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.

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 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.

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.

Cardiac baroreflex dysfunction in patients with pulmonary arterial hypertension at rest and during orthostatic stress: Role of the peripheral chemoreflex

2021 ◽  
Author(s):  
Marcelle Paula-Ribeiro ◽  
Indyanara C. Ribeiro ◽  
Liliane C. Aranda ◽  
Talita M. Silva ◽  
Camila M. Costa ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Early Stage ◽  
Pressure Fluctuations ◽  
Sit To Stand ◽  
Peak Aerobic Capacity ◽  
Pulmonary Arterial ◽  
Peripheral Chemoreflex

The baroreflex integrity in early-stage pulmonary arterial hypertension (PAH) remains uninvestigated. A potential baroreflex impairment could be functionally relevant and possibly mediated by enhanced peripheral chemoreflex activity. Thus, we investigated 1) the cardiac baroreflex in non-hypoxemic PAH; 2) the association between baroreflex indexes and peak aerobic capacity (i.e., V̇O2peak); and 3) the peripheral chemoreflex contribution to the cardiac baroreflex. Nineteen patients and 13 age- and sex-matched healthy adults (HA) randomly inhaled either 100% O2 (peripheral chemoreceptors inhibition) or 21% O2 (control session), while at rest and during a repeated sit-to-stand maneuver. Beat-by-beat analysis of R-R intervals and systolic blood pressure provided indexes of cardiac baroreflex sensitivity (cBRS) and effectiveness (cBEI). The PAH group had lower cBEIALL at rest (mean ± SD: PAH = 0.5 ± 0.2 vs HA = 0.7 ± 0.1 a.u., P = 0.02) and lower cBRSALL (PAH = 6.8 ± 7.0 vs HA = 9.7 ± 5.0 ms mmHg-1, P < 0.01) and cBEIALL (PAH = 0.4 ± 0.2 vs HA= 0.6 ± 0.1 a.u., P < 0.01) during the sit-to-stand maneuver versus the HA group. The cBEI during the sit-to-stand maneuver was independently correlated to V̇O2peak (partial r = 0.45, P < 0.01). Hyperoxia increased cBRS and cBEI similarly in both groups at rest and during the sit-to-stand maneuver. Therefore, cardiac baroreflex dysfunction was observed under spontaneous and, most notably, provoked blood pressure fluctuations in non-hypoxemic PAH, was not influenced by the peripheral chemoreflex, and was associated with lower V̇O2peak suggesting it could be functionally relevant.

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.

Does leukotriene C4 mediate hypoxic vasoconstriction in isolated ferret lungs?

1990 ◽  
Vol 68 (1) ◽  
pp. 253-259 ◽  
Author(s):  
C. M. Tseng ◽  
M. McGeady ◽  
T. Privett ◽  
A. Dunn ◽  
J. T. Sylvester
Keyword(s):  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Physiological Salt Solution ◽  
Leukotriene C4 ◽  
Prostaglandin F2 Alpha ◽  
Pulmonary Vasoconstriction ◽  
Vasoconstrictor Response ◽  
Hypoxic Vasoconstriction ◽  
Pulmonary Arterial

To evaluate leukotriene (LT) C4 as a mediator of hypoxic pulmonary vasoconstriction, we examined the effects of FPL55712, a putative LT antagonist, and indomethacin, a cyclooxygenase inhibitor, on vasopressor responses to LTC4 and hypoxia (inspired O2 tension = 25 Torr) in isolated ferret lungs perfused with a constant flow (50 ml.kg-1.min-1). Pulmonary arterial injections of LTC4 caused dose-related increases in pulmonary arterial pressure during perfusion with physiological salt solution containing Ficoll (4 g/dl). FPL55712 caused concentration-related inhibition of the pressor response to LTC4 (0.6 micrograms). Although 10 micrograms/ml FPL55712 inhibited the LTC4 pressor response by 61%, it did not alter the response to hypoxia. At 100 microgram/ml, FPL55712 inhibited the responses to LTC4 and hypoxia by 73 and 71%, respectively, but also attenuated the vasoconstrictor responses to prostaglandin F2 alpha (78% at 8 micrograms), phenylephrine (68% at 100 micrograms), and KCl (51% at 40 mM). At 0.5 microgram/ml, indomethacin significantly attenuated the pressor response to arachidonic acid but did not alter responses to LTC4 or hypoxia. These results suggest that in isolated ferret lungs 1) the vasoconstrictor response to LTC4 did not depend on release of cyclooxygenase products and 2) LTC4 did not mediate hypoxic vasoconstriction.

