Pulmonary Circulation and Systemic Circulation: Similar Problems, Different Solutions

The extraction of α-angiotensin and its aminopeptidase-resiistant analogue β-angiotensin by the pulmonary, hepatoportal, femoral, and renal vascular beds was studied in normal anesthetized dogs and rats by comparing the systemic pressor responses to infusions into the afferent and efferent vessel of each organ. The extraction percentage of both peptides by the pulmonary circulation was negligible whereas it averaged 70% for α-angiotensin and 63% for the β-analogue in the other three systemic vascular beds studied. It is concluded that the main process responsible for the clearing of angiotensin from the systemic circulation is not the activity of circulating angiotensinases but rather occurs in the tissues.

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Maladaptive Pulmonary Vascular Responses to Chronic Sustained and Chronic Intermittent Hypoxia in Rat

Antioxidants ◽

10.3390/antiox11010054 ◽

2021 ◽

Vol 11 (1) ◽

pp. 54

Author(s):

Jesus Prieto-Lloret ◽

Elena Olea ◽

Ana Gordillo-Cano ◽

Inmaculada Docio ◽

Ana Obeso ◽

...

Keyword(s):

Pulmonary Hypertension ◽

Carotid Body ◽

Pulmonary Circulation ◽

Intermittent Hypoxia ◽

Pulmonary Arteries ◽

Systemic Circulation ◽

Systemic Hypertension ◽

Chronic Intermittent Hypoxia ◽

Respiratory Disorder ◽

Obstructive Sleep

Chronic sustained hypoxia (CSH), as found in individuals living at a high altitude or in patients suffering respiratory disorders, initiates physiological adaptations such as carotid body stimulation to maintain oxygen levels, but has deleterious effects such as pulmonary hypertension (PH). Obstructive sleep apnea (OSA), a respiratory disorder of increasing prevalence, is characterized by a situation of chronic intermittent hypoxia (CIH). OSA is associated with the development of systemic hypertension and cardiovascular pathologies, due to carotid body and sympathetic overactivation. There is growing evidence that CIH can also compromise the pulmonary circulation, causing pulmonary hypertension in OSA patients and animal models. The aim of this work was to compare hemodynamics, vascular contractility, and L-arginine-NO metabolism in two models of PH in rats, associated with CSH and CIH exposure. We demonstrate that whereas CSH and CIH cause several common effects such as an increased hematocrit, weight loss, and an increase in pulmonary artery pressure (PAP), compared to CIH, CSH seems to have more of an effect on the pulmonary circulation, whereas the effects of CIH are apparently more targeted on the systemic circulation. The results suggest that the endothelial dysfunction evident in pulmonary arteries with both hypoxia protocols are not due to an increase in methylated arginines in these arteries, although an increase in plasma SDMA could contribute to the apparent loss of basal NO-dependent vasodilation and, therefore, the increase in PAP that results from CIH.

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Effect of high intra-alveolar O2 tensions on pulmonary circulation in perfused lungs of dogs

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1965.208.1.130 ◽

1965 ◽

Vol 208 (1) ◽

pp. 130-138 ◽

Cited By ~ 5

Author(s):

G. J. A. Cropp

Keyword(s):

Blood Flow ◽

Pulmonary Vascular Resistance ◽

Vascular Resistance ◽

Pulmonary Circulation ◽

Time Course ◽

Systemic Circulation ◽

The Body ◽

Arterial Blood ◽

Pulmonary Parenchyma ◽

Pulmonary Arterial

The resistance to blood flow in the pulmonary circulation of dogs (PVR) increased when their lungs were ventilated with 95–100% oxygen and were perfused with blood that recirculated only through the pulmonary circulation; the systemic circulation was perfused independently. This increase in PVR occurred even when nerves were cut or blocked but was abolished by inhaled isopropylarterenol aerosol. Elevation of intra-alveolar Po2 without increase in pulmonary arterial blood Po2 was sufficient to increase pulmonary vascular resistance. The pulmonary venules or veins were thought to be the likely site of the constriction. These reactions were qualitatively similar to those produced by injection of serotonin or histamine into the pulmonary circulation. The time course of the response and failure to obtain it when the blood was perfused through the remainder of the body before it re-entered the pulmonary circulation are compatible with a theory that high intra-alveolar O2 tension activates a vasoconstrictor material in the pulmonary parenchyma.

