Micropuncture Measurement of Lung Microvascular Pressure Profile in 3- to 4-Week-Old Rabbits

Raj, J. Usha; Chen, P; Navazo, Lucía

doi:10.1203/00006450-198611000-00009

Cited by 15 publications

(8 citation statements)

References 22 publications

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“…Although in the adult lung, much of the resistance is in the microvascular segment, in the young human and in young rabbits, pulmonary vascular resistance has been shown to reside mainly in the arteries and veins, with a shift to the microvascular segment occurring with increasing age (14). Structural and pharmacological changes in response to chronic hypoxia are similar in large muscular and resistance arteries (10,15).…”

mentioning

confidence: 79%

Porcine Pulmonary Artery and Bronchial Responses to Endothelin-1 and Norepinephrine on Recovery from Hypoxic Pulmonary Hypertension

Schindler

Hislop²,

Haworth³

2006

Pediatr Res

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Many infants recovering from acute lung disease and pulmonary hypertension still have evidence of reactive airways disease at one year of age, suggesting longer-term airway effects. We hypothesized that parallel changes in smooth muscle would occur in airways and pulmonary arteries from animals with pulmonary hypertension and during normoxic recovery. Thus, two-hour-old piglets were subjected to 3 d chronic hypobaric hypoxia and 3-d-old piglets were subjected to 11 d hypoxia. Some animals were allowed to recover in room air for 3 or 6 d. The amount of smooth muscle and responses of isolated paired bronchial and pulmonary artery rings to endothelin-1 (ET-1) and norepinephrine were studied at the end of hypoxic exposure, on recovery and in age-matched control animals. In all hypoxia induced pulmonary hypertensive animals, smooth muscle area and ET-1 contractile response was increased in the pulmonary arteries and bronchi. Norepinephrine-induced relaxant response was impaired significantly in both bronchi and pulmonary arteries. After 3 d recovery, pulmonary arterial smooth muscle area decreased by 65%, and ET-1-induced contractile responses were normal for age. In the airways, ET-1 contractile response only normalized after six days and bronchial smooth muscle was still increased. After 6 d recovery pulmonary arterial norepinephrineinduced relaxant response had returned to normal, but bronchial response remained impaired. Thus during pulmonary hypertension, both bronchial and pulmonary arterial smooth muscle area and contractile responses are increased. On recovery, regression of bronchial structural and functional abnormalities is slower than in pulmonary arteries. A natomically, the pulmonary arteries and airways lie in close proximity and local mediator release may affect both bronchial and pulmonary vascular reactivity. Pulmonary hypertension in children with congenital heart disease is associated not only with an elevated pulmonary arterial vascular resistance and medial smooth muscle hypertrophy, but also with increased respiratory system resistance and bronchial smooth muscle hypertrophy (1).Fifty percent of infants requiring Extra Corporeal Membrane Oxygenation (ECMO) for persistent pulmonary hypertension of the newborn still required pulmonary medications after six months, despite ECMO utilizing a strategy of lung rest to prevent lung injury (2). Twenty-six percent of infants who participated in the UK randomized ECMO trial, many of whom had severe persistent pulmonary hypertension, still had evidence of reactive airways disease with cough and wheeze at one year of age, and 8% still required regular pulmonary medications (3). These changes could be due to the damaging effects of high pressure and the high FiO 2 used during the mechanical ventilation given before instituting ECMO (4), however pulmonary hypertension may have contributed to the end result by affecting both the pulmonary arteries and bronchi. The clinical findings also suggest that any bronchial changes, once present, are slow to re...

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mentioning

confidence: 79%

Porcine Pulmonary Artery and Bronchial Responses to Endothelin-1 and Norepinephrine on Recovery from Hypoxic Pulmonary Hypertension

Schindler

Hislop²,

Haworth³

2006

Pediatr Res

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“…He also found that this effect was exaggerated in the presence of red blood cells. In our study, the osmolarity of the perfusates ranged from 265 to 340 mosm/l, and in group 5, 6, and 7 In general, the effect of an increase in blood flow and total arteriovenous pressure drop is a decrease in pulmonary vascular resistance that is mainly due to vascular distension and recruitment. Some of the reduction in total resistance is also due to a reduction in apparent viscosity of blood.…”

Section: Effect Of Dextran-induced Increases In Perfusate Viscosity Omentioning

confidence: 56%

“…We accepted p<0.05 as indicative of statistical significance. 7. In group 7 lungs, at the lower flow rate (30+7 ml* kg`.…”

Section: Data Analysesmentioning

confidence: 93%

Comparison of dextran and hematocrit effects in the pulmonary microcirculation.

