Vagal control of pulmonary vascular resistance in the turtle Chrysemys scripta

1977 ◽  
Vol 55 (2) ◽  
pp. 359-367 ◽  
Author(s):  
William K. Milsom ◽  
B. Lowell Langille ◽  
David R. Jones
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Sympathetic Innervation ◽  
Pulmonary Arteries ◽  
Lung Parenchyma ◽  
Distal Segment ◽  
Cholinergic Innervation ◽  
Pulmonary Flow ◽  
Induced Changes

We have directly examined the control of pulmonary vascular resistance in the turtle Chrysemys scripta to determine the way in which pulmonary vasoregulation is achieved. The pulmonary circulation of the turtle Chrysemys scripta receives a strong excitatory cholinergic innervation from the vagus nerve. The major site of vasoconstrictor activity is in the extrinsic pulmonary artery proximal to the lung with only weak constrictor activity evident in the intrinsic arteries and arterioles within the lung parenchyma. No cholinergic innervation is evident in the segment of the extrinsic pulmonary artery proximal to the origin of the arterial ligament (ligamentum Botalli) and all vagally induced changes in flow resistance reside in the much narrower segment distal to this site. Vagal stimulation in an intact preparation produces sufficient constriction in the distal segment of extrinsic pulmonary artery to totally occlude pulmonary flow. The pulmonary arteries appear to be devoid of sympathetic innervation.

A bronchial epithelium-derived factor reduces pulmonary vascular tone in the newborn rat

2004 ◽  
Vol 96 (4) ◽  
pp. 1399-1405 ◽  
Author(s):  
J. Belik ◽  
J. Pan ◽  
R. P. Jankov ◽  
A. K. Tanswell
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Arteries ◽  
Bronchial Epithelium ◽  
Force Generation ◽  
Phosphatidylinositol 3 Kinase ◽  
Newborn Rat ◽  
No Release ◽  
Phosphatidylinositol 3

The factors accounting for the maintenance of a low pulmonary vascular resistance postnatally are not completely understood. The aim of this study was to test the hypothesis that bronchial epithelium produces a factor capable of relaxing adjacent pulmonary arterial smooth muscle. We studied fourth-generation intralobar pulmonary arteries and bronchi of 4- to 8-day-old rats. Arteries were mounted on a wire myograph, alone or with the adjacent bronchus. The presence of the attached bronchus significantly reduced pulmonary artery force generation induced by the thromboxane analog (U-46619) or KCl whether the endothelium was present or absent ( P < 0.01). The converse was not true in that bronchial force generation was not affected when studied with the adjacent pulmonary artery. Mechanical removal of the bronchial epithelium or addition of the nitric oxide (NO) synthase (NOS) nonspecific ( NG-monomethyl-l-arginine) or the specific neuronal NOS (7-nitroindazole) inhibitors increased arterial force generation to levels comparable to the isolated artery preparation. Wortmannin, a phosphatidylinositol 3-kinase inhibitor, significantly decreased ( P < 0.01) NO release of pulmonary arteries only when the adjacent bronchus was present. We conclude that bronchial epithelium in the newborn rat produces a factor capable of lowering pulmonary vascular muscle tone. This relaxant effect can be suppressed by NOS and phosphatidylinositol 3-kinase kinase inhibition, suggesting an action via NOS phosphorylation and NO release. We speculate that such a mechanism may be operative in vivo and plays an important role in control of pulmonary vascular resistance in the early postnatal period.

Serial changes in pulmonary haemodynamics during human pregnancy: a non-invasive study using Doppler echocardiography

1991 ◽  
Vol 80 (2) ◽  
pp. 113-117 ◽  
Author(s):  
Stephen C. Robson ◽  
Stewart Hunter ◽  
Richard J. Boys ◽  
William Dunlop
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Vascular Resistance ◽  
Pulmonary Artery Pressure ◽  
Vascular Resistance ◽  
Cross Sectional ◽  
Artery Pressure ◽  
Non Invasive ◽  
Pulmonary Flow ◽  
Pulmonary Haemodynamics ◽  
Significant Change

