Adrenal component to pulmonary hypertension caused by nicotine administration in the dog

1980 ◽  
Vol 49 (1) ◽  
pp. 66-72 ◽  
Author(s):  
M. B. Maron ◽  
D. A. Rickaby ◽  
C. A. Dawson
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Left Atrial ◽  
Venous Return ◽  
Venous Blood ◽  
Main Pulmonary Artery ◽  
Mixed Venous Blood ◽  
Lung Lobe ◽  
Nicotine Administration ◽  
Lower Lung

In this study, we investigated the possibility that the adrenal gland contributes to nicotine-induced pulmonary hypertension using a canine left lower lung lobe (LLL) preparation that was pump-perfused with mixed venous blood at constant flow and outflow pressure. Main pulmonary artery, left atrial, and LLL arterial pressures were monitored to assess the responses of the animal's intact right lung and isolated LLL. With the adrenal venous return intact, injection of 10-26 micrograms/kg nicotine into the left ventricle or ascending aorta resulted in a 42% increase in LLL arterial pressure and a 70% increase in the pulmonary arterial-left atrial pressure gradient (Ppa-Pla). When the adrenal venous return was interrupted, the increases in LLL arterial pressure and Ppa-Pla were reduced to 6 and 10%, respectively. The LLL response could be eliminated by alpha-adrenergic receptor blockade, suggesting that adrenal catecholamines may contribute to the pulmonary hypertension induced by nicotine infusion.

Adrenal component to pulmonary hypertension induced by elevated cerebrospinal fluid pressure

1979 ◽  
Vol 47 (1) ◽  
pp. 153-160 ◽  
Author(s):  
M. B. Maron ◽  
C. A. Dawson
Keyword(s):  
Pulmonary Hypertension ◽  
Cerebrospinal Fluid ◽  
Intact Animal ◽  
Venous Pressure ◽  
Venous Blood ◽  
Fluid Pressure ◽  
Cerebrospinal Fluid Pressure ◽  
Mixed Venous Blood ◽  
Vasoactive Agent ◽  
Lung Lobe

In this study we investigated the possibility that a circulating vasoactive agent contributes to the pulmonary hypertension elicited by elevated cerebrospinal fluid pressure (PCSF) using a denervated canine left lower lung lobe (LLL) preparation that was pump perfused with mixed venous blood at constant flow and venous pressure. Raising the PCSF to an average 190 Torr resulted in a 34.3% increase in LLL inflow pressure. This response was eliminated by adrenal venous occlusion and also by alpha-blockade of the LLL. The results indicated that adrenal catecholamines were responsible for the LLL response. The passively induced elevation of left atrial pressure (Pla) that occurs in the intact animal during elevated PCSF was stimulated in the LLL by raising the outflow pressure. This maneuver attenuated the increase in LLL vascular resistance and suggested that the elevation in Pla seen in the intact animal could mask humorally mediated responses of the magnitude we observed.

Carbon Dioxide Equilibration in Canine Lungs during Rebreathing and Acute Alkalosis

1979 ◽  
Vol 57 (5) ◽  
pp. 385-388 ◽  
Author(s):  
R. D. Latimer ◽  
G. Laszlo
Keyword(s):  
Whole Blood ◽  
Base Excess ◽  
Venous Blood ◽  
Main Pulmonary Artery ◽  
Mixed Venous Blood ◽  
Arterial Blood ◽  
Significant Difference ◽  
Venous Pco2 ◽  
Pulmonary Arterial ◽  
Gas Pressures

1. The left lower lobe of the lungs of six anaesthetized dogs were isolated by the introduction of a bronchial cannula at thoracotomy. Catheters were introduced into the main pulmonary artery and a vein draining the isolated lobe. 2. Blood-gas pressures and pH were measured across the isolated lobe and compared with gas pressures in alveolar samples from the lobe. 3. When the isolated lobe was allowed to reach gaseous equilibrium with pulmonary arterial blood for 30 min, there was no significant difference between alveolar and pulmonary venous Pco2. Mean values of whole-blood base excess were similar in pulmonary arterial and pulmonary venous blood. 4. After injection of 20 ml of 8·4% sodium bicarbonate solution into a peripheral vein, Pco2, pH and plasma bicarbonate concentrations rose in the mixed venous blood. There was no change of whole-blood base excess across the lung, indicating that HCO−3, as distinct from dissolved CO2, did not enter lung tissue in measurable amounts. 5. No systematic alveolar—pulmonary venous Pco2 differences were demonstrated in this preparation other than those explicable by maldistribution of lobar blood flow.

