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JAMA Cardiology Jan 2022The recognition of the pulmonary circulation is a complex evolution in medical history and draws on theories across eras and cultures. (Review)
Review
IMPORTANCE
The recognition of the pulmonary circulation is a complex evolution in medical history and draws on theories across eras and cultures.
OBSERVATIONS
This narrative review summarizes evidence suggesting that the recognition of pulmonary circulation is older than the time of Ibn Nafis. The theory of pulmonary circulation originated in ancient Persia (ad 224-637), was overshadowed by Greek theory from the 11th century, and reestablished by Ibn Nafis in the 13th century.
CONCLUSIONS AND RELEVANCE
The findings of this review may help contextualize the story of the discovery of pulmonary circulation in ancient Persian and Greek theories before Ibn Nafis.
Topics: Cardiology; Greece; History, 15th Century; History, 16th Century; History, 17th Century; History, 18th Century; History, 19th Century; History, 20th Century; History, Ancient; History, Medieval; Humans; Persia; Pulmonary Circulation
PubMed: 34550308
DOI: 10.1001/jamacardio.2021.3520 -
Current Hypertension Reports Dec 2013The pulmonary circulation is a high-flow and low-pressure circuit. The functional state of the pulmonary circulation is defined by pulmonary vascular pressure-flow... (Review)
Review
The pulmonary circulation is a high-flow and low-pressure circuit. The functional state of the pulmonary circulation is defined by pulmonary vascular pressure-flow relationships conforming to distensible vessel models with a correction for hematocrit. The product of pulmonary arterial compliance and resistance is constant, but with a slight decrease as a result of increased pulsatile hydraulic load in the presence of increased venous pressure or proximal pulmonary arterial obstruction. An increase in left atrial pressure is transmitted upstream with a ratio ≥1 for mean pulmonary artery pressure and ≤1 the diastolic pulmonary pressure. Therefore, the diastolic pressure gradient is more appropriate than the transpulmonary pressure gradient to identify pulmonary vascular disease in left heart conditions. Exercise is associated with a decrease in pulmonary vascular resistance and an increase in pulmonary arterial compliance. Right ventricular function is coupled to the pulmonary circulation with an optimal ratio of end-systolic to arterial elastances of 1.5-2.
Topics: Animals; Exercise; Heart; Humans; Hypertension; Lung; Pulmonary Circulation; Vascular Resistance
PubMed: 24097187
DOI: 10.1007/s11906-013-0396-6 -
Seminars in Respiratory and Critical... Oct 2023The pulmonary circulation is a low-pressure, low-resistance circuit whose primary function is to deliver deoxygenated blood to, and oxygenated blood from, the pulmonary... (Review)
Review
The pulmonary circulation is a low-pressure, low-resistance circuit whose primary function is to deliver deoxygenated blood to, and oxygenated blood from, the pulmonary capillary bed enabling gas exchange. The distribution of pulmonary blood flow is regulated by several factors including effects of vascular branching structure, large-scale forces related to gravity, and finer scale factors related to local control. Hypoxic pulmonary vasoconstriction is one such important regulatory mechanism. In the face of local hypoxia, vascular smooth muscle constriction of precapillary arterioles increases local resistance by up to 250%. This has the effect of diverting blood toward better oxygenated regions of the lung and optimizing ventilation-perfusion matching. However, in the face of global hypoxia, the net effect is an increase in pulmonary arterial pressure and vascular resistance. Pulmonary vascular resistance describes the flow-resistive properties of the pulmonary circulation and arises from both precapillary and postcapillary resistances. The pulmonary circulation is also distensible in response to an increase in transmural pressure and this distention, in addition to recruitment, moderates pulmonary arterial pressure and vascular resistance. This article reviews the physiology of the pulmonary vasculature and briefly discusses how this physiology is altered by common circumstances.