1. Serial pulmonary haemodynamic investigations were performed in 13 women before conception, at monthly intervals throughout pregnancy, and then at 6 months after delivery. 2. Mean pulmonary artery pressure was calculated from pulsed Doppler pulmonary velocities. Pulmonary flow was measured by Doppler and cross-sectional echocardiography. These two measurements were used to calculate pulmonary vascular resistance. 3. Mean non-pregnant pulmonary artery pressure was 13.8 mmHg and no significant change was demonstrated during pregnancy. 4. Pulmonary flow increased from 4.88 to 7.19 litres/min during pregnancy. 5. Pulmonary vascular resistance decreased from 2.85 resistance units before pregnancy to 2.17 resistance units at 8 weeks gestation. Thereafter there was no further significant change, values returning to pre-pregnant levels by 6 months after delivery.

Large pulmonary arteries and the control of pulmonary vascular resistance in the newborn

1994 ◽  
Vol 72 (11) ◽  
pp. 1464-1468 ◽  
Author(s):  
J. Belik
Keyword(s):  
Mechanical Properties ◽  
Smooth Muscle ◽  
Pulmonary Artery ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Arteries ◽  
Isometric Tension ◽  
Force Generation ◽  
Myogenic Response ◽  
Capacitance Vessels

In the immediate neonatal period the pulmonary vascular resistance is higher than later in life. The role of maturational differences in the smooth muscle mechanical properties of large capacitance vessels in this response has not been previously studied. To this end, we studied the smooth muscle isometric and isotonic mechanical properties, as well as the myogenic response of large extralobar pulmonary arteries in newborn and adult guinea pigs. Compared with the adult, the newborn pulmonary vascular smooth muscle generates less force and has a similar shortening capacity but longer isometric and isotonic relaxation half times. The myogenic response could be elicited in 80% of the newborn and 70% of the adult vessels. A 20% increase in vessel diameter resulted in force generation equivalent to 46 + 5.1 % of maximal isometric tension in the newborn. Such a response was significantly greater than observed for the adult vessels (14 ± 2.8%; p < 0.001). Our results showed significant maturational differences in the mechanical properties of the large pulmonary artery smooth muscle in the newborn. We speculate that the presence of myogenic response in large pulmonary capacitance vessels and the observed greater magnitude of stretch-induced force generation in the newborn may play an important role in the maintenance of a higher pulmonary vascular resistance in the neonatal period.Key words: myogenic response, pulmonary artery, newborn.

Increased pulmonary vascular resistance and defective pulmonary artery filling in caveolin-1−/− mice

2008 ◽  
Vol 294 (5) ◽  
pp. L865-L873 ◽  
Author(s):  
Nikolaos A. Maniatis ◽  
Vasily Shinin ◽  
Dean E. Schraufnagel ◽  
Shigenori Okada ◽  
Stephen M. Vogel ◽  
...  
Keyword(s):  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Type I Collagen ◽  
Pulmonary Arteries ◽  
Lung Parenchyma ◽  
Negative Regulator ◽  
Pulmonary Vasculature ◽  
Type I ◽  
Caveolin 1 ◽  
Pulmonary Vasodilation

Caveolin-1, the structural and signaling protein of caveolae, is an important negative regulator of endothelial nitric oxide synthase (eNOS). We observed that mice lacking caveolin-1 ( Cav1−/−) had twofold increased plasma NO levels but developed pulmonary hypertension. We measured pulmonary vascular resistance (PVR) and assessed alterations in small pulmonary arteries to determine the basis of the hypertension. PVR was 46% greater in Cav1−/− mice than wild-type (WT), and increased PVR in Cav1−/− mice was attributed to precapillary sites. Treatment with NG-nitro-l-arginine methyl ester (l-NAME) to inhibit NOS activity raised PVR by 42% in WT but 82% in Cav1−/− mice, indicating greater NO-mediated pulmonary vasodilation in Cav1−/− mice compared with WT. Pulmonary vasculature of Cav1−/− mice was also less reactive to the vasoconstrictor thromboxane A2 mimetic (U-46619) compared with WT. We observed redistribution of type I collagen and expression of smooth muscle α-actin in lung parenchyma of Cav1−/− mice compared with WT suggestive of vascular remodeling. Fluorescent agarose casting also showed markedly decreased density of pulmonary arteries and artery filling defects in Cav1−/− mice. Scanning electron microscopy showed severely distorted and tortuous pulmonary precapillary vessels. Thus caveolin-1 null mice have elevated PVR that is attributed to remodeling of pulmonary precapillary vessels. The elevated basal plasma NO level in Cav1−/− mice compensates partly for the vascular structural abnormalities by promoting pulmonary vasodilation.

