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Circulation Jan 1966
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Basic Research in Cardiology May 2017Vasopressors are widely used in resuscitation, ventricular failure, and sepsis, and often induce pulmonary hypertension with undefined mechanisms. We hypothesize that...
Vasopressors are widely used in resuscitation, ventricular failure, and sepsis, and often induce pulmonary hypertension with undefined mechanisms. We hypothesize that vasopressor-induced pulmonary hypertension is caused by increased pulmonary blood volume and tested this hypothesis in dogs under general anesthesia. In normal hearts (model 1), phenylephrine (2.5 μg/kg/min) transiently increased right but decreased left cardiac output, associated with increased pulmonary blood volume (63% ± 11.8, P = 0.007) and pressures in the left atrium, pulmonary capillary, and pulmonary artery. However, the trans-pulmonary gradient and pulmonary vascular resistance remained stable. These changes were absent after decreasing blood volume or during right cardiac dysfunction to reduce pulmonary blood volume (model 2). During double-ventricle bypass (model 3), phenylephrine (1, 2.5 and 10 μg/kg/min) only slightly induced pulmonary vasoconstriction. Vasopressin (1U and 2U) dose-dependently increased pulmonary artery pressure (52 ± 8.4 and 71 ± 10.3%), but did not cause pulmonary vasoconstriction in normally beating hearts (model 1). Pulmonary artery and left atrial pressures increased during left ventricle dysfunction (model 4), and further increased after phenylephrine injection by 31 ± 5.6 and 43 ± 7.5%, respectively. In conclusion, vasopressors increased blood volume in the lung with minimal pulmonary vasoconstriction. Thus, this pulmonary hypertension is similar to the hemodynamic pattern observed in left heart diseases and is passive, due to redistribution of blood from systemic to pulmonary circulation. Understanding the underlying mechanisms may improve clinical management of patients who are taking vasopressors, especially those with coexisting heart disease.
Topics: Animals; Dogs; Hemodynamics; Hypertension, Pulmonary; Pulmonary Circulation; Vasoconstrictor Agents
PubMed: 28258299
DOI: 10.1007/s00395-017-0611-8 -
European Heart Journal Dec 2016
Topics: Pulmonary Circulation
PubMed: 28062589
DOI: 10.1093/eurheartj/ehw537 -
Romanian Journal of Morphology and... 2011Bronchial circulation has three components: a systemic arterial component represented by the bronchial arteries; a pulmonary venous component represented by the...
Bronchial circulation has three components: a systemic arterial component represented by the bronchial arteries; a pulmonary venous component represented by the pulmonary veins; and a systemic venous component represented by the bronchial veins. We have used vascular casting, microscope dissection coupled with tracers and light microscopy to define the detailed anatomy of the pulmonary venous compartment of the bronchial circulation. We have found that the extrapulmonary drainage territory of the pulmonary veins correlate with the forming pattern of the right superior pulmonary vein. In the case of a large apical venous trunk, pulmonary veins drain the venous blood of the main bronchia, terminal portion of the trachea and of the tracheobronchial lymph nodes. In the case of the systemic venous drainage of the extrapulmonary airways, we constantly found a pulmonary component which drains the venous blood from the subcarinal lymph nodes and the medial side of the main bronchia.
Topics: Humans; Pulmonary Circulation; Pulmonary Veins
PubMed: 21655643
DOI: No ID Found -
Federation Proceedings Sep 1978
Topics: Pulmonary Circulation
PubMed: 689170
DOI: No ID Found -
Clinics in Perinatology Mar 2024Fetal lungs have fewer and smaller arteries with higher pulmonary vascular resistance (PVR) than a newborn. As gestation advances, the pulmonary circulation becomes more... (Review)
Review
Fetal lungs have fewer and smaller arteries with higher pulmonary vascular resistance (PVR) than a newborn. As gestation advances, the pulmonary circulation becomes more sensitive to changes in pulmonary arterial oxygen tension, which prepares them for the dramatic drop in PVR and increase in pulmonary blood flow (PBF) that occur when the baby takes its first few breaths of air, thus driving the transition from fetal to postnatal circulation. Dynamic and intricate regulatory mechanisms control PBF throughout development and are essential in supporting gas exchange after birth. Understanding these concepts is crucial given the role the pulmonary vasculature plays in the development of complications with transition, such as in the setting of persistent pulmonary hypertension of the newborn and congenital heart disease. An improved understanding of pulmonary vascular regulation may reveal opportunities for better clinical management.