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O79. Nitrite-associated hypoxic vasodilatation in man: The pulmonary circulation is more susceptible to the vasodilator effects of nitrite than the systemic circulation

Nitric Oxide ◽

10.1016/j.niox.2008.06.080 ◽

2008 ◽

Vol 19 ◽

pp. 38

Author(s):

Thomas E. Ingram ◽

Andrew G. Pinder ◽

Ellen Pittaway ◽

Alan G. Fraser ◽

Philip E. James

Keyword(s):

Pulmonary Circulation ◽

Systemic Circulation

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Roles of uptake1 and catechol-O-methyltransferase in removal of circulating catecholamines in the rabbit

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1994.267.6.e814 ◽

1994 ◽

Vol 267 (6) ◽

pp. E814-E821 ◽

Cited By ~ 2

Author(s):

B. Friedgen ◽

T. Halbrugge ◽

K. H. Graefe

Keyword(s):

Pulmonary Circulation ◽

Systemic Circulation ◽

Before And After ◽

Definite Role

Anesthetized rabbits were simultaneously infused with [3H]norepinephrine (NE), [3H]epinephrine (Epi), [3H]dopamine (DA), and [3H]isoproterenol (Iso), and their plasma clearances and fractional extractions across the systemic (ERS), as well as pulmonary (ERP), circulation were determined before and after blockade of uptake1 by desipramine (2 mg/kg). Desipramine reduced the clearance of NE, Epi, and DA by 39, 13, and 14%, respectively, but did not affect Iso clearance. Similar results were obtained with respect to the effects of desipramine on ERS. By contrast, desipramine reduced ERP of NE and DA (which for both amines was markedly lower than ERS) by > 70%; its effect on the very low ERP of Epi was not determinable. Comparison of the desipramine-sensitive components of ERS and ERP indicated that for uptake1 NE was the preferred substrate in the systemic circulation and DA was preferred in the pulmonary circulation. In the absence and presence of desipramine, catechol-O-methyltransferase inhibition had no effect on the clearance of NE, Epi, and DA and decreased Iso clearance by 25%. Hence the contribution by uptake1 to the removal of circulating catecholamines depends on the type of amine and on whether the systemic or pulmonary circulation is considered. Moreover catechol-O-methyltransferase does not appear to contribute to the clearance of NE, Epi, and DA but plays a definite role in the removal of circulating Iso.

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Carl J. Wiggers and the pulmonary circulation: a young man in search of excellence

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.1998.274.4.l467 ◽

1998 ◽

Vol 274 (4) ◽

pp. L467-L474 ◽

Cited By ~ 1

Author(s):

John T. Reeves

Keyword(s):

Pulmonary Circulation ◽

Pulmonary Arterial Pressure ◽

Systemic Circulation ◽

Right Atrial ◽

High Fidelity ◽

Left Heart ◽

Sound Recording ◽

Pulmonary Arterial ◽

The Relationship ◽

Lung Microcirculation

Oddly, Carl Wiggers (1883–1962), who is remembered for his work on the systemic circulation, may be considered the “American father of the pulmonary circulation.” In nearly 20 papers published in the American Journal of Physiology between 1909 and 1925, he reported the first reliable pressure contours in the pulmonary artery, inquired into the relationship between respiration and pulmonary arterial pressure, examined right atrial and right ventricular function, and demonstrated how right and left heart dynamics relate to heart sounds. He also stimulated direct visualization of the lung microcirculation. Method and concept are inextricably linked in the progress of science. His contributions to the pulmonary circulation were based on his high-fidelity pressure and sound recording instruments, which he ultimately applied in the left heart. Wiggers’ search for excellence in method brought him well-deserved fame in the systemic circulation, but the search began in the lung.