The peculiarities of pulmonary macro- and microhemodynamics changes after treatment with agonists and blockers of cholinoceptors

2021 ◽  
Vol 20 (4) ◽  
pp. 35-44
Author(s):  
Vadim I. Evlakhov ◽  
Ilya Z. Poyassov ◽  
Tatiana P. Berezina
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Vascular Resistance ◽  
Pulmonary Artery Pressure ◽  
Vascular Resistance ◽  
Venous Return ◽  
Filtration Coefficient ◽  
Artery Pressure ◽  
Capillary Filtration ◽  
Capillary Filtration Coefficient ◽  
Pulmonary Microcirculation

Background. The pulmonary arterial and venous vessels are innervated by parasympathetic cholinergic nerves. However, the studies, performed on the isolated rings of pulmonary vessels, can not give answer to the question about the role of cholinergic mechanisms in the changes of pulmonary circulation in full measure. Aim. The comparative analysis of the changes of the pulmonary macro- and microhemodynamics after acetylcholine, atropine, pentamine and nitroglycerine treatment. Materials and methods. The study was carried out on the anesthetized rabbits in the condition of intact circulation with the measurement of the pulmonary artery pressure and flow, venae cavae flows, cardiac output, and also on isolated perfused lungs in situ with stabilized pulmonary flow with measurement of the perfused pulmonary artery pressure, capillary hydrostatic pressure, capillary filtration coefficient and calculation of the pulmonary vascular resistance, pre- and postcapillary resistances. Results. In the conditions of intact circulation after acetylcholine, pentamine and nitroglycerine treatment the pulmonary artery pressure and flow decreased, the pulmonary vascular resistance did not change as a result of decreasing of pulmonary artery flow and left atrial pressure due to diminution of venous return and venae cavaе flows. On perfused isolated lungs acetylcholine caused the increasing of pulmonary artery pressure, capillary hydrostatic pressure, pulmonary vascular resistance, pre- and postcapillary resistance and capillary filtration coefficient. After M-blocker atropine treatment the indicated above parameters of pulmonary microcirculation increased, on the contrary, after N-blocker pentamine treatment they decreased. Nitroglycerine infusion caused less decreasing of the parameters of pulmonary microcirculation in comparison with effects of pentamine, but capillary filtration coefficient decreased to a greater extent. These data indicate that nitroglycerine decreases endothelial permeability of pulmonary microvessels. Conclusion. After activation or blockade of cholinergic mechanisms in the condition of intact circulation the calculated parameter of pulmonary vascular resistance is depended from the ratio of the pulmonary artery pressure and flow and left atrial pressure, which are determined by the venous return. The different character of the changes of pulmonary microcirculatory parameters after M-blocker atropine and N-blocker pentamine treatment is evidence of reciprocal relations of M- and N-cholinoceptors in the nervous regulation of the pulmonary microcirculatory bed.

scholarly journals Effects of acute Rho kinase inhibition on chronic hypoxia-induced changes in proximal and distal pulmonary arterial structure and function

2011 ◽  
Vol 110 (1) ◽  
pp. 188-198 ◽  
Author(s):  
Rebecca R. Vanderpool ◽  
Ah Ram Kim ◽  
Robert Molthen ◽  
Naomi C. Chesler
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Arteries ◽  
Rho Kinase ◽  
Pressure Flow ◽  
Kinase Inhibition ◽  
Pulmonary Vasoconstriction ◽  
Pulsatile Pressure ◽  
Arterial Structure ◽  
Pulmonary Arterial ◽  
Induced Changes