Topics: Pregnancy; Infant, Newborn; Female; Humans; Lung; Fetus; Pulmonary Circulation; Prenatal Care; Vascular Resistance
PubMed: 38325936
DOI: 10.1016/j.clp.2023.11.003 -
Anesthesiology Apr 2015Hypoxic pulmonary vasoconstriction (HPV) represents a fundamental difference between the pulmonary and systemic circulations. HPV is active in utero, reducing pulmonary... (Review)
Review
Hypoxic pulmonary vasoconstriction (HPV) represents a fundamental difference between the pulmonary and systemic circulations. HPV is active in utero, reducing pulmonary blood flow, and in adults helps to match regional ventilation and perfusion although it has little effect in healthy lungs. Many factors affect HPV including pH or PCO2, cardiac output, and several drugs, including antihypertensives. In patients with lung pathology and any patient having one-lung ventilation, HPV contributes to maintaining oxygenation, so anesthesiologists should be aware of the effects of anesthesia on this protective reflex. Intravenous anesthetic drugs have little effect on HPV, but it is attenuated by inhaled anesthetics, although less so with newer agents. The reflex is biphasic, and once the second phase becomes active after about an hour of hypoxia, this pulmonary vasoconstriction takes hours to reverse when normoxia returns. This has significant clinical implications for repeated periods of one-lung ventilation.
Topics: Anesthetics, Inhalation; Animals; Humans; Hypoxia; Lung; Pulmonary Circulation; Vasoconstriction
PubMed: 25587641
DOI: 10.1097/ALN.0000000000000569 -
Indian Heart Journal 2017The diagnosis of idiopathic dilatation of pulmonary artery is challenging because its clinical recognition is difficult and various other causes of dilated pulmonary... (Review)
Review
The diagnosis of idiopathic dilatation of pulmonary artery is challenging because its clinical recognition is difficult and various other causes of dilated pulmonary artery need to be excluded. The clinical findings mimic various common cardiac disorders and both invasive and non-invasive investigations should be done to arrive at the diagnosis. It is a known clinical entity but etiology and pathophysiology are largely unknown. The current echocardiographic and catheterization based diagnostic criteria, may not be satisfied completely in a particular patient and need to be revisited in view of newer imaging modalities. There is paucity of information about the natural history of the disease with attendant lack of clarity in treatment guidelines. Certain cases may progress to huge dilatation and consequent serious implications. It is a rare disease and is the diagnosis of exclusion.
Topics: Dilatation, Pathologic; Humans; Pulmonary Artery; Pulmonary Circulation; Ultrasonography, Doppler; Vascular Diseases
PubMed: 28228295
DOI: 10.1016/j.ihj.2016.07.009 -
The American Review of Respiratory... Oct 1989
Review
Topics: Humans; Hyperplasia; Hypertrophy; Lung; Mesoderm; Pulmonary Circulation; Vascular Diseases
PubMed: 2679262
DOI: 10.1164/ajrccm/140.4.1093 -
Nihon Rinsho. Japanese Journal of... Nov 2008Remodeling of the lung's vascular structure is the critical abnormality in the various types of pulmonary hypertension, including pulmonary arterial hypertension.... (Review)
Review
Remodeling of the lung's vascular structure is the critical abnormality in the various types of pulmonary hypertension, including pulmonary arterial hypertension. Pulmonary hypertension consists of some structural changes and an adaptation to its presence (perhaps reversible component, including vasoconstriction). However, once pulmonary hypertension is a recognizable clinical problem, its basis is structural. The research for mediators of cell injury and tissue remodeling has been one of the most active fields of biomedical study. It offers an embarrassingly wide array of candidates for the cellular events. The normal structure of the lung's vascular bed holds the key to its remodeling. The cast of cells is similar at all levels of the pulmonary vascular bed, yet the various segments have special features and different patterns of response.
Topics: Humans; Hypertension, Pulmonary; Pulmonary Artery; Pulmonary Circulation
PubMed: 19051719
DOI: No ID Found