Topics: Humans; Vasoconstriction; Vascular Resistance; Lung; Pulmonary Circulation; Hypoxia; Blood Pressure
PubMed: 37816344
DOI: 10.1055/s-0043-1770059 -
Comprehensive Physiology Jul 2011Two selective pressures have shaped the evolution of the pulmonary circulation. First, as animals evolved from heterothermic ectotherms to homeothermic endoderms with... (Review)
Review
Two selective pressures have shaped the evolution of the pulmonary circulation. First, as animals evolved from heterothermic ectotherms to homeothermic endoderms with their corresponding increase in the ability to sustain high oxygen consumptions, the blood-gas barrier had to become successively thinner, and also provide an increasingly large area for diffusive gas exchange. Second, the barrier had to find a way to maintain its mechanical integrity in the face of extreme thinness, and this was assisted by the increasing separation of the pulmonary from the systemic circulation. A remarkable feature throughout the evolution of air-breathing vertebrates has been the tight conservation of the tripartite structure of the blood-gas barrier with its three layers: capillary endothelium, extracellular matrix, and alveolar epithelium. The strength of the barrier can be ascribed to the very thin layer of type IV collagen in the extracellular matrix. In the phylogenic progression from amphibia and reptiles to mammals and birds, the blood-gas barrier became successively thinner. Also, the area increased greatly reflecting the greater oxygen demands of the organism. The gradual separation of the pulmonary from the systemic circulation continued from amphibia through reptiles to mammals and birds. Only in the last two classes are the circulations completely separate with the result that the pulmonary capillary pressures can be maintained low enough to avoid stress failure of the blood-gas barrier. Remarkably, the barrier is generally much thinner in birds than mammals, and it is also much more uniform in thickness. These advantages for gas exchange can be explained by the support of avian pulmonary capillaries by the surrounding air capillaries. This arrangement was made possible by the adoption of the flow-through system of ventilation in birds as opposed to the reciprocating pattern in mammals.
Topics: Animals; Biological Evolution; Gills; Humans; Lung; Phylogeny; Pulmonary Circulation; Pulmonary Gas Exchange; Vertebrates
PubMed: 23733652
DOI: 10.1002/cphy.c090001 -
Terapevticheskii Arkhiv 2006
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General Pharmacology Jun 19961. Neutral endopeptidase (NEP) EC 3.4.24.11 is a zinc-metallopeptidase which is partly responsible for the degradation of atrial natriuretic peptide (ANP) in vivo. 2.... (Review)
Review
1. Neutral endopeptidase (NEP) EC 3.4.24.11 is a zinc-metallopeptidase which is partly responsible for the degradation of atrial natriuretic peptide (ANP) in vivo. 2. ANP inhibits vascular smooth muscle cell proliferation, and elicits vasorelaxation of the systemic and, more potently, the pulmonary vasculature. Plasma ANP levels are elevated in human disease states characterized by pulmonary hypertension, and in animal models of these diseases. 3. However, the short in vivo half-life of ANP suggests that it has limited therapeutic potential. Therefore, it has been hypothesized that inhibition of the metabolism of ANP may prove successful in the treatment of pulmonary hypertension. 4. Several inhibitors of NEP have been shown to reduce the development of pulmonary hypertension secondary to chronic hypoxia in rats. In addition, the inhibitor SCH 42495, partially reversed the established cardio-pulmonary remodelling associated with this disease model, without elevating plasma ANP levels. 5. The physiological actions of ANP are many of the properties desirable in a treatment for pulmonary hypertension. Thus, attenuating the metabolism of this peptide using NEP inhibitors, should potentially enhance the effects of ANP, either by maintaining plasma levels or at a local, tissue level.
