Enhancement of the pulmonary vasoconstriction reaction to alveolar hypoxia in systemic high blood pressure

1989 ◽  
Vol 76 (6) ◽  
pp. 589-594 ◽  
Author(s):  
Maurizio D. Guazzi ◽  
Marco Berti ◽  
Elisabetta Doria ◽  
Cesare Fiorentini ◽  
Claudia Galli ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Arterial Pressure ◽  
High Blood Pressure ◽  
Pulmonary Arterial Pressure ◽  
Systemic Hypertension ◽  
Pulmonary Vasoconstriction ◽  
Arteriolar Resistance ◽  
Alveolar Hypoxia ◽  
Pulmonary Arterial

1. In systemic hypertension the pulmonary vessels show an excessive tone at rest and hyper-react to adrenoceptor stimulation. Alterations in Ca2+ handling by the vascular smooth muscle cells seem to underlie these disorders. Alveolar hypoxia also constricts pulmonary arteries, increasing the intracellular Ca2+ availability for smooth muscle contraction. This suggests the hypothesis that hypoxic pulmonary vasoconstriction depends on similar biochemical disorders, and that the response to the hypoxic stimulus may be emphasized in high blood pressure. 2. In 21 hypertensive and 10 normotensive men, pulmonary arterial pressure and arteriolar resistance have been evaluated during air respiration and after 15 min of breathing 17, 15 and 12% oxygen in nitrogen. Curves relating changes in pulmonary arterial pressure and arteriolar resistance to the oxygen content of inspired gas had a similar configuration in the two populations, but in hypertension were steeper and significantly shifted to the left of those in normotension, reflecting a lower threshold and an enhanced vasoconstrictor reactivity. 3. This pattern was not related to differences in severity of the hypoxic stimulus, degree of hypocapnia and respiratory alkalosis induced by hypoxia, and plasma catecholamines. 4. The association of high blood pressure with enhanced pulmonary vasoreactivity to alveolar hypoxia could have clinical implications in patients who are chronically hypoxic and have systemic hypertension.

Effect of chronic hypoxia on pulmonary vascular pressures in isolated lungs of newborn pigs

1994 ◽  
Vol 77 (6) ◽  
pp. 2853-2862 ◽  
Author(s):  
C. D. Fike ◽  
M. R. Kaplowitz
Keyword(s):  
Smooth Muscle ◽  
Arterial Pressure ◽  
Chronic Hypoxia ◽  
Pulmonary Arterial Pressure ◽  
Muscle Tone ◽  
Before And After ◽  
Alveolar Hypoxia ◽  
Pulmonary Arterial ◽  
Newborn Pigs ◽  
Isolated Lungs

Our purposes were to determine whether chronic alveolar hypoxia altered pulmonary vascular pressures in lungs of newborn pigs, evaluate the contribution of smooth muscle tone to alterations in pulmonary vascular pressures, and examine whether chronic hypoxia altered pulmonary vascular reactivity to acute hypoxia. We kept 24- to 72-h-old pigs in chambers filled with room air (control) or 11–12% O2 (chronic hypoxia) for either 3–5 (short) or 10–12 (long) days. We used isolated lungs and applied micropuncture and vascular occlusion techniques to measure pressure in 10- to 30-microns-diam venules and inflow occlusion and outflow occlusion pressures before and after the addition of the smooth muscle dilator papaverine or before and after inflation of the lungs with a hypoxic gas mixture. For pigs in both the short and long groups, pulmonary arterial pressure was the only vascular pressure that was greater in chronically hypoxic than in control lungs. Increased smooth muscle tone was the primary source of the change in pulmonary arterial pressure with short hypoxia, whereas morphometric changes contributed to the change in pulmonary arterial pressure with long hypoxia. Exposure of newborn pigs to different lengths of alveolar hypoxia is a useful model to study postnatal pulmonary hypertension in newborns and infants.