Pulmonary hypertension with muscular exercise in the newborn calf

1965 ◽  
Vol 20 (2) ◽  
pp. 249-252 ◽  
Author(s):  
John T. Reeves ◽  
James E. Leathers
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
Muscular Exercise ◽  
Arterial Oxygen ◽  
Mixed Venous Blood ◽  
Fetal Life ◽  
Pulmonary Vasoconstriction ◽  
Pulmonary Arterial

Two types of pulmonary hypertension occur with muscular exercise (walking) in the calf on the day of birth: a) Pulmonary arterial pressure increased in all calves during exercise. The increase was greatest in the youngest calves. Pulmonary arterial pressures did not rise to systemic levels and arterial oxygen saturations remained normal. Pulmonary hypertension subsided in 2 min after stopping exercise. Pulmonary arterial pressure rose again when exercise was repeated. Both an increased pulmonary flow and pulmonary vasoconstriction may have contributed to the increased pulmonary arterial pressure during exercise. b) Pulmonary hypertension was observed in five calves for 30-50 min after exercise ceased. When pulmonary arterial pressure exceeded aortic pressure, arterial oxygen unsaturation occurred. This pulmonary hypertension which occurred only once per calf resembled"spontaneous" pulmonary vasoconstriction observed in resting calves on the day of birth. It is postulated that some substance remaining in the lung after fetal life, rather than the acutely reduced oxygenation of mixed venous blood, initiated this pressor response. hypoxia; pulmonary vasoconstriction Submitted on May 11, 1964

Modulation of vascular reactivity to serotonin in the dog lung

1991 ◽  
Vol 71 (1) ◽  
pp. 217-222 ◽  
Author(s):  
W. F. Hofman ◽  
W. F. Jackson ◽  
H. el-Kashef ◽  
I. C. Ehrhart
Keyword(s):  
Arterial Pressure ◽  
Vascular Reactivity ◽  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
Venous Occlusion ◽  
Lung Lobe ◽  
Lower Lung ◽  
Pulmonary Arterial ◽  
Pressure Changes ◽  
Related Increase

Experiments were conducted to compare the effects of cyclooxygenase inhibition (COI) on vascular reactivity to serotonin (5-HT) in the isolated blood-perfused canine left lower lung lobe (LLL) and in isolated canine intrapulmonary lobar artery rings with and without a functional endothelium. LLLs (n = 6), perfused at constant blood flow, were challenged with bolus doses of 50, 100, and 250 micrograms 5-HT before COI, after COI with 45 microM meclofenamate, and after infusion of prostacyclin (PGI2) during COI. Lobar vascular resistance was segmentally partitioned by venous occlusion. Pulmonary arterial pressure increased from 13.5 +/- 1.0 to 16.3 +/- 0.8 cmH2O (P less than 0.01) after COI but declined to 13.1 +/- 1.1 cmH2O (P less than 0.01) subsequent to PGI2 infusion (91.3 +/- 14.5 ng.min-1.g LLL-1). The pulmonary arterial pressure changes were related to changes in postcapillary resistance. The dose-dependent pressor response to 5-HT was potentiated by COI (P less than 0.01) but reversibly attenuated (P less than 0.05) by PGI2 infusion. Isolated intrapulmonary artery rings (2–4 mm diam) exhibited a dose-related increase in contractile tension to 5-HT. The response to 5-HT was enhanced (P less than 0.05) in rings devoid of a functional endothelium. However, COI (10 microM indomethacin) did not alter (P greater than 0.05) the dose-related increase in contractile tension to 5-HT in rings with an intact endothelium. Our results suggest that both PGI2 and endothelium-derived relaxing factors modulate pulmonary vascular reactivity to 5-HT.(ABSTRACT TRUNCATED AT 250 WORDS)

Pulmonary vasoconstrictor responses to graded decreases in precapillary blood PO2 in intact-chest cat

1981 ◽  
Vol 51 (4) ◽  
pp. 1009-1016 ◽  
Author(s):  
A. L. Hyman ◽  
R. T. Higashida ◽  
E. W. Spannhake ◽  
P. J. Kadowitz
Keyword(s):  
Arterial Pressure ◽  
Pressor Response ◽  
Venous Blood ◽  
Pulmonary Veins ◽  
Right Atrial ◽  
Mixed Venous Blood ◽  
Arterial Blood ◽  
Vasoconstrictor Response ◽  
Pulmonary Arterial ◽  
Alveolar Capillary