Topics: Animals; Atrial Natriuretic Factor; Humans; Neprilysin; Pulmonary Circulation; Rats
PubMed: 8853287
DOI: 10.1016/0306-3623(95)02051-9 -
Seminars in Respiratory and Critical... Dec 2023The right ventricle plays a pivotal role in patients with pulmonary hypertension (PH). Its adaptation to pressure overload determines a patient's functional status as... (Review)
Review
The right ventricle plays a pivotal role in patients with pulmonary hypertension (PH). Its adaptation to pressure overload determines a patient's functional status as well as survival. In a healthy situation, the right ventricle is part of a low pressure, high compliance system. It is built to accommodate changes in preload, but not very well suited for dealing with pressure overload. In PH, right ventricular (RV) contractility must increase to maintain cardiac output. In other words, the balance between the degree of RV contractility and afterload determines stroke volume. Hypertrophy is one of the major hallmarks of RV adaptation, but it may cause stiffening of the ventricle in addition to intrinsic changes to the RV myocardium. Ventricular filling becomes more difficult for which the right atrium tries to compensate through increased stroke work. Interaction of RV diastolic stiffness and right atrial (RA) function determines RV filling, but also causes vena cava backflow. Assessment of RV and RA function is critical in the evaluation of patient status. In recent guidelines, this is acknowledged by incorporating additional RV parameters in the risk stratification in PH. Several conventional parameters of RV and RA function have been part of risk stratification for many years. Understanding the pathophysiology of RV failure and the interactions with the pulmonary circulation and right atrium requires consideration of the unique RV anatomy. This review will therefore describe normal RV structure and function and changes that occur during adaptation to increased afterload. Consequences of a failing right ventricle and its implications for RA function will be discussed. Subsequently, we will describe RV and RA assessment in clinical practice.
Topics: Humans; Hypertension, Pulmonary; Heart Ventricles; Pulmonary Circulation; Heart Failure; Stroke Volume; Ventricular Function, Right; Ventricular Dysfunction, Right
PubMed: 37487527
DOI: 10.1055/s-0043-1770117 -
Minerva Anestesiologica May 2000Nitric oxide (NO) is synthetized throughout the body by the enzyme NO synthase (NOS), cyclic GMP transduction pathway causes pulmonary vasodilatation anti-platelets... (Review)
Review
Nitric oxide (NO) is synthetized throughout the body by the enzyme NO synthase (NOS), cyclic GMP transduction pathway causes pulmonary vasodilatation anti-platelets aggregation and inhibition of leukocyte adhesion. Inducible NOS is expressed in leukocytes in response to a variety of inflammatory stimuli and can be inhibited by corticosteroids. Inhaled NO is a selective pulmonary vasodilator. In USA inhaled NO was approved by FDA for hypoxemic respiratory failure in infants and children. In adults it may be useful in various clinical therapy: pulmonary hypertension, lung transplantation, ARDS but new clinical investigations are necessary.
Topics: Administration, Inhalation; Humans; Lung; Nitric Oxide; Pulmonary Circulation
PubMed: 10965707
DOI: No ID Found -
Acta Anaesthesiologica Scandinavica.... 1990
Review
Topics: Blood Pressure; Cardiac Output; Humans; Positive-Pressure Respiration; Pressure; Pulmonary Circulation; Respiration, Artificial; Respiratory Mechanics
PubMed: 2291390
DOI: 10.1111/j.1399-6576.1990.tb03223.x -
American Heart Journal Oct 2016Pulmonary hypertension is usually related to obstruction of pulmonary blood flow at the level of the pulmonary arteries (eg, pulmonary embolus), pulmonary arterioles... (Review)
Review
Pulmonary hypertension is usually related to obstruction of pulmonary blood flow at the level of the pulmonary arteries (eg, pulmonary embolus), pulmonary arterioles (idiopathic pulmonary hypertension), pulmonary veins (pulmonary venoocclusive disease) or mitral valve (mitral stenosis and regurgitation). Pulmonary hypertension is also observed in heart failure due to left ventricle myocardial diseases regardless of the ejection fraction. Pulmonary hypertension is often regarded as a passive response to the obstruction to pulmonary flow. We review established fluid dynamics and physiology and discuss the mechanisms underlying pulmonary hypertension. The important role that the right ventricle plays in the development and maintenance of pulmonary hypertension is discussed. We use principles of thermodynamics and discuss a potential common mechanism for a number of disease states, including pulmonary edema, through adding pressure energy to the pulmonary circulation.
Topics: Humans; Hydrodynamics; Hypertension, Pulmonary; Pulmonary Circulation; Thermodynamics
PubMed: 27659877
DOI: 10.1016/j.ahj.2016.07.003