Thrombin receptor activation peptide induces pulmonary vasoconstriction

1994 ◽  
Vol 266 (2) ◽  
pp. C448-C454 ◽  
Author(s):  
H. Lum ◽  
T. T. Andersen ◽  
J. W. Fenton ◽  
A. B. Malik
Keyword(s):  
Smooth Muscle ◽  
Arterial Pressure ◽  
Guinea Pig ◽  
Smooth Muscle Cells ◽  
Pulmonary Arterial Pressure ◽  
Muscle Cells ◽  
Receptor Activation ◽  
Thrombin Receptor ◽  
Pulmonary Vasoconstriction ◽  
Pulmonary Arterial

We investigated the involvement of the 14-residue thrombin receptor activating peptide SFLLRNPNDKYEPF (TRAP-14) in mediating the pulmonary vasoconstriction in response to alpha-thrombin. Isolated guinea pig lungs were uniformly perfused with Ringer-albumin solution at a constant flow of 28 ml/min. Addition of TRAP-14 or human alpha-thrombin to the perfusate caused dose-dependent increases of pulmonary arterial pressure within 1 min. TRAP-14 at 1 microM increased pulmonary arterial pressure to a similar extent as 10 nM alpha-thrombin (i.e., increase of 7.7 +/- 0.8 and 7.4 +/- 0.9 cmH2(0) from baseline, respectively). The increases in pulmonary venous resistance induced by TRAP-14 and alpha-thrombin were two- to fivefold greater than the increases in pulmonary arterial resistance, indicating that both agonists mediated pulmonary hypertension secondary to pulmonary venoconstriction. Stimulation of cultured guinea pig pulmonary artery smooth muscle cells with 100 microM TRAP-14 or 10 nM alpha-thrombin increased cytosolic Ca2+ concentration about five- to sevenfold over baseline. The increase in cytosolic Ca2+ concentration in smooth muscle cells was not observed with a subsequent challenge with either agonist, indicating desensitization. In the perfused lungs, an initial stimulation with alpha-thrombin or TRAP-14 desensitized the lungs to either agonist. The alpha-thrombin-desensitized lungs remained refractile to alpha-thrombin after 1 h of perfusion with fresh Ringer solution, whereas the TRAP-14-desensitized lungs recovered 79% of the vasoconstrictor response by 10 min and 93% of the response by 30 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Enhancement of the pulmonary vasoconstriction reaction to alveolar hypoxia in systemic high blood pressure

1991 ◽  
Vol 80 (4) ◽  
pp. 403-403 ◽  
Author(s):  
D. Guazzi Maurizio ◽  
Berti Marco ◽  
Doria Elisabetta ◽  
Fiorentini Cesare ◽  
Galli Claudia ◽  
...  
Keyword(s):  
Blood Pressure ◽  
High Blood Pressure ◽  
Pulmonary Vasoconstriction ◽  
Alveolar Hypoxia

Effect of hypoxia on pulmonary artery pressure of dogs

1964 ◽  
Vol 207 (6) ◽  
pp. 1314-1318 ◽  
Author(s):  
Benson R. Wilcox ◽  
W. Gerald Austen ◽  
Harvey W. Bender
Keyword(s):  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Pulmonary Artery Pressure ◽  
Pulmonary Arterial Pressure ◽  
Venous Pressure ◽  
Artery Pressure ◽  
Pulmonary Vasoconstriction ◽  
Systemic Hypoxia ◽  
Pump Output ◽  
Pulmonary Arterial

The mechanism by which the pulmonary artery pressure rises in response to hypoxia has never been clearly demonstrated. This problem was reinvestigated in experiments utilizing separate pulmonary and systemic perfusion systems. These vascular beds were perfused in such a fashion that a change in pulmonary artery pressure could only result from changes in vasomotor tone. Alveolar-pulmonary vein hypoxia was usually associated with a slight fall in pulmonary artery pressure. Systemic hypoxia resulted in elevation of pulmonary arterial pressure in 10 of the 12 animals tested with a constant-flow and constant-pulmonary venous pressure. In addition, all animals with systemic desaturation showed an increased venous return. When the "cardiac output" (pump output) was increased to match this return, the elevation in pulmonary artery pressure increased. It was concluded that the pulmonary arterial pressure elevation seen with hypoxia is the result of active pulmonary vasoconstriction coupled with an increased pulmonary blood flow.

