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.

Capillary filtration coefficient, vascular resistance, and compliance in isolated mouse lungs

1999 ◽  
Vol 87 (4) ◽  
pp. 1421-1427 ◽  
Author(s):  
James C. Parker ◽  
Mark N. Gillespie ◽  
Aubrey E. Taylor ◽  
Sherri L. Martin
Keyword(s):  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Vascular Function ◽  
Vascular Occlusion ◽  
Filtration Coefficient ◽  
Longitudinal Distribution ◽  
Mouse Lung ◽  
Control Group ◽  
Capillary Filtration ◽  
Capillary Filtration Coefficient

Although many recently produced transgenic mice possess gene alterations affecting pulmonary vascular function, there are few baseline measurements of vascular resistance and permeability. Therefore, we excised the lungs of C57/BL6 mice and perfused them with 5% bovine serum albumin in RPMI-1640 culture medium at a nominal flow of 0.5 ml/min and ventilated them with 20% O2-5% CO2-75% N2. The capillary filtration coefficient, a sensitive measurement of hydraulic conductivity, was unchanged over 2 h (0.33 ± 0.03 ml ⋅ min−1 ⋅ cmH2O−1 ⋅ 100 g−1) in a control group ventilated with low peak inflation pressures (PIP) but increased 4.3-fold after high PIP injury. Baseline pulmonary vascular resistance was 6.1 ± 0.4 cmH2O ⋅ ml−1 ⋅ min ⋅ 100 g−1 and was distributed 34% in large arteries, 18% in small arteries, 14% in small veins, and 34% in large veins on the basis of vascular occlusion pressures. Baseline vascular compliance was 5.4 ± 0.3 ml ⋅ cmH2O−1 ⋅ 100 g−1 and decreased significantly with increased vascular pressures. Baseline pulmonary vascular resistance was inversely related to both perfusate flow and microvascular pressure and increased to 202% of baseline after infusion of 10−4 M phenylephrine due to constriction of large arterial and venous segments. Thus isolated mouse lung vascular permeability, vascular resistance, and the longitudinal distribution of vascular resistance are similar to those in other species and respond in a predictable manner to microvascular injury and a vasoconstrictor agent.

Effects of Acutely Induced Changes in Arterial pH on Pulmonary Vascular Resistance during Normoxia and Hypoxia in Awake Dogs

1972 ◽  
Vol 42 (3) ◽  
pp. 277-287 ◽  
Author(s):  
O. G. Thilenius ◽  
Carol Derenzo
Keyword(s):  
Cardiac Output ◽  
Pulmonary Artery ◽  
Pulmonary Vascular Resistance ◽  
Pulmonary Artery Pressure ◽  
Vascular Resistance ◽  
Main Pulmonary Artery ◽  
Compensatory Mechanisms ◽  
Artery Pressure ◽  
Arterial Ph ◽  
Small Rise

1. Awake dogs with chronically implanted catheters (pulmonary artery, left atrium, aorta) and electromagnetic flow probe (main pulmonary artery) underwent five types of experiments in succession: (1) slow infusion of 0·4 m-hydrochloric acid; (2) rapid infusion of 1·0 m-sodium bicarbonate; (3) exposure to 30 min of hypoxia (10% O2); (4) exposure to hypoxia after arterial pH had been lowered to 7·30; (5) exposure to hypoxia after pH had been increased to 7·55. Intravascular pressures, pulmonary vascular resistance, cardiac output, arterial gas tension and pH were studied. 2. Acute acidosis (pH 7·21) resulted in a small rise in pulmonary artery pressure, cardiac output and pulmonary vascular resistance, associated with a decrease in Pa,co2. Acute alkalosis (pH 7·61) was accompanied by a small rise in pulmonary artery pressure, marked increase in cardiac output, a fall in pulmonary vascular resistance and mild elevation in Pa,co2. During acidosis hypoxia resulted in a more pronounced rise in pulmonary vascular resistance than during alkalosis (P < 0·01). 3. The study provides evidence that in the intact, awake dog with its compensatory mechanisms acute alkalosis decreases pulmonary vascular resistance by decreasing vascular tone and/or recruitment of pulmonary vascular channels; it diminishes the vasoconstrictive response to hypoxia; conversely, mild acidosis increases the pulmonary vascular resistance slightly and enhances vasoconstriction during hypoxia to a small extent.