The effects of graded changes in pulmonary lobar arterial blood PO2 and ventilatory hypoxia were investigated in the intact-chest cat under conditions of controlled lobar blood flow. A reduction in precapillary PO2 from systemic arterial levels to below 60 Torr increased lobar arterial pressure. Ventilation with 10% O2 increased lobar arterial pressure, and responses to ventilatory hypoxia and precapillary hypoxemia were independent but additive. The magnitude of the pressor response to precapillary hypoxemia was similar in experiments in which the lung was autoperfused with right atrial blood or cross-perfused with aortic blood from a donor cat breathing 10% O2. During retrograde perfusion of the ventilated lung, a reduction in pulmonary venous PO2 to 40 Torr did not affect inflow pressure. The present data suggest that sensor sites upstream to the alveolar-capillary region in segments of lobar artery unexposed to alveolar gas sense a reduction in precapillary blood PO2 and elicit a pulmonary vasoconstrictor response. The sensor site in the precapillary segment is independent of sensors in the alveolar-capillary-exposed segment region, and the effects of stimulation of both sensors on the pulmonary vascular bed are additive. In addition, the present data indicate that sensors in the pulmonary veins do not sense a reduction in PO2 in venous blood and elicit a vasoconstrictor response. These data suggest that the mixed venous blood PO2 may exert an important regulatory role in controlling pulmonary arterial pressure and pulmonary vascular resistance in the cat under normal and pathological conditions.

scholarly journals The Role of the Gills and Branchiostegites in Gas Exchange in a Bimodally Breathing Crab, Holthuisana Transversa: Evidence for a Facultative Change in the Distribution of the Respiratory Circulation

1984 ◽  
Vol 111 (1) ◽  
pp. 103-121 ◽  
Author(s):  
H. H. TAYLOR ◽  
PETER GREENAWAY
Keyword(s):  
Gas Exchange ◽  
Venous Return ◽  
Venous Blood ◽  
Mixed Venous Blood ◽  
Substantial Fraction ◽  
Air Breathing ◽  
Arterial Circulation ◽  
Circulation Patterns ◽  
Gill Lamellae

The respiratory circulation was investigated in air-breathing and waterbreathing Holthuisana transversa von Martens by analysis of the distribution of radioactive microspheres injected into the haemocoel at seven locations. The gills and putative lungs (branchiostegites and membraneous thoracic walls) both trap approximately 90% of the microspheres entrained in their afferent circulations. The main blood supply to the branchiostegites is from the venous sinuses and constitutes a substantial fraction of the total venous return, which is consistent with earlier inferences, based on morphological information, of their possible involvement in gas exchange. In airbreathing crabs, a mechanism exists which directs a greater proportion of the total venous return via the lungs. From the sinus at the base of walking leg 2, the ratio lung: gill flow was estimated as 86.9: 13.1 ± 5.7% in hydrated crabs that had been air-breathing for more than 1 day, and 19.5:80.5 ± 7.12% in water-breathers. A factor in this circulatory switch may be an increase in branchial resistance in air caused by surface tension of water adherent to the gill lamellae. The direct arterial circulation to the gills represents about 3% of cardiac output and is therefore an insignificant component of the total respiratory circulation. Patterns of microsphere distribution among different gills and different regions of the lung provide information on flow patterns within the thoracic sinus. Neither the thoracic sinus as a whole nor the inf rabranchial sinuses can be considered as reservoirs of truly mixed venous blood in H. transversa.

Analysis of responses to sarafotoxin 6a and sarafotoxin 6c in the pulmonary vascular bed of the cat

1991 ◽  
Vol 71 (5) ◽  
pp. 2019-2025 ◽  
Author(s):  
T. J. McMahon ◽  
J. S. Hood ◽  
P. J. Kadowitz
Keyword(s):  
Arterial Pressure ◽  
Left Atrial ◽  
Lower Lobe ◽  
Thromboxane A2 ◽  
Aortic Pressure ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Lung Lobe ◽  
Vascular Bed ◽  
Pulmonary Vascular Bed

Pulmonary vascular responses to sarafotoxins 6a and 6c (S6a and S6c) were investigated in the intact-chest cat under constant flow conditions. Injections of S6a and S6c into the perfused lobar artery caused dose-related increases in lobar arterial pressure, increased left atrial pressure, and produced biphasic changes in systemic arterial (aortic) pressure. When left atrial pressure was maintained constant, injections of S6a, S6c, and endothelin 1 (ET-1) caused dose-related increases in lobar arterial pressure. The increases in lobar arterial pressure in response to S6a and S6c were not altered by treatment with a cyclooxygenase inhibitor or a thromboxane receptor blocking agent. Increases in lobar arterial pressure in response to S6a and S6c were not altered when airflow to the left lower lung lobe was interrupted by bronchial occlusion, and pressor responses were not diminished when the left lower lobe was perfused with low-molecular-weight dextran. Under conditions of controlled blood flow and constant left atrial pressure, S6a, S6b, S6c, and ET-1 had similar pressor activity, whereas the thromboxane A2 mimic, U-46619, had far greater activity when compared on a nanomolar basis. The present studies demonstrate that S6a and S6c have significant vasoconstrictor activity in the feline pulmonary vascular bed. These data suggest that pulmonary vasoconstrictor responses to the endothelin peptides are not dependent on release of cyclooxygenase products and the activation of thromboxane A2 receptors, alterations in bronchomotor tone, or interaction with formed elements in blood.

