Effects of Blood Flow and Left Atrial Pressure on Pulmonary Venous Resistance

Kuramoto, Kizuku; Rodbard, Simon

doi:10.1161/01.res.11.2.240

Cited by 28 publications

(6 citation statements)

References 17 publications

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“…The latter effect is of importance since wide fluctuations in left atrial pressure can strongly influence calculated pulmonary resistance independent of neural effects on vessel caliber (17,22,23). However, enhanced vascular resistance together with elevated mean arterial pressure and essentially unchanged mean left atrial pressure during left stellate ganglion stimulation is a strong indication of vasoconstriction.…”

Section: Discussionmentioning

confidence: 99%

Sympathetic Control of Pulmonary Vascular Impedance in Anesthetized Dogs

Pace

1971

Circulation Research

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The effects of left stellate ganglion stimulation on pulmonary hydraulic input impedance was evaluated in 21 experiments on open-chest dogs anesthetized with chloralose. The stellate ganglion was stimulated at 1, 2, 5, 10, and 20 cps, and impedance spectra were generated at each frequency. Control spectra were characterized by frequency-dependent oscillations in impedance magnitude. Generally, impedance minimums occurred between 2 and 3 cps and maximums between 4 and 6 cps. Stellate ganglion stimulation caused elevations in impedance magnitude and shifted the impedance curve upward. The average control impedance magnitude at the minimum was 4780 dyne sec cm-8 kg ± 262 SE and was increased to 8280 ± 452 during stimulation at 20 cps, while the frequency of the first harmonic in the control averaged 2.50 ± 0.08 SE cps and was 3.10 ± 0.08 during stimulation at 20 cps. Maximum activation of sympathetic outflows (10-20 cps) caused the impedance curve to flatten, attenuating frequency dependent oscillations characteristic of control spectra. The administration of propranolol attenuated cardiogenic increases in pulmonary pressure and flow during stellate ganglion stimulation, but elevations in pulmonary vascular impedance still occurred, indicating that this was not dependent on changes in harmonic content of the flow pulse that attended changes in heart rate and stroke volume. Frequency dependent oscillations in impedance magnitude were usually enhanced during left stellate ganglion stimulation following propranolol. The results indicate that sympathetic nerve stimulation increases the opposition to pulsatile flow; since pulmonary vascular resistance was relatively less affected, the input impedance becomes a greater fraction of the total opposition that must be overcome in moving blood through the lungs. KEY WORDS propranololFourier analysis right ventricular function stellate ganglion stimulation pulmonary arteries• The pioneer studies of I. deB. Daly et al. demonstrated that sympathetic nerve stimulation increased the opposition to steady flow through artificially perfused lungs, thus establishing the existence of a sympathetic innervation to pulmonary vessels which could produce a direct vasomotor response (1 with stellate ganglion stimulation in isolated lung lobes perfused with pulsatile flow was an increase in arterial pulse pressure with an insignificant effect on the level of mean pressure (2). This resulted from generalized stiffening of large pulmonary arteries rather than from constriction of smaller muscular arterioles. Further studies showed that stellate ganglion stimulation reduced the volume distensibility of the main pulmonary artery and increased the elastic modulus of the arterial wall; thus these studies established a physical basis for the observed increases in pulsatile pressure (3).Since stiffening of conduit vessels tends to augment pressure pulsations, a major hemodynamic consequence of activation of sympathetic pathways to the pulmonary vasculature

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Section: Discussionmentioning

confidence: 99%

Sympathetic Control of Pulmonary Vascular Impedance in Anesthetized Dogs

Pace

1971

Circulation Research

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“…This concept is supported by radiographic (Kjellberg and Olsson, 1954) and experimental (Little, 1960) observations. The contribution in the regulation of the pulmonary venous pressure and blood flow has also been attributed to the sleeves ensheathing the veins in physiological and experimental conditions (Eliakim and Aviado, 1961;Kuramoto andRodbard, 1962, Smith andCoxe, 1951;Gilbert, Hinshaw, Kuida, and Visscher, 1958;Rudolph, Gootman, Golinko, and Scarpelli, 1961). Descriptions of active expulsion of blood from the veins into the atria, facilitating the filling of the atria, have also appeared in the literature (Carrow and Calhoun, 1964).…”

Section: Discussionmentioning

confidence: 99%

Myocardial atrio-venous junctions and extensions (sleeves) over the pulmonary and caval veins: Anatomical observations in various mammals