Raj

Anderson

1991

Circulation Research

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We have compared the effects of an increase in perfusate viscosity induced by dextran and by hematocrit (Hct) on segmental vascular resistance in the pulmonary circulation and the effect of flow on microvascular resistance in lungs perfused with dextran and red blood cells. We isolated and perfused lungs of 39 neonatal rabbits weighing 670±250 g. To determine the effect of dextran, group 1 (n =8) lungs were perfused with both 5% and 20o dextran 70 solutions (Hct, -25%); to determine the effect of Hct, group 2 (n=5) lungs were perfused alternately with 5% and 40% Hct solutions (5% dextran 70). In group 1 and group 2 lungs, experiments were done at constant flow and pressure. Group 3 and group 4 (each n=4) lungs were perfused with 5% and 20% dextran 70, respectively (0 Hct); group 5 (n =5), with 10% dextran 70; group 6 (n=7), with 5% dextran 500; and group 7 (n=6), with 20% dextran 70 (Hct, -5%). All lungs were perfused in zone 3; airway and left atrial pressures were 6 and 8 cm H20, respectively. To partition the circulation, we measured pressures in the pulmonary artery and left atrium continuously and pressures in 20-50-,um arterioles and 20-50-gm venules by micropuncture.We found that an increase in both the concentration and molecular weight of dextran increased perfusate viscosity and the resistance in all three longitudinal vascular segments: arteries, microvessels, and veins. However, Hct-induced increases in perfusate viscosity resulted in an increase in arterial and venous resistances alone, with no increase in microvascular resistance. In group 1 and group 7 lungs, which were perfused with 20% dextran 70 but with varying Hcts, a greater than 50%o increase in flow rate resulted in a greater decrease in microvascular resistance in group 1 lungs that had a higher Hct. Our results indicate that dextran-induced viscosity effects are present in all three vascular segments of the pulmonary circulation, whereas Hct effects are found mainly in arteries and veins greater than 50 ,um in diameter. Microvascular resistance is altered by flow rate and may also be influenced by dextran-red blood cell interactions. (Circulation Research 1991;68:1108-1116 T he pulmonary circulation is comprised of a complex network of blood vessels, with each successive segment (arterial, microvascular, and venous) demonstrating unique pressure-flow characteristics. The differences in the responses of these three vascular segments to a variety of stimuli are, in part, due to the intrinsic vasomotor properties of the blood vessels as well as their passive viscoelastic properties. In addition, the microrheological behavior of blood may vary in the three segments of the pulmonary vasculature, leading to different hemodynamic events in the three vascular segments. The interactions of plasma constituents with the various circulating cells in blood are complex. In general, our knowledge of blood rheology is derived from in vitro studies using cone-plate viscometers and microtube viscometry. However, results from in vivo studies appear to be i...

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“…A predominant ar terial resistance in lungs of younger animals has been described in some species [15][16][17], consistent with morphometric findings of a thicker smooth muscle coat in pulmonary ar teries in the neonatal period with a decrease in muscle mass and increase in vessel luminal diameter with increasing age [10,20]. How ever, we did not find any differences in the vascular pressure profile in lungs of 2-to 3-week-old, 5-to 6-week-old and adult ferrets, making this explanation unlikely.…”

Section: Discussionmentioning

confidence: 99%

“…We have previously shown that in the fer ret, the longitudinal distribution of segmental vascular resistance in the lung is similar in neonatal, juvenile and adult ferrets [19], un like the rabbit in which the contribution of arteries, microvessels and veins to total pul monary vascular resistance changes with age [17], Also, in both neonatal and adult ferret lungs, both arteries and veins constrict with hypoxia to the same degree [18]. The mecha nisms of the age-related differences in PTXinduced pulmonary vasodilation are not clear but we can speculate on some possibilities.…”

Section: Age-related Differences In Ptx Effectsmentioning

confidence: 99%

Age-Related Differences in Vascular Effects of Pentoxifylline in Isolated Perfused Ferret Lungs

1992

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We have determined the magnitude and sites of action of pentoxifylline (PTX), a methylxanthine derivative, in the adult and 3- to 4-week old ferret pulmonary circulation. Lungs of 8 ferrets, four 3- to 4-week-old and 4 adult, were isolated and perfused with blood. During perfusion, blood flow was kept constant, as were airway and left atrial pressures (6 and 8 cm H(2)O respectively, zone 3 conditions). In all lungs, pulmonary artery pressure was measured continuously and the circulation was partitioned into arteries, microvessels and veins, by measurement of pressures in 20-50 μm diameter subpleural arterioles and venules using the micropipette-servonulling method. Pressures were obtained in each lung during baseline, after vasoconstriction with hypoxia, and again after the infusion of PTX, 20 mg/kg, during hypoxia. We found that with hypoxia, total vascular resistance increased by ~90% in both adult and neonatal lungs; arterial and venous resistances increased by 100-180% in both age groups, with little change in microvascular resistance. PTX resulted in a significant decrease in total vascular resistance, due to a decrease in resistance in both arteries and veins. The decrease in resistance with PTX was greater in adult lungs (of the increase in resistance induced by hypoxia, 80% was eliminated by PTX) than in 3- to 4-week-old lungs (51 % elimination of tone induced by hypoxia). This difference was mainly due to a smaller reduction in arterial resistance with PTX in 3- to 4-week-old lungs. We conclude that PTX is a powerful pulmonary vasodilator in ferrets and that its effectiveness as a vasodilator depends on the age of the animal, the older animal showing greater responsiveness.

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Micropuncture Measurement of Lung Microvascular Pressure Profile in 3- to 4-Week-Old Rabbits

Cited by 15 publications

References 22 publications

Porcine Pulmonary Artery and Bronchial Responses to Endothelin-1 and Norepinephrine on Recovery from Hypoxic Pulmonary Hypertension

Porcine Pulmonary Artery and Bronchial Responses to Endothelin-1 and Norepinephrine on Recovery from Hypoxic Pulmonary Hypertension

Comparison of dextran and hematocrit effects in the pulmonary microcirculation.

Age-Related Differences in Vascular Effects of Pentoxifylline in Isolated Perfused Ferret Lungs

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