Pulmonary Circulation

Grover, Robert F.; Wagner, Wiltz W.; McMurtry, Ivan F.; Reeves, John Τ.

doi:10.1002/cphy.cp020304

Cited by 34 publications

(54 citation statements)

References 311 publications

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“…At an elevation of 3,000 m, Pi,O 2 is one third lower than at sea level. People born and living in Leadville, Colorado, USA, 3,100 m above sea level (ASL), have mild PH (mean PAP524 mmHg) [92]. At the elevation of 5,000 m, Pi,O2 equals 75 mmHg.…”

Section: Intermittent Hypoxia In Copd Patients On Long-term Oxygen Trmentioning

confidence: 99%

Effects of intermittent hypoxia on pulmonary haemodynamics: animal models versus studies in humans

Zieliński¹

2005

European Respiratory Journal

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The aim of this review was to analyse the effects of intermittent hypoxia (IH) on pulmonary haemodynamics, comparing results of animal experiments with results of clinical studies.In animal investigations even short hypoxic exposure, continuously or in short repeated episodes mimicking obstructive sleep apnoea (OSA), leads to pulmonary artery remodelling and to pulmonary hypertension (PH). Results of investigations on effects of nocturnal IH on pulmonary haemodynamics in patients with chronic obstructive pulmonary disease (COPD) are discordant. Earlier studies reported the development of mild PH in subjects desaturating during sleep, while more recent investigations did not confirm those findings.Alveolar IH developing during apnoeic episodes during sleep in OSA patients is a diseaseinduced model to study its effects on pulmonary haemodynamics. In the majority of studies in OSA patients pulmonary arterial pressure remained within normal values. PH was found in patients with OSA accompanied by COPD and/or extreme obesity.People commuting between lowland and high altitude due to their employment, are also repeatedly exposed to IH. Results of clinical investigations suggest that it did not lead to the development of permanent PH.The mechanisms of discrepancies between effects of intermittent hypoxia in animal models and in humans remain to be studied.

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Section: Intermittent Hypoxia In Copd Patients On Long-term Oxygen Trmentioning

confidence: 99%

Effects of intermittent hypoxia on pulmonary haemodynamics: animal models versus studies in humans

Zieliński¹

2005

European Respiratory Journal

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“…Under physiological conditions, pulmonary arterioles are thin-walled vessels with the media occupying only 7% of the vessel thickness. The major finding in remodeled vessels caused by a chronic stimulus like hypoxia is the increase in SMCs in already muscularized arteries and extension of SMCs into vessels that are normally thin and nonmuscular (12) and thickening of the adventitial layer (13). Thickening of the adventitial layer is the result of marked proliferation of the fibroblasts, which has been shown to be modulated by protein kinase C and mitogen-activated protein kinase (14).…”

Section: Vascular Remodelingmentioning

confidence: 99%

Management of Pulmonary Hypertension: Physiological and Pharmacological Considerations for Anesthesiologists

Fischer¹,

Aken²,

Rkle³

2003

Anesthesia & Analgesia

171

108

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F or decades the pulmonary circulation was not considered as important as the systemic ("greater") circulation. However, pulmonary hypertension can arise because of many diseases of the heart and lung. Therefore, increasing efforts in research have been undertaken leading to a profound increase in understanding pulmonary vascular physiology and pathophysiology. This review discusses basic physiology, clinical concepts, and treatment options for pulmonary hypertension and the related right ventricular heart failure focusing on secondary pulmonary hypertension in patients during anesthetic procedures. Physiology of Pulmonary CirculationThe pulmonary vascular bed is a high-flow, lowpressure circulation system. Pulmonary vessels have less resistance in comparison to the systemic circulation under normal conditions because of higher compliance of pulmonary precapillary arterioles with a thinner media and less smooth muscle cells (SMCs) compared with the corresponding systemic arterioles. In addition, the cross-sectional area of the pulmonary vascular bed is large and highly distensible with recruitable vessels available to accommodate increase in flow resulting in low pressure and low resistance.In contrast to the systemic arteries, pulmonary vessels constrict with hypoxia (Euler-Liljestrand reflex) and relax in the presence of hyperoxia. Furthermore, changes in cardiac output (CO), airway pressure, and gravity affect the pulmonary more than the systemic circulation. Increases in CO distend open vessels and recruit previously closed vessels. Therefore, the crosssectional area of pulmonary circulation enlarges and results in a decrease in pulmonary vascular resistance (PVR). An increase in CO has very little effect on pulmonary arterial pressure (PAP) because of the recruitment and distension of pulmonary vessels. An increased PAP or left atrial pressure (LAP) may also distend and recruit pulmonary vessels. Clinically, this means that enhanced CO caused by the administration of inotropic drugs or enlarged blood volume will passively decrease PVR.

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“…The historical concepts (233) and anatomy (635) of the pulmonary circulation, comparative physiology (686), effects of exercise (445) and high altitude (233), the mechanics (172) and distribution of blood flow (217,220), and mechanisms matching ventilation and perfusion (161,172,220) have been covered extensively in previous reviews. In this article, we will focus on reviewing the basics of the lung circulation (pulmonary and bronchial), normal development and transition at birth, and vasoregulation.…”

Section: Introductionmentioning

confidence: 99%

Lung Circulation

Suresh

Shimoda

2016

Comprehensive Physiology

104

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The circulation of the lung is unique both in volume and function. For example, it is the only organ with two circulations: the pulmonary circulation, the main function of which is gas exchange, and the bronchial circulation, a systemic vascular supply that provides oxygenated blood to the walls of the conducting airways, pulmonary arteries and veins. The pulmonary circulation accommodates the entire cardiac output, maintaining high blood flow at low intravascular arterial pressure. As compared with the systemic circulation, pulmonary arteries have thinner walls with much less vascular smooth muscle and a relative lack of basal tone. Factors controlling pulmonary blood flow include vascular structure, gravity, mechanical effects of breathing, and the influence of neural and humoral factors. Pulmonary vascular tone is also altered by hypoxia, which causes pulmonary vasoconstriction. If the hypoxic stimulus persists for a prolonged period, contraction is accompanied by remodeling of the vasculature, resulting in pulmonary hypertension. In addition, genetic and environmental factors can also confer susceptibility to development of pulmonary hypertension. Under normal conditions, the endothelium forms a tight barrier, actively regulating interstitial fluid homeostasis. Infection and inflammation compromise normal barrier homeostasis, resulting in increased permeability and edema formation. This article focuses on reviewing the basics of the lung circulation (pulmonary and bronchial), normal development and transition at birth and vasoregulation. Mechanisms contributing to pathological conditions in the pulmonary circulation, in particular when barrier function is disrupted and during development of pulmonary hypertension, will also be discussed.

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Pulmonary Circulation

Cited by 34 publications

References 311 publications

Effects of intermittent hypoxia on pulmonary haemodynamics: animal models versus studies in humans

Effects of intermittent hypoxia on pulmonary haemodynamics: animal models versus studies in humans

Management of Pulmonary Hypertension: Physiological and Pharmacological Considerations for Anesthesiologists

Lung Circulation

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