CO modulates pulmonary vascular response to acute hypoxia: relation to endothelin

2004 ◽  
Vol 286 (1) ◽  
pp. H137-H144 ◽  
Author(s):  
Fan Zhang ◽  
Jun Ichi Kaide ◽  
LiMing Yang ◽  
Houli Jiang ◽  
Shuo Quan ◽  
...  
Keyword(s):  
Pulmonary Arterial Pressure ◽  
Acute Hypoxia ◽  
Isometric Tension ◽  
Vascular Response ◽  
Tension Development ◽  
Pulmonary Vasoconstriction ◽  
Pulmonary Arterial ◽  
Hypoxic Gas Mixture ◽  
Concentration Response Curve ◽  
Krebs Buffer

Pulmonary intralobar arteries express heme oxygenase (HO)-1 and -2 and release carbon monoxide (CO) during incubation in Krebs buffer. Acute hypoxia elicits isometric tension development (0.77 ± 0.06 mN/mm) in pulmonary vascular rings treated with 15 μmol/l chromium mesoporphyrin (CrMP), an inhibitor of HO-dependent CO synthesis, but has no effect in untreated vessels. Acute hypoxia also induces contraction of pulmonary vessels taken from rats injected with HO-2 antisense oligodeoxynucleotides (ODN), which decrease pulmonary HO-2 vascular expression and CO release. Hypoxia-induced contraction of vessels treated with CrMP is attenuated ( P < 0.05) by endothelium removal, by CO (1–100 μmol/l) in the bathing buffer, and by endothelin-1 (ET-1) receptor blockade with L-754142 (10 μmol/l). CrMP increases ET-1 levels in pulmonary intralobar arteries, particularly during incubation in hypooxygenated media. CrMP also causes a leftward shift in the concentration-response curve to ET-1, which is offset by exogenous CO. In anesthetized rats, pretreatment with CrMP (40 μmol/kg iv) intensifies the elevation of pulmonary artery pressure elicited by breathing a hypoxic gas mixture. However, acute hypoxia does not elicit augmentation of pulmonary arterial pressure in rats pretreated concurrently with CrMP and the ET-1 receptor antagonist L-745142 (15 mg/kg iv). These data suggest that a product of HO activity, most likely CO, inhibits hypoxia-induced pulmonary vasoconstriction by reducing ET-1 vascular levels and sensitivity.

Role of airway nitric oxide on the regulation of pulmonary circulation by carbon dioxide

2001 ◽  
Vol 91 (3) ◽  
pp. 1121-1130 ◽  
Author(s):  
Yasushi Yamamoto ◽  
Hitoshi Nakano ◽  
Hiroshi Ide ◽  
Toshiyuki Ogasa ◽  
Toru Takahashi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Arterial Pressure ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
No Synthase ◽  
No Production ◽  
Pulmonary Vasoconstriction ◽  
Exhaled No ◽  
Progressive Hypoxia ◽  
Pulmonary Arterial

The effects of hypercapnia (CO2) confined to either the alveolar space or the intravascular perfusate on exhaled nitric oxide (NO), perfusate NO metabolites (NOx), and pulmonary arterial pressure (Ppa) were examined during normoxia and progressive 20-min hypoxia in isolated blood- and buffer-perfused rabbit lungs. In blood-perfused lungs, when alveolar CO2concentration was increased from 0 to 12%, exhaled NO decreased, whereas Ppa increased. Increments of intravascular CO2levels increased Ppa without changes in exhaled NO. In buffer-perfused lungs, alveolar CO2 increased Ppa with reductions in both exhaled NO from 93.8 to 61.7 (SE) nl/min ( P < 0.01) and perfusate NOx from 4.8 to 1.8 nmol/min ( P < 0.01). In contrast, intravascular CO2 did not affect either exhaled NO or Ppa despite a tendency for perfusate NOx to decline. Progressive hypoxia elevated Ppa by 28% from baseline with a reduction in exhaled NO during normocapnia. Alveolar hypercapnia enhanced hypoxic Ppa response up to 50% with a further decline in exhaled NO. Hypercapnia did not alter the apparent K m for O2, whereas it significantly decreased the V max from 66.7 to 55.6 nl/min. These results suggest that alveolar CO2 inhibits epithelial NO synthase activity noncompetitively and that the suppressed NO production by hypercapnia augments hypoxic pulmonary vasoconstriction, resulting in improved ventilation-perfusion matching.

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