Hypoxic pulmonary hypertension (HPH) is initially a disease of the small pulmonary arteries. Its severity is usually quantified by pulmonary vascular resistance (PVR). Acute Rho kinase inhibition has been found to reduce PVR toward control values in animal models, suggesting that persistent pulmonary vasoconstriction is the dominant mechanism for increased PVR. However, HPH may also cause proximal arterial changes, which are relevant to right ventricular (RV) afterload. RV afterload can be quantified by pulmonary vascular impedance, which is obtained via spectral analysis of pulsatile pressure-flow relationships. To determine the effects of HPH independent of persistent pulmonary vasoconstriction in proximal and distal arteries, we quantified pulsatile pressure-flow relationships before and after acute Rho kinase inhibition and measured pulmonary arterial structure with microcomputed tomography. In control lungs, Rho kinase inhibition decreased 0 Hz impedance (Z0), which is equivalent to PVR, from 2.1 ± 0.4 to 1.5 ± 0.2 mmHg·min·ml−1 ( P < 0.05) and tended to increase characteristic impedance (ZC) from 0.21 ± 0.01 to 0.22 ± 0.01 mmHg·min·ml−1. In HPH lungs, Rho kinase inhibition decreased Z0 ( P < 0.05) without affecting ZC. Microcomputed tomography measurements performed on lungs after acute Rho kinase inhibition demonstrated that HPH significantly decreased the unstressed diameter of the main pulmonary artery (760 ± 60 vs. 650 ± 80 μm; P < 0.05), decreased right pulmonary artery compliance, and reduced the frequency of arteries of diameter 50–100 μm (both P < 0.05). These results demonstrate that acute Rho kinase inhibition reverses many but not all HPH-induced changes in distal pulmonary arteries but does not affect HPH-induced changes in the conduit arteries that impact RV afterload.

Pressure-induced smooth muscle cell depolarization in pulmonary arteries from control and chronically hypoxic rats does not cause myogenic vasoconstriction

2005 ◽  
Vol 98 (3) ◽  
pp. 1119-1124 ◽  
Author(s):  
Jay S. Naik ◽  
Scott Earley ◽  
Thomas C. Resta ◽  
Benjimen R. Walker
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Cell Membrane ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Arteries ◽  
Barometric Pressure ◽  
Cell Membrane Potential ◽  
Intraluminal Pressure ◽  
Dose Dependent

Chronic obstructive pulmonary diseases, as well as prolonged residence at high altitude, can result in generalized airway hypoxia, eliciting an increase in pulmonary vascular resistance. We hypothesized that a portion of the elevated pulmonary vascular resistance following chronic hypoxia (CH) is due to the development of myogenic tone. Isolated, pressurized small pulmonary arteries from control (barometric pressure ≅ 630 Torr) and CH (4 wk, barometric pressure = 380 Torr) rats were loaded with fura 2-AM and perfused with warm (37°C), aerated (21% O2-6% CO2-balance N2) physiological saline solution. Vascular smooth muscle (VSM) intracellular Ca2+ concentration ([Ca2+]i) and diameter responses to increasing intraluminal pressure were determined. Diameter and VSM cell [Ca2+]i responses to KCl were also determined. In a separate set of experiments, VSM cell membrane potential responses to increasing luminal pressure were determined in arteries from control and CH rats. VSM cell membrane potential in arteries from CH animals was depolarized relative to control at each pressure step. VSM cells from both groups exhibited a further depolarization in response to step increases in intraluminal pressure. However, arteries from both control and CH rats distended passively to increasing intraluminal pressure, and VSM cell [Ca2+]i was not affected. KCl elicited a dose-dependent vasoconstriction that was nearly identical between control and CH groups. Whereas KCl administration resulted in a dose-dependent increase in VSM cell [Ca2+]i in arteries taken from control animals, this stimulus elicited only a slight increase in VSM cell [Ca2+]i in arteries from CH animals. We conclude that the pulmonary circulation of the rat does not demonstrate pressure-induced vasoconstriction.

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