressure, central venous pressure and left atrial pressure were noted as hemodynamic data. Nitrite levels were 4.64 +/- 0.67 mumol in the right atrium and 4.84 +/- 0.95 mumol in the left atrium before protamine administration. The difference was insignificant statistically. These measurements were 4.85 +/- 0.92 in the right atrium and 5.28 +/- 0.66 mumol in the left atrium after protamine administration. This increase was significant (p < 0.05). The measurements of nitrate levels were completely parallel with those of nitrite. Mean arterial pressures were 78.9 +/- 7.59 mm-Hg before protamine and 74.1 +/- 8.55 mm-Hg after protamine (p = 0.03). The changes in other hemodynamic parameters were not significant. Protamine augments NO production and prevents the pulmonary circulation from possible vasoconstriction.
Aged↗
Mechanism of epinephrine pulmonary edema. With special reference to relation of venous return to pulmonary circulation.
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Epinephrine↗
[Therapeutic problems in pulmonary circulation disorders].
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Humans↗
Pulmonary circulation, extravascular water, and solute flux as determined by positron emission tomography.
Pulmonary edema is the result of an increased transpulmonary flux of water and solute and a concomitant insufficiency of lung lymphatic drainage. Although this pathogenetic concept seems well-established, the microcirculatory details of pulmonary edema formation and its ultimate resolution are still poorly understood. For example, how do regional changes in pulmonary blood flow affect the resolution of pulmonary edema, and in turn, how do they affect pulmonary gas exchange? When does vascular permeability return to normal after acute lung injury? Is the severity of the permeability defect related to prognosis, and can therapy hasten either the resolution of altered permeability or the accumulation of extravascular lung water? These and similar questions are approachable with positron emission tomography (PET) and are outlined in this brief review.
Animals↗
[Effects of various forms of hypoxia and physical stress on pulmonary circulation].
In healthy persons, without respiratory abnormalities, by physical exercise and hypoxia pulmonary hypertension can be induced. It could be shown that increasing physical exercise has a more pronounced influence upon the value of PAP, whereas increasing hypoxia has a more pronounced influence upon PO2-V.
Adult↗
[Congenital pulmonary lymphangiectasis. One new case with complete blockage of the return venous pulmonary circulation and marked interstitial emphysema].
In this unusual case of bilateral congenital pulmonary lymphangiectasia with complete block of pulmonary venous return, the radiological diagnosis was made difficult by the association of the lymphangiectasia with bilateral interstitial emphysema. Routine dissection of the heart, considered to be normal since the cardio-thoracic index was only 0.45, relealed the true cause of death. The heart was the site of extreme hypoplasia of the left heart with complete mitral and aortic atresia. The ostium secundum being completely closed, the left atrium, after receiving the pulmonary veins, was completely blocked. It communicated neither with the right atrium, nor with the non-existent left ventricule.
Humans↗
Irreversibility of birth-related changes in the pulmonary circulation.
We hypothesized that establishing conditions of hypoxia and fluid filling of the airways in lungs of newborns would reproduce the high levels of pulmonary vascular resistance (PVR) observed in the fetal state. We assessed the hemodynamics of the left pulmonary circulation of 1- to 3-day-old lambs during a variety of airway states while attempting to reestablish fetal conditions. Eleven animals were studied during both normoxemia and hypoxemia in a baseline airway state with a positive end-expiratory pressure (PEEP) of 4 cm H2O, and in experimental airway states, of atelectasis, and fluid filling to 15 and 30 mL/kg and with PEEP of 12 cm H2O. PVR increased while pulmonary blood flow decreased with all airway state changes as compared to baseline, suggesting a passive mechanism for these changes. With the addition of hypoxemia there was a further increase in PVR in all states accompanied by an increase in pulmonary blood flow, indicating that active vasoconstriction was responsible for the increase in PVR. The combined effects of hypoxemia and fluid filling, designed to approximate the fetal state, increased PVR to only 20-30% of fetal values. Thus, additional factors appear to be important in maintaining the high PVR of the fetal state. We speculate that ventilation of the lungs at birth irreversibly alters these factors.
Animals↗
[Dyspnea in cardiac and emphysematous patients and some problems of the gas exchange. V. Calculation of the venous blood mixture with arterialized blood in the pulmonary circulation].
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Blood Circulation↗
Ventilatory effects of high and pulsatile blood flow in the pulmonary circulation.
The mechanism of ventilatory stimulation that accompanies increases in cardiac output is unknown. Previous studies addressing this issue have been inconclusive. However, only steady pulmonary blood flow was used. The effect of flow pulsatility merits consideration, because increasing cardiac output raises not only mean pulmonary arterial pressure but also pulse pressure; mechanoreceptors with an important dynamic component to their responses may cause a response to pulsatile, but not steady, flow. Studies were done on anesthetized cats (n = 4) and dogs (n = 4). The right pulmonary artery was cannulated within the pericardium, and systemic blood was pumped from the left atrium to the right pulmonary artery. The right pulmonary circulation was perfused at different levels of flow, which was either steady or pulsatile. Steady-state flow of up to 150 ml.kg-1.min-1 (270 ml.kg-1.min-1 when corrected for the proportion of lung tissue perfused) did not affect breathing pattern. When high pulmonary flow was made pulsatile (pulse pressure approximately 23 mmHg), breath duration decreased from 3.7 +/- 0.72 to 3.4 +/- 0.81 (SD) s (P less than 0.01), representing a change in frequency of only 9%. There was no change in peak inspiratory activity. It was concluded that pulmonary vascular mechanoreceptors are not likely to contribute significantly to the increase in ventilation in association with increases in cardiac output.
Animals↗