scholarly journals A multiscale model of vascular function in chronic thromboembolic pulmonary hypertension

2021 ◽  
Author(s):  
Mitchel J. Colebank ◽  
M. Umar Qureshi ◽  
Sudarshan Rajagopal ◽  
Richard A Krasuski ◽  
Mette S. Olufsen
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Main Pulmonary Artery ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Large Artery ◽  
Wave Reflections ◽  
Thromboembolic Pulmonary Hypertension ◽  
Optimal Target ◽  
Pulmonary Arterial

Chronic thromboembolic pulmonary hypertension (CTEPH) is caused by recurrent or unresolved pulmonary thromboemboli, leading to perfusion defects and increased arterial wave reflections. CTEPH treatment aims to reduce pulmonary arterial pressure and reestablish adequate lung perfusion, yet patients with distal lesions are inoperable by standard surgical intervention. Instead, these patients undergo balloon pulmonary angioplasty (BPA), a multi-session, minimally invasive surgery that disrupts the thromboembolic material within the vessel lumen using a catheter balloon. However, there still lacks an integrative, holistic tool for identifying optimal target lesions for treatment. To address this insufficiency, we simulate CTEPH hemodynamics and BPA therapy using a multiscale fluid dynamics model. The large pulmonary arterial geometry is derived from a computed tomography (CT) image, whereas a fractal tree represents the small vessels. We model ring- and web-like lesions, common in CTEPH, and simulate normotensive conditions and four CTEPH disease scenarios; the latter includes both large artery lesions and vascular remodeling. BPA therapy is simulated by simultaneously reducing lesion severity in three locations. Our predictions mimic severe CTEPH, manifested by an increase in mean proximal pulmonary arterial pressure above 20 mmHg and prominent wave reflections. Both flow and pressure decrease in vessels distal to the lesions and increase in unobstructed vascular regions. We use the main pulmonary artery (MPA) pressure, a wave reflection index, and a measure of flow heterogeneity to select optimal target lesions for BPA. In summary, this study provides a multiscale, image-to-hemodynamics pipeline for BPA therapy planning for inoperable CTEPH patients.

Circulating neuropeptide Y does not produce pulmonary hypertension during massive sympathetic activation

1992 ◽  
Vol 73 (1) ◽  
pp. 117-122 ◽  
Author(s):  
S. A. Lang ◽  
M. B. Maron ◽  
K. C. Maender ◽  
C. F. Pilati
Keyword(s):  
Pulmonary Hypertension ◽  
Neuropeptide Y ◽  
Sympathetic Activation ◽  
Pulmonary Hemodynamics ◽  
Vasoactive Agent ◽  
Lung Lobe ◽  
Lower Lung ◽  
Capillary Pressures ◽  
Additional Lobes

We tested the possibility that neuropeptide Y (NPY) may contribute to the pulmonary hypertension that occurs after massive sympathetic activation produced by intracisternal veratrine administration in the chloralose-anesthetized dog. In six dogs, veratrine caused arterial NPY-like immunoreactivity (NPY-LI) to rise from 873 +/- 150 (SE) pg/ml to peak values of 3,780 +/- 666 pg/ml by 60–120 min. (In 3 animals, adrenalectomy significantly reduced the increases in NPY-LI.) In five additional dogs, we infused porcine NPY for 30 min in doses that increased arterial NPY-LI to 8,354 +/- 1,514 pg/ml and observed only minor changes in pulmonary hemodynamics. In three isolated perfused canine left lower lung lobe (LLL) preparations, increasing doses of NPY were administered, producing levels of plasma NPY-LI, at the highest dose, that exceeded those observed after veratrine administration by three orders of magnitude. No changes in LLL arterial or double-occlusion capillary pressures were observed at any dose. Similarly, no changes in LLL hemodynamics were observed in three additional lobes when NPY was administered while norepinephrine was being infused. We conclude that it is unlikely that NPY plays a role as a circulating vasoactive agent in producing the pulmonary hypertension and edema that occur in this model.

Sign in / Sign up

Export Citation Format

Share Document