Pulmonary vasodilation by acetazolamide during hypoxia is unrelated to carbonic anhydrase inhibition

2007 ◽  
Vol 292 (1) ◽  
pp. L178-L184 ◽  
Author(s):  
Claudia Höhne ◽  
Philipp A. Pickerodt ◽  
Roland C. Francis ◽  
Willehad Boemke ◽  
Erik R. Swenson
Keyword(s):  
Carbonic Anhydrase ◽  
Pulmonary Artery ◽  
Pulmonary Vascular Resistance ◽  
Pulmonary Artery Pressure ◽  
Vascular Resistance ◽  
Low Dose ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Artery Pressure ◽  
Pulmonary Vasoconstriction ◽  
Mean Pulmonary Artery Pressure

Acute hypoxic pulmonary vasoconstriction can be inhibited by high doses of the carbonic anhydrase inhibitor acetazolamide. This study aimed to determine whether acetazolamide is effective at dosing relevant to human use at high altitude and to investigate whether its efficacy against hypoxic pulmonary vasoconstriction is dependent on carbonic anhydrase inhibition by testing other potent heterocyclic sulfonamide carbonic anhydrase inhibitors. Six conscious dogs were studied in five protocols: 1) controls, 2) low-dose intravenous acetazolamide (2 mg·kg−1·h−1), 3) oral acetazolamide (5 mg/kg), 4) benzolamide, a membrane-impermeant inhibitor, and 5) ethoxzolamide, a membrane-permeant inhibitor. In all protocols, unanesthetized dogs breathed spontaneously during the first hour (normoxia) and then breathed 9–10% O2 for the next 2 h. Arterial oxygen tension ranged between 35 and 39 mmHg during hypoxia in all protocols. In controls, mean pulmonary artery pressure increased by 8 mmHg and pulmonary vascular resistance by 200 dyn·s·cm−5 ( P <0.05). With intravenous acetazolamide, mean pulmonary artery pressure and pulmonary vascular resistance remained unchanged during hypoxia. With oral acetazolamide, mean pulmonary artery pressure increased by 5 mmHg ( P < 0.05), but pulmonary vascular resistance did not change during hypoxia. With benzolamide and ethoxzolamide, mean pulmonary artery pressure increased by 6–7 mmHg and pulmonary vascular resistance by 150–200 dyn·s·cm−5 during hypoxia ( P < 0.05). Low-dose acetazolamide is effective against acute hypoxic pulmonary vasoconstriction in vivo. The lack of effect with two other potent carbonic anhydrase inhibitors suggests that carbonic anhydrase is not involved in the mediation of hypoxic pulmonary vasoconstriction and that acetazolamide acts on a different receptor or channel.

Stability of pulmonary artery pressure during emboli-induced pulmonary edema in dogs

1965 ◽  
Vol 208 (6) ◽  
pp. 1263-1266
Author(s):  
H. Weisberg ◽  
R. T. Jortner ◽  
I. K. Kline ◽  
A. Ellis ◽  
L. N. Katz
Keyword(s):  
Cardiac Output ◽  
Pulmonary Artery ◽  
Pulmonary Edema ◽  
Pulmonary Vascular Resistance ◽  
Pulmonary Artery Pressure ◽  
Vascular Resistance ◽  
Pressure Rise ◽  
Vascular Effects ◽  
Artery Pressure ◽  
Pressure Changes

Changes in some facets of cardiovascular hemodynamics occurring after acute unilateral pulmonary starch embolization were studied in the anesthetized closed-chest dog. While bilateral pulmonary edema and reduced cardiac output occurred in starch-embolized dogs, these phenomena were not seen in control animals. Pulmonary arterial pressure changes were not significant during the present experiments, but the consistent rise in pulmonary vascular resistance after embolization indicates that the latter may be a better index of pulmonary vascular effects of emboli than are pressure changes. The fall in cardiac output was of sufficient magnitude to more completely neutralize the pulmonary artery pressure rise usually expected with increased pulmonary vascular resistance following pulmonary embolization.

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