M&B 22948, a cGMP phosphodiesterase inhibitor, is a pulmonary vasodilator in lambs

1993 ◽  
Vol 264 (1) ◽  
pp. H252-H258 ◽  
Author(s):  
D. A. Braner ◽  
J. R. Fineman ◽  
R. Chang ◽  
S. J. Soifer
Keyword(s):  
Smooth Muscle ◽  
Arterial Pressure ◽  
Smooth Muscle Cell ◽  
Vascular Tone ◽  
Pulmonary Arterial Pressure ◽  
Cell Concentration ◽  
Phosphodiesterase Inhibitor ◽  
Relaxing Factor ◽  
Pulmonary Arterial ◽  
Endothelium Derived Relaxing Factor

To investigate the hypothesis that pulmonary vascular tone and endothelium-dependent pulmonary vasodilation are mediated by changes in the vascular smooth muscle cell concentration of cGMP, we studied the hemodynamic effects of M&B 22948, a selective guanosine 3',5'-cyclic monophosphate (cGMP) phosphodiesterase inhibitor, in eight intact newborn lambs. At rest, M&B 22948 (1.0-2.5 mg/kg) selectively decreased pulmonary arterial pressure (by 8.5 +/- 6.6 to 10.3 +/- 4.5%, P < 0.05). Similarly, M&B 22948 (0.5-5.0 mg/kg) produced selective dose-dependent decreases in pulmonary arterial pressure during pulmonary hypertension induced either by U46619 (by 7.7 +/- 4.2 to 44.2 +/- 4.4%, P < 0.05) or by alveolar hypoxia (by 9.5 +/- 6.2 to 29.0 +/- 11.0%, P < 0.05). In addition, M&B 22948 augmented the pulmonary vasodilating effects of acetylcholine and ATP (both endothelium- and cGMP-dependent vasodilators) but not isoproterenol (an endothelium-independent and cAMP-dependent vasodilator). Because M&B 22948 inhibits the breakdown of cGMP, this study supports the in vitro data that changes in the vascular smooth muscle cell concentration of cGMP, in part, may regulate pulmonary vascular tone and mediate endothelium-dependent vasodilator responses in the pulmonary circulation. In addition, N omega-nitro-L-arginine (an inhibitor of endothelium-derived relaxing factor synthesis) blocked the vasodilating effects of M&B 22948, suggesting that the majority of endogenous cGMP is generated by the release of endothelium-derived relaxing factor.

Hypoxia and angiotensin II infusion redistribute lung blood flow in lambs

1985 ◽  
Vol 58 (3) ◽  
pp. 812-818 ◽  
Author(s):  
T. N. Hansen ◽  
A. L. Le Blanc ◽  
A. L. Gest
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Lymph Flow ◽  
Filtration Pressure ◽  
Alveolar Hypoxia ◽  
Pulmonary Arterial ◽  
Lung Lymph ◽  
Lung Lymph Flow

To assess the effects of alveolar hypoxia and angiotensin II infusion on distribution of blood flow to the lung we performed perfusion lung scans on anesthetized mechanically ventilated lambs. Scans were obtained by injecting 1–2 mCi of technetium-labeled albumin macroaggregates as the lambs were ventilated with air, with 10–14% O2 in N2, or with air while receiving angiotensin II intravenously. We found that both alveolar hypoxia and infusion of angiotensin II increased pulmonary vascular resistance and redistributed blood flow from the mid and lower lung regions towards the upper posterior region of the lung. We assessed the effects of angiotensin II infusion on filtration pressure in six lambs by measuring the rate of lung lymph flow and the protein concentration of samples of lung lymph. We found that angiotensin II infusion increased pulmonary arterial pressure 50%, lung lymph flow 90%, and decreased the concentration of protein in lymph relative to plasma. These results are identical to those seen when filtration pressure increases during alveolar hypoxia. We conclude that alveolar hypoxia and angiotensin II infusion both increase fluid filtration in the lung by increasing filtration pressure. The increase in filtration pressure may be the result of a redistribution of blood flow in the lung with relative overperfusion of vessels in some areas and transmission of the elevated pulmonary arterial pressure to fluid-exchanging sites in those vessels.