Nathan

Gloobe

1970

Thorax

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The myocardial fibres of the posterior wall of the atrio-venous junctions were examined in 35 large domestic mammals. In the majority of specimens a common pattern in the course and organization of the fibres could be observed. The most obvious features were the following: (1) a main circular fascicle surrounding the pulmonary trunks; (2) fibres encircling the atriovenous junctions; and (3) myocardial sleeves extending along the veins, occasionally as far as the lung. The superior part of the left atrial wall was consistently thicker than the inferior section. Individual variations of this wall between the various trunks followed one of four patternsvertical, oblique, horizontal or criss-crossed. Differences between mammal and human hearts were found regarding the number of pulmonary trunks, the presence of the oblique vein of the left atrium, and the extension of the myocardial sleeves on the caval vein. This extension on the caval vein continues over the end of the azygos vein in animals. The functional significance of the structures described in this study is discussed.The presence of sleeves of atrial myocardium continuing over the pulmonary veins and venae cavae have been observed in various mammals and human hearts (Favaro, 1910;Brown, 1913;Papez, 1920;Auer, 1948;Los and Dankmeijer, 1956;Neill, 1956; Thomas, 1959;Klavins, 1963;Kosir, 1964;Carrow and Calhoun, 1964;Nathan and Eliakim, 1966). Although these sleeves are commonly neglected in anatomical textbooks and medical literature (Bourdelle, 1920;Bruni and Zimmerl, 1951 ;Sisson, 1953 ;Miller, Christensen, and Evans, 1964;May, 1964), they may perhaps be of functional importance. Previous studies in dogs (Eliakim, Stern, and Nathan, 1961) and humans (Nathan and Eliakim, 1966) disclosed that the atrial wall around the superior veins was thicker and the sphincter-like arrangement of the fibres was generally more distinct around the superior veins. It was also observed that the myocardial sleeves of the superior veins usually extended further towards th2 lung than did the sleeves of the inferior veins.In the present work, hearts of large mammals were studied with the hope that their dissection might contribute more anatomical details about the atrio-pulmonary and atrio-caval vein junctions, in order to permit a better understanding of the functions of these structures. MATERIAL AND METHODSThe hearts of 35 animals-17 sheep, 9 cattle, 5 pigs, 2 donkeys, 1 horse, and 1 camel-of various ages, both male and female, were dissected for the present study. The heart, pulmonary vessels, and part of the lungs were removed together in all cases. The anterior caval vein was cut above the opening of the azygos vein and the posterior caval vein was cut at the level of the diaphragm. The atria were separated from the ventricles at the level of the atrioventricular sulcus, so that they could be examined from both the inner and outer aspects. Using a micrometer caliper with a rachet stop, the thickness of the posterior wall of the left atrium was measured at a constant pressure...

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“…Thus in the adult lung, because the pulmonary veins are thin walled and sparsely innervated, they act mainly as conduit vessels to drain oxygenated blood into the left ventricle (32,85). However, other investigators, from measurement of venular pressures using small catheters, have found that a substantial portion of the total pulmonary vascular resistance is in veins (75,92,147). Similarly, from detailed morphometric measurements of cat lung, 49% of the total vascular resistance was calculated to be in veins, which the authors attributed to the branching pattern of the veins and the viscoelastic properties of the vessel walls (169).…”

Section: Contribution Of Veins To Total Pulmonary Vascular Resistancementioning

confidence: 99%

Role of veins in regulation of pulmonary circulation

Gao¹,

Raj²

2005

American Journal of Physiology-Lung Cellular and Molecular Phys

104

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Pulmonary veins have been seen primarily as conduit vessels; however, over the past two decades, a large amount of evidence has accumulated to indicate that pulmonary veins can exhibit substantial vasoactivity. In this review, the role of veins in regulation of the pulmonary circulation, particularly during the perinatal period and under certain pathophysiological conditions, is discussed. In the fetus, pulmonary veins contribute a significant fraction to total pulmonary vascular resistance. At birth, the veins as well as the arteries relax in response to endothelium-derived nitric oxide and dilator prostaglandins, thereby assisting in the fall in pulmonary vascular resistance. These effects are oxygen dependent and modulated by cGMP-dependent protein kinase. Under chronic hypoxic conditions, pulmonary veins undergo remodeling and demonstrate substantial constriction and hypertrophy. In a number of species, including the human, pulmonary veins are also the primary sites of action of certain vasoconstrictors such as endothelin and thromboxane. In various pathological conditions, there is an increased synthesis of these vasoactive agents that may lead to pulmonary venous constriction, increased microvascular pressures for fluid filtration, and formation of pulmonary edema. In conclusion, the significant role of veins in regulation of the pulmonary circulation needs to be appreciated to better prevent, diagnose, and treat lung disease.

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Effects of Blood Flow and Left Atrial Pressure on Pulmonary Venous Resistance

Cited by 28 publications

References 17 publications

Sympathetic Control of Pulmonary Vascular Impedance in Anesthetized Dogs

Sympathetic Control of Pulmonary Vascular Impedance in Anesthetized Dogs

Myocardial atrio-venous junctions and extensions (sleeves) over the pulmonary and caval veins: Anatomical observations in various mammals

Role of veins in regulation of pulmonary circulation

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