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HDL Cholesterol as a Marker of Disease Severity and Prognosis in Patients with Pulmonary Arterial Hypertension

International Journal of Molecular Sciences ◽

10.3390/ijms20143514 ◽

2019 ◽

Vol 20 (14) ◽

pp. 3514 ◽

Cited By ~ 5

Author(s):

Kamil Jonas ◽

Grzegorz Kopeć

Keyword(s):

Pulmonary Arterial Hypertension ◽

Arterial Hypertension ◽

Vascular Endothelium ◽

Pulmonary Circulation ◽

Density Lipoprotein ◽

Hdl Cholesterol ◽

Systemic Circulation ◽

Pulmonary Arterial ◽

The Impact

The impact of high-density lipoprotein (HDL) cholesterol on the development of atherosclerosis and diseases of systemic circulation has been well documented both in experimental and registry studies. Recent discoveries in pulmonary arterial hypertension (PAH) revealed a significant impact of HDL on pulmonary artery vasoreactivity and patients’ prognosis. The vasoprotective activity of HDL primarily involves vascular endothelium that also plays a central role in pulmonary arterial hypertension (PAH) pathobiology. However, the exact mechanism in which this lipoprotein fraction exerts its effect in pulmonary circulation is still under investigation. This paper reviews potential vasoprotective mechanisms of HDL in pulmonary circulation and presents current clinical reports on the role of HDL in PAH patients.

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Pulmonary fate of histamine, isoproterenol, physalaemin, and substance P

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y70-100 ◽

1970 ◽

Vol 48 (10) ◽

pp. 681-684 ◽

Cited By ~ 23

Author(s):

Jean-Claude Boileau ◽

Lucien Campeau ◽

Pierre Biron

Keyword(s):

Substance P ◽

Cardiac Catheterization ◽

Pulmonary Circulation ◽

Systemic Circulation ◽

Small Degree ◽

Vasodilator Agents ◽

Single Passage ◽

Important Site

The biological inactivation of four vasodilator agents during a single passage through the pulmonary circulation was studied by means of an assay based on systemic depressor responses. Isoproterenol was tested in humans undergoing cardiac catheterization and in anesthetized normal dogs. Histamine and physalaemin were tested in anesthetized normal rats and dogs; substance P was tested in rats. The degree of inactivation of these four vasodilator agents was either negligible or small, rarely exceeding 15%. It is concluded that the lung is not an important site for the removal of these substances from the circulation. The small degree of pulmonary inactivation of histamine suggests that it could play some role as a "circulating" hormone. Unlike bradykinin, the "tachykinins" physalaemin and substance P undergo little pulmonary inactivation. The absence of lung inactivation of isoproterenol explains its entry into the systemic circulation when given by inhalation.

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Where Breath Meets Blood—Lung Perfusion

Just Enough Physiology ◽

10.1093/med/9780199797790.003.0015 ◽

2011 ◽

pp. 122-128

Author(s):

James R. Munis

Keyword(s):

Pulmonary Circulation ◽

Systemic Circulation ◽

Lung Perfusion ◽

High Flow ◽

Substantial Part ◽

Efficient System ◽

Low Resistance ◽

Vascular Bed ◽

Pulmonary Capillaries ◽

Flow Through

The pulmonary circulation is a low-resistance, low-pressure, high-flow system because its primary function is to oxygenate blood. For that reason, pulmonary circulation is different from systemic circulation. Because resistance is lower in pulmonary circulation, pressures across the pulmonary vascular bed also are substantially lower. An efficient system includes inherently low resistance. This allows the entire cardiac output to flow through without high-pressure areas, thereby diminishing the danger of rupturing thin gas-exchange surfaces. One other consequence of low resistance is that the pulmonary circulation is unusually susceptible to the effects of gravity. No substantial part of the cerebral circulation collapses in the head-up position because it is held open by the rigid cranium and the architecture of the venous sinuses. Pulmonary circulation is different. There is less ‘stenting open’ of pulmonary capillaries, and they are therefore more likely to partially or fully collapse when transmural pressure becomes negative.

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