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 by endogenous opioids of pulmonary vasoconstrictor response to acute lung injury

1988 ◽  
Vol 64 (5) ◽  
pp. 1823-1828 ◽  
Author(s):  
A. T. Scardella ◽  
J. A. Neubauer ◽  
N. H. Edelman ◽  
T. V. Santiago
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Lung Injury ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Endogenous Opioids ◽  
Pulmonary Perfusion ◽  
Base Line ◽  
Injured Lung ◽  
Pulmonary Arterial

The effects of endogenously generated opioids on distribution of pulmonary perfusion (as assessed by radiolabeled microspheres) and overall gas exchange in acute acid-induced lung injury were studied. In 14 anesthesized dogs, sufficient acid was given to one lung to double shunt fraction (Qs/Qt) from 14.2 +/- 0.8 to 32.4 +/- 2.6% (SE). This resulted in a significant decrease in Po2 from 495 +/- 9 to 136 +/- 21 Torr, cardiac output from 2.47 +/- 0.27 to 1.46 +/- 0.15 1/min, and blood pressure from 139 +/- 3 to 116 +/- 5 mmHg and a significant rise in pulmonary arterial pressure from 9.6 +/- 0.8 to 14.9 +/- 0.8 mmHg. After acid instillation, microsphere distribution to the injured lung segments decreased to 50% of the base-line value. At the same time, microsphere distribution in the normal segments increased to 160% of base line. In 7 of the 14 dogs the effects of naloxone (1 mg/kg) given after lung injury were compared with the other 7 animals that were given saline. Naloxone administration caused a significant redistribution of regional pulmonary perfusion such that microsphere distribution in the injured lung segments increased by a factor of 2 at 35 min compared with the animals given saline. Consistent with this finding, Qs/Qt in the naloxone group increased to 34.7 +/- 5.0% at 35 min, whereas that of the saline group decreased to 28.2 +/- 2.5%. The difference between the two groups was significant at 35 min. These changes occurred without further alterations in cardiac output, pulmonary arterial pressure, or systemic blood pressure in either group.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals STUDIES IN ASTHMA

1929 ◽  
Vol 49 (1) ◽  
pp. 21-31 ◽  
Author(s):  
Stephen Went ◽  
Cecil K. Drinker
Keyword(s):  
Blood Pressure ◽  
Pulmonary Artery ◽  
Anaphylactic Shock ◽  
Pulmonary Arterial Pressure ◽  
Early Stage ◽  
Horse Serum ◽  
Foreign Protein ◽  
Marked Contrast ◽  
Pulmonary Vasoconstriction ◽  
Pulmonary Arterial

1. Sheep serum in doses below 0.3 cc. intravenously produces no pulmonary vasoconstriction in the guinea pig. Guinea pigs have consequently been sensitized with this substance and anaphylactic shock produced by doses of O.1 and 0.2 cc. 2. Pressure in the pulmonary artery has been measured by the method of Drinker and Went (2) and recorded photographically in a new and convenient manner. 3. At a very early stage in anaphylactic shock the pulmonary arterial pressure falls markedly and this fall seems to precede the appearance of bronchiolar obstruction. 4. The fall in pulmonary blood pressure in anaphylactic shock is in marked contrast to the rise in pressure resulting from intravenous injection of toxic foreign protein, such as horse serum.

scholarly journals THE PULMONARY ARTERIAL PRESSURE IN NORMAL ALBINO RATS AND THE EFFECT THEREON OF EPINEPHRINE

1934 ◽  
Vol 59 (2) ◽  
pp. 173-180 ◽  
Author(s):  
F. J. C. Smith ◽  
Granville A. Bennett
Keyword(s):  
Blood Pressure ◽  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Direct Determination ◽  
Albino Rats ◽  
Satisfactory Method ◽  
Pulmonary Arterial ◽  
Nembutal Anesthesia

1. A satisfactory method for the direct determination of the pulmonary arterial pressure in rats is described. 2. The arithmetical mean of the blood pressure in the pulmonary artery in a series of thirty-four normal albino rats under nembutal anesthesia is 256 mm. H20 (18.8 mm. Hg). 3. Intravenous epinephrine causes an abrupt but briefly sustained rise in the pulmonary arterial pressure with a gradual return to normal.

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